Quick answer

What is NAD+?

NAD+ (nicotinamide adenine dinucleotide) is a coenzyme made by every living cell. Chemically it’s a dinucleotide and contains no amino acids. Scientists study it for its roles in energy metabolism, DNA repair and the biology of ageing. In the UK you’ll see it sold as a supplement, offered by private clinics and supplied as a material for lab research. It has no UK medicine licence.

• A dinucleotide: two nucleotides linked by phosphates, with no amino acids anywhere in it
• Most of the anti-ageing evidence comes from mice; human trials mainly use its precursors, NR and NMN
• UK status: no MHRA licence, and research material is for lab use only

In the UK, one molecule wears three different labels. NAD+ turns up as a capsule on a pharmacy shelf, as a drip in a private clinic and as a dry powder in a research freezer, and each version answers to its own set of rules. The chemistry underneath never changes, and neither does the evidence.

That evidence is deep in some places and thin in others. Cell and mouse work on NAD+ goes back decades, while human trials mostly test its precursors for a few weeks at a time. To keep the two apart, every result below names where it came from (cells, animals or people) before we reach the age-decline argument, the NMN and NR comparison and the law on each supply route.

Apexion supplies NAD+ for laboratory research only. It’s not for human or veterinary use, and the page gives no medical advice. Our Research Use Only notice lists the full terms.

What Is NAD+?

NAD+ is a small helper molecule, or coenzyme, that hundreds of enzymes rely on to complete their reactions. It’s assembled from two nucleotides: one holds a nicotinamide group and the other holds adenine, and two phosphates bridge them. Every cell in every organism makes it.

The story goes back to 1906. The biochemists Harden and Young were studying how yeast juice ferments sugar, and they noticed that boiling part of the extract didn’t destroy a small factor the reaction needed. They called it a “co-ferment”. Working out its full structure took several more decades, and it’s now among the most researched molecules in biochemistry.

Here are the core identity details, checked against PubChem’s NAD+ record:

Field	Detail
Name	Nicotinamide adenine dinucleotide (oxidised form, NAD+)
Type	Coenzyme; a dinucleotide
Formula	C21H27N7O14P2
Molecular weight	~663.4 g/mol (free acid)
CAS number	53-84-9
Apexion format	NAD+ 500mg, a pre-filled research pen prepared to order in the UK for laboratory handling
UK status	Research material; no MHRA marketing authorisation

NAD+ vs NADH

NAD+ and NADH are the same compound in two states. The oxidised form, NAD+, is the “empty” one, ready to pick up electrons, and NADH is the “loaded” reduced form carrying them.

The pair works like a shuttle bus. During glycolysis and the Krebs cycle, enzymes strip electrons from sugars and fats and hand them to NAD+, which becomes NADH. NADH then delivers them to Complex I of the mitochondrial electron transport chain and turns back into NAD+. Those electrons power the pumps that make ATP, the cell’s energy currency.

Its sister molecule, NADP+, has an additional phosphate and mainly supports building reactions and antioxidant defences.

Is NAD+ a Peptide?

No. A peptide forms when amino acids hook together via peptide bonds, and NAD+ contains none of them. Its parts are nicotinamide, two ribose sugars, two phosphates and adenine. Chemists group it with ATP and the nucleotides that make up RNA.

So why do UK peptide suppliers list it? It comes down to logistics. NAD+ arrives as a dry research material, is kept cold and dry like peptide stock, and ends up in the labs that study mitochondria alongside peptides including MOTS-c and SS-31. Suppliers simply follow those orders.

Feature	NAD+	A peptide (MOTS-c)
Made from	Two nucleotides	Sixteen amino acids
Linkage	Pyrophosphate bridge	Peptide bonds
Mass	~663 g/mol	~2,175 g/mol
Has a sequence?	No	Yes (MRWQEMGYIFYPRKLR)
How it’s identified	UV at 260 nm plus mass	Mass plus sequence

Our MOTS-c vs SS-31 vs NAD+ comparison places the three mitochondrial research compounds next to each other, while the What Is MOTS-c? guide covers the peptide in depth.

What Does NAD+ Do in Cells?

NAD+ has two separate jobs. As a redox cofactor, it ferries electrons and returns to the pool, switching back and forth between its two forms without being used up. As a co-substrate, it’s consumed outright by three enzyme families: sirtuins, PARPs and CD38. Most consumer pages blur the two, yet the difference explains nearly every research question about NAD+.

Job 1, the recyclable carrier. The shuttle described above is a closed loop. A cell can run the same NAD+ molecule through it again and again, so this job barely changes the total amount in the cell. The ratio of NAD+ to NADH does move, though, and it tells researchers how hard the energy machinery is working.

Job 2, the consumable fuel. Here NAD+ is spent:

• Sirtuins (SIRT1 to SIRT7) cleave NAD+ to remove acetyl tags from proteins, a step tied to gene regulation and mitochondrial function in cultured cells and rodents.
• PARPs, PARP1 above all, spend NAD+ assembling poly(ADP-ribose) tags that mark damaged DNA for repair.
• CD38 is an enzyme found on and inside many cell types that degrades NAD+ and generates messenger molecules such as cyclic ADP-ribose.

Every one of these reactions frees a nicotinamide and leaves the original NAD+ gone. A 2014 review by Shin-ichiro Imai and Leonard Guarente in Trends in Cell Biology linked dropping NAD+ supply in animal models with weaker sirtuin activity, which is why consumption drives most ageing research.

How Cells Make NAD+

Since Job 2 keeps draining the pool, cells must keep resupplying it. They use three routes:

• De novo synthesis: a long pathway beginning with tryptophan, an amino acid.
• The Preiss-Handler pathway: a shorter route from nicotinic acid, one form of vitamin B3.
• The salvage pathway: recycles the nicotinamide released by those three enzyme families. The enzyme NAMPT turns nicotinamide into NMN, and NMNAT enzymes turn NMN into NAD+. NR enters the same pathway after NRK enzymes convert it to NMN.

Salvage supplies most of the NAD+ in mammalian cells, according to the 2021 review by Covarrubias and colleagues in Nature Reviews Molecular Cell Biology. That’s also where NR and NMN come in, since both are steps on that route.

What Is NAD+ Studied For?

NAD+ turns up in five main research areas. Each one carries a different weight of evidence, so here’s the model behind each:

• Mitochondria and energy production (cells, animals). Researchers track the NAD+/NADH ratio as a readout of how the electron transport chain is running, and study the separate mitochondrial NAD+ pool used by SIRT3, SIRT4 and SIRT5.
• Sirtuin and PARP signalling, DNA repair (in vitro, animals). Lab work examines how NAD+ supply limits sirtuin activity and how heavy DNA damage drains NAD+ through PARP1.
• Ageing and healthspan (mice, worms). Studies in mice and the worm C. elegans test what happens to ageing markers when NAD+ levels are raised or lowered. A 2018 review by Rajman, Chwalek and Sinclair in Cell Metabolism gathers the in vivo animal evidence for NAD-boosting molecules.
• Metabolic research (mice; human precursor trials). Mouse studies look at NAD+ in muscle, liver and fat tissue. In humans, small trials have given NMN or NR and measured metabolic markers. The 2021 NMN trial by Yoshino and colleagues in Science is the best known, and it tested NMN, a precursor.
• Neurodegeneration and cardiovascular models (preclinical). Cell and rodent models of nerve and heart tissue examine how NAD+ supply relates to mitochondrial stress in those cells.

Labs often study NAD+ beside other mitochondrial compounds, such as the peptides in our SS-31 UK research overview.

Does NAD+ Decline With Age?

It depends on the tissue and the method. Rodent studies consistently report lower NAD+ in several older tissues, and some human tissue studies agree. Human whole-blood measurements tell a different story, and a large 2026 study reported stable levels across age groups. The idea is well supported in mice and still open in people.

The “NAD+ falls with age” claim has deep roots. A 2020 review by McReynolds, Chellappa and Baur in Experimental Gerontology summarised the animal and human data pointing to decline. Part of the explanation comes from mice: a 2016 mouse study led by Camacho-Pereira found that CD38 climbs with age, and CD38-knockout animals held on to their NAD+.

Other researchers asked harder questions. A 2021 review by Peluso and colleagues in Nutrients carried the pointed title “Universal Truth or Confounded Consensus?”, noting that differences in tissue, sampling and measurement method could explain some of the reported drops. Vinten and colleagues, writing in Nature Metabolism in 2025, summed up the human picture:

“Evidence for an age-related decline in NAD+ levels in humans has been consistently observed only in a limited number of studies.”

Vinten et al., Nature Metabolism, 2025

A University of Amsterdam team then published, in June 2026, a multi-cohort study titled “Human whole-blood NAD+ levels do not vary with age or lifestyle interventions”. Blood is mostly red cells with no mitochondria, so whole blood may simply not mirror what happens in muscle, skin or brain. You’ll often see a “50% drop by middle age” figure online. We couldn’t trace it to a primary human study, so we’ve left it out.

NAD+ vs NMN vs NR: How the Molecules Differ

NMN and NR are building-block molecules (precursors) that the salvage pathway turns into NAD+. The order runs NR to NMN to NAD+. They differ in size, in how they reach the inside of a cell and in how much human trial data exists for each. Results from NR or NMN studies describe those molecules and shouldn’t be read as NAD+ data.

Feature	NAD+	NMN	NR
Molecular weight	~663.4 g/mol	~334.2 g/mol	~255.3 g/mol (cation); chloride salt ~290.7
Getting into cells	Enters poorly; enzymes on the cell surface (CD38, CD73) break it into smaller pieces first	Debated: often turned into NR before crossing the membrane, with a proposed direct transporter in mouse gut	Taken up by nucleoside transporters, then converted to NMN by NRK1/2
Place in salvage pathway	End product	One step before NAD+ (via NMNAT)	Two steps before NAD+
Human trial data	Very little; small pilot studies	A growing set of small, short trials	The largest set of human trials of the three

Rachel Pojednic, a nutritional biochemist on the Stanford faculty, summed up the cell-entry problem to NPR in May 2026: NAD+ has “no easy door” into the cell from outside. The 2025 Nature Metabolism review pulls together the human precursor studies published to date and compares their tissue-specific effects.

What Does the Research on NAD+ Actually Show?

The strongest NAD+ data come from cells and animals, where the mechanisms are mapped in detail. Human data come mostly from precursor trials of NR and NMN, which reliably raise blood NAD+ markers but show mixed effects on function. No large controlled trials of intravenous NAD+ have been published.

Area	Model	What was reported	Evidence level
Sirtuin activity	Animal models (review)	Lower NAD+ tracks with lower sirtuin activity (Imai & Guarente 2014)	Preclinical
NAD+ loss with age	Mice	CD38 rises with age; CD38-knockout mice keep NAD+ (Camacho-Pereira 2016)	Animal
NAD-boosting molecules	Rodents (review)	Precursors raised tissue NAD+ across many models (Rajman 2018)	Animal
NR in adults	6-week human crossover trial	Blood-cell NAD+ went up with NR (Martens 2018)	Human precursor trial, biomarker
NMN in adults	10-week trial, 25 postmenopausal women	Muscle insulin sensitivity rose vs placebo; other metabolic markers unchanged (Yoshino 2021)	Human precursor trial, small
Blood NAD+ and age	Several human cohorts	Whole-blood NAD+ stable with age; increased after NR (Trętowicz 2026)	Human observational + trial
IV NAD+	Humans	Small pilot studies only (NPR, May 2026)	No controlled trials

Even with those limits, researchers inside the field stay enthusiastic about the science itself. “When you look at the wide breadth of data in the NAD+ sciences, it’s vast and being done by some of the best scientists, truly in the world,” Pojednic told NPR.

Why Is NAD+ Research Debated?

Four questions keep the debate going:

• Mice and humans. Results that look strong in rodents haven’t carried over cleanly into short human trials, and routes and timescales differ between the two.
• The age-decline question. As covered above, tissue and blood data point in different directions.
• Marketing ahead of evidence. NPR’s May 2026 report and a piece in The Conversation both noted that nearly all NAD+ ageing research has come from cells or animals.
• Tumour-cell metabolism. Many tumour cell lines lean heavily on NAMPT and the salvage pathway, as a 2022 review in Cancers describes. That leads some researchers to ask whether raising NAD+ could also support those cells. It remains a theoretical question, untested in controlled studies.

Is NAD+ Legal in the UK?

Yes. NAD+ can be bought, sold and held lawfully in the UK (checked October 2026). It doesn’t appear under the Misuse of Drugs Act, and the MHRA hasn’t granted it a marketing authorisation. That second point carries real weight: no seller can present NAD+ as a treatment for any condition. Which rules apply depends on how it’s supplied.

Three regulatory routes exist:

• Research material. Supplied to labs for in vitro and analytical work, with nothing said about use in people. That’s the route Apexion uses.
• Food supplements. These come under the Food Standards Agency’s novel-food rules. The FSA register lists nicotinamide riboside chloride as an authorised novel food (NOVEL-96) for England, Scotland and Wales. A search of the same register for “nicotinamide” returned no NMN entry when we checked on 17 October 2026.
• Clinic services. Private clinics that offer NAD+ fall under medicines and advertising rules. In February 2025, the Observer reported that the MHRA had taken action against seven clinics, requiring them to remove treatment claims.

So what makes something a medicine in law? The MHRA explains its test in Guidance Note 8, updated in August 2026: the MHRA classes a product as medicinal either by “presentation” (the claims made for it) or by “function” (what it does in the body). For how UK law handles research compounds generally, see our guide to whether peptides are legal in the UK.

Can You Buy NAD+ in the UK?

Yes, through three distinct regulatory categories. Research suppliers sell it into laboratories as a reagent, for lab use only. Supplement retailers sell precursors such as NR as food, within the novel-food rules. Clinics operate under medicines and advertising law. Each category carries its own obligations, and research material belongs to none of the other two. Our Research Use Only notice spells out the conditions for research supply.

Is NAD+ a Licensed Medicine in the UK?

No. A search of the MHRA Products database shows no marketing authorisation for NAD+ (checked October 2026). The Observer’s 2025 report also noted that NAD+ isn’t approved for use on the NHS. With no licence, it can’t be advertised as a treatment for any disease.

Is NAD+ Being Researched in the UK?

Yes, mostly through precursor studies. The NHS Health Research Authority holds a research summary for a Cambridge study, “To study the role of nicotinamide riboside in inducing mitochondrial biogenesis”, with Professor Patrick Chinnery as the contact. It received a favourable ethics opinion in May 2017 (REC reference 17/EE/0120). Its ClinicalTrials.gov record (NCT03432871) lists it as completed.

A second HRA entry, NADMet, describes a University of Birmingham crossover study in healthy older men. It looked at whether NR changes how skeletal muscle handles energy. Both studies tested NR, a precursor, so neither reports on NAD+ itself.

How to Verify Research-Grade NAD+

A batch’s certificate of analysis (COA) is the one document that shows what a specific lot contains. For NAD+, the checks differ from a peptide COA, because there’s nothing like a residue sequence to confirm. Here’s what a solid one shows:

Check	Look for
Lot number	Same lot code as printed on the item received
HPLC purity	UV detection at ~260 nm (the adenine ring), with the method stated
Identity	Mass spectrometry consistent with ~663.4
Breakdown peaks	Nicotinamide and ADP-ribose listed with amounts
Lab and date	An independent lab named, with an analysis date
Form	Free acid or sodium salt stated, since this changes the weight

Red flags include dosing charts, anti-ageing claims, a certificate missing its lot code, and any “NAD+ peptide” listed with an amino-acid sequence. That last one is a giveaway, because NAD+ has no sequence.

Apexion’s research materials carry typical HPLC-verified purity of ≥98%, each batch is tracked, and the NAD+ product page publishes batch results once they’re verified. Our batch verification guide, the quality assurance page and the Quality and Batch Verification hub explain how to check a lot.

How Should NAD+ Be Stored?

Dry NAD+ lasts longest cold, dry and shielded from light. The usual long-term setting is −20 °C. Sigma-Aldrich’s β-NAD product information notes that the powder is highly hygroscopic, meaning it pulls water from the air. Moisture and heat both speed up the break at the nicotinamide-ribose bond.

In solution, NAD+ is far less stable. It degrades fast in alkaline conditions and at raised temperatures, and neutral to slightly acidic solutions hold up best. Phosphate and carbonate buffers also speed up its breakdown, according to the same Sigma data. Our research storage and handling guide goes deeper on cold-chain basics.

Frequently Asked Questions

The Bottom Line

To sum up, this dinucleotide coenzyme gets recycled by every cell as an electron carrier and spent as fuel by three enzyme families. Cell and animal research on it runs deep. Human data mostly come from NR and NMN trials, and the age-decline story looks different depending on what’s measured. Selling and holding it is lawful in the UK, no medicine licence exists for it, and the rules depend on how it’s supplied.

For lab work, see the NAD+ 500mg research material and its batch documentation, or browse the full mitochondrial research range.

For laboratory research use only. Not for human or veterinary use. Apexion Biolabs supplies NAD+ as a reagent for in vitro and analytical work. The article gives general information only. It isn’t medical advice and contains no dosing or administration guidance. The Research Use Only notice has the full terms.

Sources

• Harden A, Young WJ (1906). The alcoholic ferment of yeast-juice. Proceedings of the Royal Society B.
• Imai S, Guarente L (2014). Trends in Cell Biology, review of NAD+ and sirtuins.
• Covarrubias AJ et al. (2021). NAD+ metabolism and its roles in cellular processes during ageing. Nature Reviews Molecular Cell Biology.
• Rajman L, Chwalek K, Sinclair DA (2018). Cell Metabolism, review of in vivo evidence for NAD-boosting molecules.
• Camacho-Pereira J et al. (2016). Cell Metabolism, CD38 and age-related NAD+ decline in mice.
• McReynolds MR, Chellappa K, Baur JA (2020). Age-related NAD+ decline. Experimental Gerontology.
• Peluso A et al. (2021). Age-dependent decline of NAD+: universal truth or confounded consensus? Nutrients.
• Trętowicz MM et al. (2026). Human whole-blood NAD+ levels do not vary with age or lifestyle interventions. Nature Metabolism.
• Vinten KT et al. (2025). NAD+ precursor supplementation in human ageing: clinical evidence and challenges. Nature Metabolism.
• Yoshino M et al. (2021). Science, randomised NMN trial.
• Martens CR et al. (2018). Nature Communications, nicotinamide riboside crossover trial.
• PubChem: Nicotinamide adenine dinucleotide (CID 5892).
• MHRA. Guidance Note 8: A guide to what is a medicinal product (August 2026).
• MHRA Products database.
• Food Standards Agency: Nicotinamide riboside chloride, NOVEL-96.
• Health Research Authority: The role of nicotinamide riboside in mitochondrial biogenesis.
• The Observer / The Guardian (23 February 2025). “It’s not ethical and it’s not medical”: how UK rehab clinics are cashing in on NAD+.
• NPR (11 May 2026). Marketers say NAD+ pills and infusions can boost longevity. What’s the evidence?
• World Anti-Doping Agency: 2026 Prohibited List.

Quick answer

What is 5-Amino-1MQ?

5-Amino-1MQ (5-amino-1-methylquinolinium) is a small synthetic molecule that blocks an enzyme called NNMT. Researchers have studied it in cell cultures and in mice, mainly for fat-cell metabolism and muscle ageing. It has never been tested in a registered human trial, and it remains unapproved everywhere.

• A quinolinium compound, built without any amino acids
• Every published finding comes from cell or animal work
• UK: uncontrolled, unlicensed and supplied for research only

Half a dozen papers make up most of the published record on 5-Amino-1MQ, and nearly all of them come from one lab in Galveston, Texas. For a compound with this much online attention, that’s a strikingly short reading list.

What the papers lack in number, they make up for in focus. They all chase one enzyme, NNMT, which operates where NAD+ recycling meets the cell’s methylation machinery. We’ll follow that enzyme from the chemistry to the mouse data, tag every result with its model (enzyme assay, cell culture or mouse) and finish with UK law as it stood in October 2026.

5-Amino-1MQ from Apexion is a laboratory research material, unsuitable for human or veterinary use. Nothing here counts as medical advice; read the Research Use Only notice for every condition of supply.

What Is 5-Amino-1MQ?

5-Amino-1MQ is a quinolinium compound: a pair of fused aromatic rings with a methyl attached to the ring’s nitrogen atom and an -NH₂ group at carbon 5. That nitrogen holds a fixed positive charge, yet the molecule still passes through cell membranes. Charged molecules rarely manage that, which is why it’s popular for cell experiments.

The name spells out the structure. “1MQ” is 1-methylquinolinium, the parent scaffold, and “5-amino” marks the added amine. That one change made the difference in the lab: in the 2018 permeability tests, the parent 1-MQ and the NNMT product 1-MNA showed no passive movement across an artificial membrane, while 5-Amino-1MQ crossed readily.

It came out of a University of Texas Medical Branch programme led by Stanley Watowich. Harshini Neelakantan and colleagues first described the methylquinolinium series in a 2017 structure-activity study in the Journal of Medicinal Chemistry. The team’s 2018 Biochemical Pharmacology paper then reported that amine-substituted versions crossed membranes well in two lab models and inhibited NNMT selectively.

PubChem (CID 950107) supplies the identifiers below:

Field	Detail
Name	5-amino-1-methylquinolinium (5-Amino-1MQ)
Type	Quinolinium small molecule
Cation	C10H11N2+ · ~159.2 g/mol
Common salt	Iodide, C10H11IN2 · ~286.1 g/mol
CAS	685079-15-6 (cation) · 42464-96-0 (iodide)
Apexion format	5-Amino-1MQ 50mg, a pre-filled 50mg research pen, made to order in the UK and prepared for laboratory handling
UK status	Research material; not controlled, no medicine licence

Is 5-Amino-1MQ a Peptide?

No. Every peptide is made of amino-acid residues held together by peptide bonds, and 5-Amino-1MQ contains neither. It’s one rigid ring system weighing about 159 g/mol as the cation.

Peptide shops in the UK list it because the metabolism labs that buy mitochondrial peptides order it too. The contrast with MOTS-c, a real peptide, is stark:

Feature	5-Amino-1MQ	MOTS-c
Chemical class	Small molecule	Peptide
Structure	Fused quinoline rings	16-residue amino-acid chain
Mass	~159 g/mol (cation)	~2,175 g/mol
Made by	Organic synthesis	Solid-phase peptide synthesis
Target studied	The enzyme NNMT	AMPK signalling

Our MOTS-c Peptide UK overview covers the peptide side.

How Does 5-Amino-1MQ Work? The NNMT Pathway

NNMT (nicotinamide N-methyltransferase) takes a methyl group from SAM (S-adenosylmethionine, the chief methyl donor in cells) and attaches it to nicotinamide. The product, 1-methylnicotinamide (1-MNA), leaves the cell’s recycling loop. 5-Amino-1MQ blocks NNMT, so in lab models more nicotinamide and SAM stay available.

That single reaction connects two busy systems: NAD+ recycling and cellular methylation. Here’s how the research chain fits together, and the model tested at each step:

1. NNMT rises in obese mice (mouse, gene knockdown). Kraus and colleagues (2014) in Nature reported higher NNMT in fat and liver tissue of obese mice. Reducing NNMT with antisense knockdown raised energy expenditure. This study used no 5-Amino-1MQ.
2. Blocking NNMT spares nicotinamide (biochemistry). With the methylation route closed, nicotinamide can return to the salvage pathway that rebuilds NAD+.
3. NAD+ and SAM rise in treated fat cells (in vitro). In cultured adipocytes, the 2018 Neelakantan study found that the inhibitors lowered 1-MNA, raised intracellular NAD+ and SAM, and suppressed lipogenesis (fat building).
4. Links to SIRT1 and energy use (mouse). Kraus’s team described NNMT as a regulator of NAD+-dependent SIRT1 signalling, and their knockdown mice burned more energy.

On selectivity, the 2018 paper reported that the methylquinolinium compounds didn’t inhibit related SAM-dependent methyltransferases or enzymes of the NAD+ salvage pathway in enzyme assays. In those assays, 5-Amino-1MQ blocked NNMT at around 1 µM (its IC₅₀, the concentration that halves enzyme activity). The team suggested the quinolinium ring docks in NNMT’s nicotinamide-binding pocket, which would explain why enzymes built around the SAM site were left alone.

Is 5-Amino-1MQ the Same as NAD+?

No. NAD+ is a natural coenzyme present in all cells, while 5-Amino-1MQ is a synthetic enzyme inhibitor. The link is indirect: by blocking NNMT, 5-Amino-1MQ affects how much nicotinamide cells can recycle into NAD+. Inside the cell, nicotinamide reaches a fork. NAMPT can send it back into the salvage pathway towards NMN and then NAD+, or NNMT can methylate it into 1-MNA, which cells excrete. Closing the NNMT branch leaves more nicotinamide for the NAMPT branch, which matches the higher NAD+ seen in treated fat cells. Our MOTS-c vs SS-31 vs NAD+ comparison covers NAD+ in more detail.

What Is 5-Amino-1MQ Studied For?

Work on 5-Amino-1MQ and its target clusters into four areas, and only the first three involve the compound itself:

• Fat-cell metabolism (in vitro). Studies in 3T3-L1 adipocytes, a standard mouse fat-cell line, measure 1-MNA, NAD+, SAM and lipogenesis after NNMT inhibition.
• Diet-induced obesity (mouse). Mice kept on a high-fat diet are used to track body composition, fat tissue and blood lipids during treatment.
• Muscle stem-cell ageing (aged mice). A 2019 study by Neelakantan and colleagues gave an NNMT inhibitor to 24-month-old mice after a controlled muscle injury and measured muscle stem-cell activity and fibre regrowth. Treated mice showed more stem-cell division and fusion, larger regrowing fibres and stronger muscle contraction than controls. The same paper repeated parts of the work in C2C12 muscle cells.
• NNMT in cancer and heart research (reviews, context only). A 2013 Nature Chemical Biology study by Ulanovskaya and colleagues described NNMT as a “metabolic methylation sink” in cancer cells. A 2025 Biomolecules review examined NNMT in cardiovascular research. Neither tested 5-Amino-1MQ.

5-Amino-1MQ in Obesity Research: What Mouse Studies Show

Three mouse studies from the same research group carry this topic. Each measured body composition, tissue weights and blood markers in mice kept on controlled diets, so the readouts are physical measurements taken in animals:

• Neelakantan 2018: diet-induced obese mice given an NNMT inhibitor showed lower body weight and white fat mass, smaller fat cells and lower plasma cholesterol than untreated controls. Food intake didn’t change.
• Sampson 2021 in Scientific Reports: obese mice switched to a lean diet were compared with and without NNMT inhibition, and the combined group reached a body composition close to that of lean-diet control mice.
• Babula 2024 in Diabetes, Obesity and Metabolism: a 28-day study in diet-induced obese mice tracked body composition, liver tissue and blood markers. The team also mapped how the compound spread through mouse plasma and tissues.

All three are mouse studies. No human data exist for any of these measures.

What Does the Research on 5-Amino-1MQ Actually Show?

The published evidence is a small set of enzyme, cell and mouse studies, almost all from one University of Texas research group. Those studies consistently report NNMT inhibition and metabolic changes in mice. No study has given 5-Amino-1MQ to people, so its effects in humans are unknown.

Study	Year	Model	What was measured	Evidence level
Kraus et al.	2014	Mice (NNMT knockdown)	NNMT levels, energy expenditure, SAM and NAD+	Animal; no 5-Amino-1MQ
Neelakantan et al.	2017	Enzyme assays	Potency across quinolinium analogues	Biochemical
Neelakantan et al.	2018	Membrane models, adipocytes, obese mice	Permeability, selectivity, metabolites, body composition	In vitro + animal
Neelakantan et al.	2019	Aged mice, C2C12 cells	Muscle stem-cell activity, fibre size, contractile force	Animal + in vitro
Sampson et al.	2021	Obese mice on a lean diet	Body composition, liver fat, fat-tissue metabolites	Animal
Babula et al.	2024	Obese mice	Body composition, glucose handling, liver tissue, tissue distribution	Animal

Three things limit how far mouse results travel:

• Metabolic rate. Mice burn energy many times faster per gram of body weight than humans do, which changes how metabolic interventions play out.
• Diet models. Diet-induced obesity in young mice develops over weeks and differs from human weight gain over years.
• Exposure. Mouse pharmacokinetics can’t predict how the compound would behave in people, and no human pharmacokinetic study exists.

Replication is the other open question. Five of the six studies above share senior authors, and the 2021 paper discloses that Watowich founded Ridgeline Therapeutics, where Neelakantan works. Independent labs haven’t yet published matching 5-Amino-1MQ results, which is normal for a young compound and is the next step the field needs.

Has 5-Amino-1MQ Been Tested in Humans?

No. A ClinicalTrials.gov search for “5-amino-1MQ”, “5-amino-1-methylquinolinium” and “NNMT inhibitor” returned no registered studies as of our 17 October 2026 search. That means there’s no human safety, tolerability or pharmacokinetic data for the compound.

That absence covers the basics researchers would want first: how the compound is absorbed, how long it stays in circulation, how it’s broken down and cleared, and whether it interacts with other substances. The only distribution data so far come from the 2024 mouse study, which tracked the compound in mouse plasma, fat, muscle and liver. Those figures describe mice and can’t be scaled to people.

For context, cancer-biology reviews flag NNMT’s role in some tumour cells as an open research question, since the enzyme reshapes methylation in those cells. That work concerns the enzyme itself and doesn’t involve 5-Amino-1MQ.

The compound holds no approval from the MHRA, the US FDA or the European Medicines Agency.

Is 5-Amino-1MQ Legal in the UK?

Yes, so long as it’s sold and held as lab research material. As of October 2026, 5-Amino-1MQ is absent from controlled-drug schedules, it has never held a UK medicine licence, and no seller may present it for human use. Its status rests on three pieces of law and one MHRA guidance note.

Law or guidance	What it covers	Position for 5-Amino-1MQ
Human Medicines Regulations 2012	Licensing and supply of medicines	No marketing authorisation; can’t be marketed as medicinal
MHRA Guidance Note 8 (August 2026)	When a product is classed as a medicine	Claims made for a product can make it medicinal by “presentation”
Misuse of Drugs Act 1971	Controlled drugs	Not listed
Psychoactive Substances Act 2016	Substances that act on the central nervous system	No published work describes it as psychoactive

No UK law names 5-Amino-1MQ directly. Its status rests on the lists it’s absent from and on how it’s offered for sale. Guidance Note 8 is the reason research suppliers stick to identity, purity and storage details in their listings: a seller that adds health claims risks turning the same compound into an unlicensed medicine in law. The rules across research compounds are set out in Are Peptides Legal in the UK?

Can You Buy 5-Amino-1MQ in the UK?

Yes. UK research suppliers sell it under research-use-only conditions. It isn’t stocked by pharmacies, and there’s no prescription route, because no licensed product contains it. Capsules or other formats marketed for consumption fall outside research supply. Our Research Use Only notice explains the conditions of sale.

Is 5-Amino-1MQ FDA Approved?

No. Neither the FDA (US), the MHRA (UK) nor the EMA (EU) has approved 5-Amino-1MQ. No approved medicine anywhere contains it, and no company has registered a human trial.

Is 5-Amino-1MQ Banned in Sport?

5-Amino-1MQ isn’t named on the WADA Prohibited List. The list’s S0 section, “Non-Approved Substances”, covers any pharmacological substance not addressed elsewhere on the list that no national health regulator has cleared for therapeutic use in humans. Such substances are banned in and out of competition. The list is applied in the UK by UK Anti-Doping.

How to Verify Research-Grade 5-Amino-1MQ

The COA (certificate of analysis) for a batch ought to confirm identity, purity and the exact salt form of the lot in hand. Salt form deserves special attention with this compound, because it changes both the molecular weight and how much active cation each milligram holds.

What to check	Why
Lot number	Ties the report to the item received
HPLC purity, with method	Shows the share of the main compound
MS identity near 159.2	Confirms the cation; the counter-ion separates in the spectrometer
¹H-NMR (ideal)	Confirms the ring structure and methyl position
Salt form stated	Iodide or chloride changes the weight per mole
Independent lab and date	Lets you trace and verify the result

Mass spectrometry for this compound is simpler than for a peptide. Run in positive mode, the cation appears as one main signal near m/z 159.09 with no added proton, and the iodide doesn’t show up in that spectrum at all. NMR adds a second check, because the N-methyl group and the ring protons give a distinctive pattern that a mislabelled quinoline wouldn’t match.

Walk away from any listing that shows dosing charts, fat-loss claims or capsules marketed for consumption. The same goes for a certificate with no lot number, or one that gives this non-peptide an amino-acid “sequence”.

Batches from Apexion are tracked, with purity typically ≥98% by HPLC, and results for this compound go up on its product page as soon as they’re verified. To check a lot yourself, use the batch verification guide, the quality assurance page or the Quality and Batch Verification hub. For format differences, see Peptide Pen vs Vial.

How Should 5-Amino-1MQ Be Stored?

As a solid, 5-Amino-1MQ keeps best cool, dry and dark, with −20 °C for long-term holding. Sigma-Aldrich’s iodide product sheet gives −20 °C and describes the powder as faint red to dark brown, so colour on its own isn’t a sign of a problem. Aromatic amines can darken with light and air over time, which is why dark, sealed storage is the default. Pens should be refrigerated and handled according to the batch sheet. Cold-chain basics are in our research storage and handling guide.

Frequently Asked Questions

The Bottom Line

5-Amino-1MQ is a membrane-permeable quinolinium molecule that inhibits NNMT. Its evidence base is a tight cluster of enzyme, cell and mouse studies, mostly from one group, and it has never been tested in a registered human trial. In the UK it’s lawful to hold as a research material, uncontrolled and unlicensed.

Researchers can review the 5-Amino-1MQ 50mg specification and batch documentation before ordering.

For laboratory research use only. Not for human or veterinary use. Apexion Biolabs sells 5-Amino-1MQ solely for bench and analytical studies. This overview is educational, offers no medical advice and includes no dosing or administration information. Conditions of sale are in the Research Use Only notice.

Sources

• Neelakantan H et al. (2017). Structure-activity relationship for small molecule inhibitors of nicotinamide N-methyltransferase. Journal of Medicinal Chemistry.
• Neelakantan H et al. (2018). Selective and membrane-permeable small molecule inhibitors of NNMT. Biochemical Pharmacology.
• Neelakantan H et al. (2019). Biochemical Pharmacology, NNMT inhibitor and aged muscle stem cells in mice.
• Sampson CM et al. (2021). Scientific Reports, NNMT inhibition with a reduced-calorie diet in mice.
• Babula et al. (2024). Diabetes, Obesity and Metabolism, NNMT inhibition in diet-induced obese mice.
• Kraus D et al. (2014). Nicotinamide N-methyltransferase knockdown in mice. Nature.
• Ulanovskaya OA et al. (2013). NNMT and the metabolic methylation sink. Nature Chemical Biology.
• Liu JR et al. (2021). Review of NNMT in metabolic research. BioMed Research International (PMC8337113).
• Jawaria et al. (2025). Review of NNMT in cardiovascular research. Biomolecules (PMC12467181).
• PubChem: 5-Amino-1-methylquinolinium, CID 950107.
• ClinicalTrials.gov search, “5-amino-1MQ” (checked 17 October 2026).
• Human Medicines Regulations 2012.
• MHRA Guidance Note 8 (August 2026).
• Misuse of Drugs Act 1971.
• Psychoactive Substances Act 2016.
• World Anti-Doping Agency: 2026 Prohibited List.
• UK Anti-Doping.

Quick answer

What is TB-500 peptide?

TB-500 is a synthetic 7-amino-acid fragment, Ac-LKKTETQ, copied from the part of thymosin beta-4 that binds actin. Scientists study it in cell and animal tissue-repair models. Most human trials so far have used full-length thymosin beta-4, and the first trial of the fragment only began in 2026. No regulator has approved it, and in the UK it’s a research material only.

• TB-500 is a fragment, not full-length thymosin beta-4
• The evidence is mostly cell and animal work
• UK: uncontrolled and unlicensed, supplied for research use only; WADA names it under S2

A search for “TB-500 peptide UK” brings up page after page of shop listings. Many of them use “TB-500” and “thymosin beta-4” as if they meant the same thing. They don’t. One is a 7-residue fragment and the other a 43-residue protein, and that mix-up runs right through the research, the trials and even some product labels.

This guide untangles it. We cover what TB-500 is, how it differs from its parent protein, how it behaves in lab models, what the research and trials show, UK law, sport and racing rules, and how a certificate reveals which molecule you’ve actually got. Each result carries two labels, the model and the compound tested, so you always know whether a result belongs to TB-500 or to full thymosin beta-4.

Apexion sells TB-500 to laboratories as a research reagent. It is never intended for people or animals, and this page offers no medical advice. Conditions of sale: Research Use Only notice.

What Is TB-500 Peptide?

TB-500 is a synthetic chain of seven amino acids, leucine-lysine-lysine-threonine-glutamate-threonine-glutamine, and the leucine at its start carries an acetyl cap. It mirrors residues 17 to 23 of thymosin beta-4, the stretch that grips actin. In short, TB-500 takes the protein’s best-known working part and leaves the other 36 residues behind.

The name started life as a product label, not a scientific term. When Hong Kong Jockey Club chemists analysed a veterinary preparation sold as TB-500 in 2012, they found its key ingredient was LKKTETQ “with artificial acetylation of the N-terminus”. Anti-doping chemists confirmed the same fragment that year, and the definition stuck.

Identifier	Value
Name	TB-500 (thymosin beta-4 fragment 17 to 23, acetylated)
Sequence	Ac-LKKTETQ (Ac-Leu-Lys-Lys-Thr-Glu-Thr-Gln)
Length	7 amino acids
Formula	C38H68N10O14 (PubChem CID 62707662)
Molecular weight	~889.0 g/mol
Source protein	Thymosin beta-4, 43 amino acids
CAS number	No single number is consistently assigned to the fragment; 77591-33-4 belongs to full-length thymosin beta-4
Form at Apexion	Pre-filled 10mg research pen, filled to order in Britain
UK position	Sold for research; unlicensed and absent from drug schedules

For lot-level identity data, open the TB-500 10mg specification and COA.

When Was Thymosin Beta-4 Discovered?

Thymosin beta-4 came out of thymus research in the United States. Allan Goldstein’s group had been separating a calf-thymus extract known as thymosin fraction 5, and in 1981 Low, Hu and Goldstein published the complete amino-acid sequence of bovine thymosin beta-4 in PNAS.

Its link to actin came a decade later. In 1991, Daniel Safer and colleagues showed that thymosin beta-4 was the same molecule as an actin-sequestering peptide they’d been studying. Later work narrowed that activity down to the LKKTETQ stretch.

TB-500 vs Thymosin Beta-4: What’s the Difference?

Thymosin beta-4 is a natural protein of 43 amino acids, weighing about 4,963 g/mol and made by most mammalian cell types, whereas TB-500 reproduces just seven of those amino acids, weighing about 889 g/mol. One is a whole protein, the other a single motif from it.

Feature	TB-500	Thymosin beta-4
Origin	Synthetic fragment	Natural protein, also made synthetically or recombinantly
Length	7 amino acids	43 amino acids
Molecular weight	~889 g/mol	~4,963 g/mol (PubChem CID 45382195)
CAS	Not consistently assigned	77591-33-4
Human trials	One Phase 1/2 study, recruiting since 2026	Several, mainly as eye drops (RGN-259)
WADA listing	Named as a derivative under S2	Named under S2

Thymosin beta-4 isn’t the only peptide researchers compare TB-500 with. Our BPC-157 vs TB-500 comparison covers the other common pairing.

How Does TB-500 Work?

In lab models, the LKKTETQ motif binds G-actin, the loose single units that cells assemble into their actin scaffolding. That binding shapes how cells change shape and move. Animal studies of thymosin beta-4 also link it to blood-vessel formation and to inflammatory signalling.

Here’s what has been seen, and where:

• G-actin binding (biochemical studies, thymosin beta-4). Thymosin beta-4 holds single actin units so they can’t join growing filaments, which lets a cell keep a ready supply for rapid rebuilding. Safer’s 1991 work established this role.
• Cell movement (cell studies, both compounds). Philp and colleagues (FASEB Journal, 2003) tested full thymosin beta-4 against its fragments in endothelial cell migration assays. The seven-amino-acid actin motif and the full protein “display near-identical activity”, while peptides missing any part of the motif were inactive.
• Blood-vessel formation (cell and tissue assays, both compounds). The same paper found the motif essential for vessel sprouting in chick aortic rings, a classic angiogenesis assay.
• Inflammatory signalling (cell studies, thymosin beta-4). In cultured eye-surface cells, Sosne and colleagues (2007) reported that thymosin beta-4 dampened NF-κB, a switch for inflammatory genes.

One 2024 finding adds a twist. A team at the Korea Institute of Science and Technology tracked how TB-500 breaks down in rats and in lab enzyme systems. In their fibroblast migration assay, a shorter breakdown product, Ac-LKKTE, was active while the parent peptide wasn’t. The authors suggest some activity credited to TB-500 may come from its metabolite. That’s a single cell study, and it’s a reason every result needs its exact compound named.

What Is TB-500 Studied For?

TB-500 and thymosin beta-4 are research tools for studying how cells move, attach and rebuild their structure. Cell cultures and animal tissue-repair models make up the bulk of it. Human data come almost entirely from full-length thymosin beta-4.

Here are the areas, with model and compound for each:

• Dermal repair models (animal, thymosin beta-4). Malinda and colleagues (1999) studied dermal repair models in rats, tracking how new tissue formed over time.
• Cardiac tissue models (mice, thymosin beta-4). Bock-Marquette and colleagues (Nature, 2004) found thymosin beta-4 formed a complex with the enzyme integrin-linked kinase and activated the survival kinase Akt in mouse cardiac cells.
• Eye-surface studies (humans, thymosin beta-4). The longest-running human programme uses thymosin beta-4 eye drops, coded RGN-259, covered in the research section below.
• Tendon and muscle models (animal, mostly thymosin beta-4). These are the thinnest area. A 2026 scoping review found tendon, ligament and muscle studies “comparatively sparse”.

What Does TB-500 Do in Lab and Animal Studies?

In cell studies, the TB-500 motif binds actin and matches full thymosin beta-4 in endothelial migration and vessel-sprouting assays (Philp 2003). In rats, TB-500 is broken down quickly into shorter pieces, which a 2024 study measured in urine for up to 72 hours. Animal tissue-repair studies have mostly used the full protein, so they say little about the fragment on its own.

What Does the Research on TB-500 Actually Show?

There’s plenty of cell and animal data, but most of it is on full thymosin beta-4. Human trials have largely tested the full protein too, mainly RegeneRx’s RGN-259 eye drops. A trial of the TB-500 fragment itself opened in 2026 and hasn’t reported.

The clearest map of the field comes from a 2026 scoping review in Applied Sciences by McGuire, Hughes, Maak and Cushman. Searching PubMed, Europe PMC and ClinicalTrials.gov through March 2026, the authors concluded that “most studies evaluated TB4 rather than TB-500.” They also noted the literature “supports the popular interest in several repair-related pathways” while remaining largely preclinical.

Research area	Model	Compound tested	Reported finding	Level of evidence
Actin binding	Biochemical	Thymosin beta-4	Holds single actin units (Safer 1991)	Preclinical
Cell migration and vessel sprouting	Cells, chick aortic rings	Both	Motif matched full protein (Philp 2003)	Preclinical
Metabolism	Rats, enzyme systems	TB-500	Rapid breakdown; one metabolite active in cells (Rahaman 2024)	Preclinical
Cardiac tissue	Mice	Thymosin beta-4	ILK and Akt activation (Bock-Marquette 2004)	Preclinical
Eye surface	Humans	Thymosin beta-4 (RGN-259)	Phase 2 and 3 trials; Phase 3 still recruiting	Human trials, protein only
Cardiovascular biomarkers	Humans	TB-500	Phase 1/2 study recruiting	Human trial, no results

The RegeneRx programme. RegeneRx and its partner ReGenTree have run several trials of RGN-259, a thymosin beta-4 eye drop, including Phase 3 ARISE studies such as NCT02597803 and NCT03937882. Another Phase 3 study, NCT05555589, was still listed as recruiting in October 2026. A second formulation, RGN-352, was planned for cardiac research, but its Phase 2 study (NCT01311518) was withdrawn before enrolling anyone. None has led to an approval.

The first fragment trial. Hudson Biotech registered a randomised, placebo-controlled Phase 1/2 study of TB-500 itself, NCT07487363, described as “Thymosin Beta 4 17-23 Fragment”. Enrolment of adult volunteers opened in February 2026, and the study tracks cardiovascular blood biomarkers.

Why animal results don’t transfer neatly. Most of the positive animal work used the full protein, not the fragment. Animal models also run under controlled diets, genetics and housing. And the 2024 metabolism study shows the fragment is broken down fast, so what reaches a tissue may not be TB-500 at all.

Is TB-500 Legal in the UK?

Yes, provided it’s handled as a lab reagent. TB-500 appears on no controlled drug schedule, and no MHRA licence has been issued for it, so British law forbids selling or promoting it for people to take.

Three laws set the limits (checked October 2026):

Legislation	Scope	TB-500’s position
Human Medicines Regulations 2012	Regulation 2 sets the medicinal-product test; regulation 46 bans selling or supplying unlicensed medicines	With no marketing authorisation, it may not be marketed as a medicine
Misuse of Drugs Act 1971	Lists class A, B and C drugs	Absent from every class
Psychoactive Substances Act 2016	Targets substances that change mood or mental functioning	No such effect on record

The subtler rule appears in MHRA Guidance Note 8. The MHRA can treat a product as a medicine purely because of how it’s presented. That covers claims on a website, testimonials, social posts and even a product name. A “TB-500” listing that promises any effect in people is presenting a medicine, research label or not.

The MHRA is actively watching this market. In April 2026 it opened an investigation into UK clinics promoting unregulated peptides. Our guide are peptides legal in the UK puts TB-500 alongside other common peptides.

Can You Buy TB-500 in the UK?

British research suppliers carry it under research-use-only terms. No pharmacy stocks it, since it holds no medicine licence. Imports are a separate risk: Border Force can seize unlicensed medicines arriving from abroad. Our conditions of sale: see the Research Use Only notice.

Do You Need a Prescription for TB-500?

No prescription route exists for TB-500 in the UK, through the NHS or privately. Prescribing requires a licensed product or a recognised route for unlicensed medicines, and TB-500 fits neither. Research suppliers deal with laboratories.

Do US Rule Changes Affect TB-500 in the UK?

No. On 23 July 2026, an advisory committee to the US FDA backed, by eight votes to six, a proposal to add BPC-157, KPV and TB-500 to the list of substances American compounding pharmacies may use, PharmExec reported. That recommendation doesn’t bind the agency, and TB-500 still holds no FDA approval. UK law is set by the MHRA and Parliament, so a US committee vote changes nothing here.

Is TB-500 Banned in Sport?

Yes. WADA’s Prohibited List places thymosin-β4 and its derivatives, naming TB-500 as an example, in class S2 under growth factors and growth factor modulators. S2 bans have no off-season, and the 2027 list, which applies from 1 January 2027, carries the same class.

In Britain, UK Anti-Doping (UKAD) enforces it, and the full text is on WADA’s Prohibited List page.

Anti-doping labs have researched how to find it. The Korea Institute of Science and Technology’s doping control centre mapped its breakdown products for testing, and its short-lived pieces are what labs look for.

Racing runs a parallel system. The Hong Kong Jockey Club’s laboratory published a method for detecting TB-500 in horse urine and plasma back in 2012. In Britain, racing’s prohibited-substance rules are set separately by the British Horseracing Authority.

TB-500 vs BPC-157

TB-500 and BPC-157 are often mentioned together, but they’re unrelated. TB-500 comes from a natural actin-binding protein. BPC-157 is a synthetic 15-residue peptide drawn from a longer natural protein, and the two share no sequence at all. In lab models they’re studied through different pathways: actin handling for TB-500, and growth-factor and nitric-oxide signalling for BPC-157.

For the full side-by-side, see BPC-157 vs TB-500, and for BPC-157 alone, the BPC-157 UK guide. Apexion also lists the BPC-157 and TB-500 20mg blend and the KLOW mix. For how multi-peptide research materials are documented, see peptide stacks explained.

How to Verify Research-Grade TB-500

Look first at the mass on the batch COA, because it reveals which molecule the pen holds. A reading near 889 means the TB-500 fragment. A reading near 4,963 means full-length thymosin beta-4. Anything else needs an explanation before the batch goes near an experiment.

The raw LC-MS spectrum adds a second check. Electrospray gives each molecule one or more extra protons, and every charge state lands at a predictable position on the mass-to-charge scale. A small peptide like the fragment shows just one or two peaks. A 43-residue protein spreads into a ladder of several. So the shape of the spectrum, not just the headline number, tells the two apart.

Item	Pass if
Lot match	Certificate and pen carry one code
HPLC purity	A percentage with its column and detector
LC-MS mass	Near 889 (fragment) or 4,963 (full protein), matching what’s sold
Stated sequence	Ac-LKKTETQ for TB-500
Salt form	Acetate or TFA stated, because counter-ions change the weighed mass
Lab and date	Independent lab named; report dated

A sequence, formula and mass that all point to the same molecule is the sign of a consistent batch. If any one of them disagrees, ask the supplier which molecule the pen holds.

Two guides go further: how to read a peptide certificate of analysis and how to verify a research peptide batch. Any lot code can be entered on the batch verification page.

How Should TB-500 Be Stored?

Keep dry powder chilled, sealed and shielded from light, with −20 °C the norm for long storage. Pre-filled pens are refrigerated, following the batch sheet’s storage note. Its two lysines and glutamine make it water-loving, so keeping moisture out of powder stocks protects the batch. The storage and handling guide gives the complete routine, while the pen vs vial comparison weighs up the two formats.

Frequently Asked Questions

The Bottom Line

TB-500 is a 7-residue synthetic copy of thymosin beta-4’s actin-binding motif. Most published research and almost every human trial used the full protein, and the first trial of the fragment is still recruiting. Under British law it remains an unlicensed, unscheduled reagent, and it appears on WADA’s banned list. The batch certificate should always confirm which molecule you have. Apexion sells it only to labs, for research.

View the TB-500 10mg specification and COA.

Disclaimer: We publish this overview for research education. TB-500 from Apexion is a laboratory reagent, never a medicine, supplement or food, and must never be used on a person or an animal. Nothing above is medical or legal advice. Legal and regulatory points reflect our October 2026 review and may change. Full terms: Research Use Only notice.

Sources

Research

• Low TL, Hu SK, Goldstein AL. PNAS, 1981. PMC319967
• Safer D, et al. Journal of Biological Chemistry, 1991. PubMed 1999398
• Malinda KM, et al. Journal of Investigative Dermatology, 1999. PubMed 10469335
• Philp D, et al. FASEB Journal, 2003. PubMed 14500546
• Bock-Marquette I, et al. Nature, 2004. PubMed 15565145
• Sosne G, et al. Experimental Eye Research, 2007. PMC2211446
• Rahaman KA, et al. Journal of Chromatography B, 2024. PubMed 38382158
• McGuire F, Hughes E, Maak T, Cushman DM. Applied Sciences, 2026. doi:10.3390/app16126202
• PubChem: TB-500, CID 62707662 and thymosin beta-4, CID 45382195

Doping detection

• Ho EN, et al. Journal of Chromatography A, 2012. PubMed 23084823
• Esposito S, et al. Drug Testing and Analysis, 2012. PubMed 22962027

Trials

• RGN-259: NCT02597803, NCT03937882, NCT05555589
• RGN-352: NCT01311518
• TB-500 fragment: NCT07487363

Sport

• WADA Prohibited List (2026 and 2027)
• UK Anti-Doping: what’s banned in sport

UK and US regulation

• Human Medicines Regulations 2012
• Misuse of Drugs Act 1971
• Psychoactive Substances Act 2016
• MHRA. Guidance Note 8: A guide to what is a medicinal product
• PharmExec: FDA panel votes on peptides, July 2026

Quick answer

What is MOTS-c peptide?

MOTS-c is a peptide of 16 amino acids, coded in mitochondrial DNA, inside the 12S rRNA region. Scientists study it mostly in cells and mice, looking at metabolism and exercise. It holds no approval from any regulator, and UK suppliers offer it purely as a research material.

• 16 amino acids, first described in 2015
• Most evidence comes from mouse and cell work; human data are mostly measured levels
• UK: not controlled, not licensed, research use only; WADA S4

Search “MOTS-c peptide UK” and nearly every result is a shop listing. A price, a vial size, a purity figure. Very few of them stop to explain what the molecule actually is, how strong the evidence behind it really is, or where UK law draws its lines.

This guide fills in those blanks. It starts with the peptide’s origin in mitochondrial DNA and the way it signals inside lab cells, then moves through the research areas, the human studies (including a Phase 2 trial that began recruiting in 2026), UK law, anti-doping rules and what a trustworthy certificate looks like. Every finding carries a label telling you where it came from, whether a cell dish, a mouse or a human volunteer.

Apexion’s MOTS-c goes to laboratories for research and nothing more. People and animals are outside its intended use, nothing here is medical advice, and our Research Use Only notice sets out the terms.

What Is MOTS-c Peptide?

MOTS-c stands for “mitochondrial open reading frame of the 12S rRNA-c”. In plain terms, it’s a short peptide whose code is tucked into a stretch of mitochondrial DNA that scientists had long assumed only made ribosomal RNA. It was first reported in 2015, in a Cell Metabolism paper from a USC team led by Changhan Lee and Pinchas Cohen.

That discovery surprised people. Every mitochondrion holds a tiny genome of its own, about 16,500 base pairs, and for decades it was thought to hold just 37 genes. MOTS-c showed that short stretches inside those genes could also code for working peptides, small enough to have been missed.

The USC team found it by scanning the 12S rRNA gene for short open reading frames, the stretches of code that could in theory be read into a protein. One candidate stood out. They then raised antibodies against it and detected the peptide in mouse tissues and in circulating blood, which told them it wasn’t just a quirk of the code.

Here’s the molecule at a glance:

Field	Detail
Name	MOTS-c (mitochondrial open reading frame of the 12S rRNA-c)
Sequence	MRWQEMGYIFYPRKLR
Length	16 amino acids
Formula	C101H152N28O22S2
Molecular weight	~2,174.6 g/mol (PubChem CID 146675088)
CAS number	1627580-64-6
Origin	Mitochondrial DNA (MT-RNR1, the 12S rRNA gene)
Form at Apexion	Pre-filled 40mg research pen, prepared to order in the UK
UK status	Research material only; no MHRA licence, not a controlled drug

Batch identity data and the certificate for our pens are listed under MOTS-c 40mg specification and COA.

Mitochondrial-Derived Peptides: MOTS-c, Humanin and SHLPs

MOTS-c belongs to a small family called mitochondrial-derived peptides, or MDPs. Merry and colleagues, reviewing the field in 2020, count eight identified so far:

• Humanin: the first one found, in 2001. It’s coded in the 16S rRNA gene and is 24 amino acids long.
• SHLP1 to SHLP6: six “small humanin-like peptides”, also coded in the 16S rRNA region.
• MOTS-c: the only known MDP coded in the 12S rRNA gene.

The same review notes there may be “tens to hundreds of potential peptide-encoding short ORFs” in mitochondrial DNA still waiting to be characterised. So the list of mitochondrial peptides is short today, and it may grow.

How Does MOTS-c Work?

In cell and mouse studies, MOTS-c acts as a metabolic signal. It slows a pathway called the folate-methionine cycle, allowing a molecule named AICAR to build up. AICAR then turns on AMPK, which works like a fuel gauge inside the cell. Under stress, MOTS-c also moves into the cell nucleus and changes which genes are active.

Here’s the chain, step by step, with the model behind each link:

1. The folate-methionine cycle slows (cells, Lee 2015). This cycle supplies building blocks for DNA and for methyl groups. MOTS-c dampens it.
2. AICAR accumulates (cells, Lee 2015). AICAR is an intermediate in purine production, and a slower folate cycle leaves more of it sitting unused.
3. AMPK switches on (cells and mouse skeletal muscle, Lee 2015). AMPK responds to low energy by nudging cells towards taking up glucose and burning fuel.
4. MOTS-c enters the nucleus (cells, Kim et al., Cell Metabolism 2018). When cultured cells were starved of glucose or put under oxidative stress, MOTS-c moved out of the cytoplasm and into the nucleus and bound to stress-response genes.

There’s a neat twist in step two. AICAR is itself a well-known lab tool for switching on AMPK, and WADA lists it in the same anti-doping section as MOTS-c. So the peptide appears to reach AMPK by raising the cell’s own supply of a compound researchers already use for the same job.

That fourth step is the striking one. It means a peptide coded by mitochondrial DNA can talk back to the nuclear genome, a two-way conversation biologists hadn’t expected.

Where “exercise mimetic” comes from. You’ll often see MOTS-c called an “exercise mimetic”. The label comes from mouse work: AMPK is the same sensor that exercise activates, and mice given MOTS-c performed better on treadmill and grip tests. No human study has shown anything of the sort, so the phrase describes what happened in mice. Nothing comparable has been recorded in people.

What Is MOTS-c Studied For?

MOTS-c serves researchers as a probe for how cells signal about their energy state, and how mitochondria pass that information along. Most of the work uses cultured cells and mice, plus a few human studies that track how much MOTS-c people already carry in muscle and circulation.

The main research areas, each with its model:

• Glucose handling (mouse, skeletal muscle): Lee’s 2015 work tracked how muscle took up and used glucose, and skeletal muscle turned out to be the main tissue responding to MOTS-c in mice. Muscle is where most glucose ends up after a meal, so it’s the natural place for a metabolic signal to show its effect.
• Exercise capacity (mouse; human levels observational): Reynolds and colleagues (Nature Communications, 2021) reported better running and grip performance in mice at young, middle and old ages. In the same paper, a small group of sedentary young men did a cycling session, and their MOTS-c levels rose during exercise. That’s an observation of natural levels, and nobody in it received the peptide.
• Ageing (aged mice; human levels by age, observational): mice that first received MOTS-c late in life still showed changes in physical-capacity measures. In people, D’Souza and colleagues (Aging, 2020) compared men of different ages and found that blood and muscle levels move in opposite directions as people get older.
• Inflammatory signalling (cell and mouse): cell cultures and mouse models have looked at how MOTS-c relates to inflammatory signalling molecules called cytokines. Because AMPK also influences these pathways, the work ties back to the same energy-sensing chain described above.
• Other preclinical models: cell and rodent studies across several tissue types, summarised in the Zheng 2023 review.

MOTS-c in Metabolic Research: What Mouse Studies Show

Many searches about MOTS-c ask about body weight. The research behind those searches is a set of mouse experiments, so that’s where the answer starts and ends.

In Lee’s 2015 paper, mice were fed a high-fat diet, a standard way of putting metabolism under stress in the lab. Researchers then compared treated mice with untreated ones eating the same food, tracking metabolic markers such as body mass and insulin response over several weeks. These are animal results under tightly controlled lab conditions. The same paper also looked at older mice with age-related changes in insulin response, which explains MOTS-c’s place in ageing research alongside metabolic work.

No human study has measured body-weight changes from MOTS-c itself. The trials of CB4211, a modified analogue, are a separate molecule and a separate question, covered below. Research-grade MOTS-c carries no weight-related claim of any kind.

What Does the Research on MOTS-c Actually Show?

There’s a lot of cell and mouse data, and almost no human data from giving the peptide itself. Human studies so far mostly measure the MOTS-c people already make. The table keeps each finding pinned to its model.

Area	Model	What researchers reported	Evidence level
Folate pathway to AMPK	Cells; mouse muscle	AICAR build-up and AMPK activation (Lee 2015)	Preclinical
Nuclear signalling	Cells	Enters the nucleus when cells are stressed (Kim 2018)	Preclinical
High-fat feeding model	Mice	Metabolic markers tracked on high-fat feed (Lee 2015)	Preclinical
Physical capacity	Mice of three ages	Better treadmill and grip measures (Reynolds 2021)	Preclinical
Exercise and natural levels	Young men	Levels rose in muscle and blood during exercise (Reynolds 2021)	Human observational
Age and natural levels	Men aged 18 to 81	Blood levels lower with age, muscle levels higher (D’Souza 2020)	Human observational
CB4211	Two adult groups	Phase 1a/1b safety study, completed 2021	Human trial of an analogue
Native MOTS-c	Adults	Phase 2 study recruiting since 2026, no results yet	Human trial, in progress

Observational vs interventional. Measuring a molecule and giving a molecule are two very different experiments. When Reynolds and D’Souza measured MOTS-c, they learned how the body’s own supply behaves. They didn’t learn what happens when someone receives extra peptide from outside. Only an interventional trial answers that, and for native MOTS-c, the first one is still running.

Why mouse results don’t carry over to people. Three reasons crop up repeatedly:

• Uniform animals. Lab mice are usually inbred, so every animal shares the same genes. People vary enormously.
• Controlled conditions. Diet, light, temperature and activity are fixed in a mouse study. Real metabolism runs under none of those controls.
• Different readouts. A treadmill time or a grip score is a mouse measure. It doesn’t map neatly onto anything a human trial would count as an outcome.

One more piece of context helps. Look at the conflict-of-interest notes on Reynolds 2021 and D’Souza 2020 and you’ll see that senior authors on both had consulting ties to CohBar, the company that developed the analogue. That’s common in early-stage science, where the discoverers are often the ones commercialising the work. Labs outside the original USC network have since run their own cell and animal studies, as the reference list of the Zheng 2023 review shows, and that wider base makes the picture sturdier.

The reviewers who’ve followed this field closely are optimistic and careful at once. As Zheng, Wei and Wang wrote in Frontiers in Endocrinology in 2023, “Understanding the detailed molecular details of MOTS-c is an ongoing endeavor.”

Has MOTS-c Been Tested in Humans?

Not as a full trial programme for MOTS-c itself. A modified version called CB4211 went through early safety testing, and a Phase 2 trial of the unmodified peptide opened in 2026. Neither has led to an approval, and no regulator in any country has authorised MOTS-c.

CB4211. CohBar, a company co-founded by Pinchas Cohen, developed CB4211 as an analogue of MOTS-c. The Phase 1a/1b trial for CB4211 (NCT03998514) enrolled healthy volunteers and a second adult group, and was completed in 2021. CohBar reported that it met its primary safety endpoint, with the other readouts treated as exploratory. No later-stage CB4211 trial was registered.

Why build an analogue at all? Natural peptides tend to break down quickly once they’re outside the cell, so drug developers often tweak the sequence to make a molecule last longer and behave more predictably. The trade-off is that the analogue’s data can’t simply be borrowed for the original peptide.

Native MOTS-c. Hudson Biotech is running a placebo-controlled Phase 2 study, NCT07505745, which opened to adult volunteers in February 2026. Its main focus is insulin sensitivity, measured against a placebo group, which makes it the first study able to say what added MOTS-c does in people. When we checked the registry in October 2026, it was still recruiting and had posted no results.

Is MOTS-c Legal in the UK?

It is, as a laboratory research material. MOTS-c is absent from the controlled drug schedules, and no MHRA licence has ever been issued for it. That means it can’t be sold, supplied or promoted for human consumption anywhere in Britain.

Three laws shape its position (checked October 2026):

Law	What it says	How it applies to MOTS-c
Human Medicines Regulations 2012	Regulation 2 sets out what counts as a medicinal product. Regulation 46 bars selling, supplying or offering an unlicensed medicinal product.	MOTS-c has no marketing authorisation, so it can’t be offered as a medicine.
Misuse of Drugs Act 1971	Places controlled drugs into classes A, B and C.	MOTS-c isn’t listed.
Psychoactive Substances Act 2016	Covers substances capable of producing a psychoactive effect, defined as one that affects mental functioning or emotional state through the central nervous system.	No psychoactive effect has been reported for MOTS-c.

The detail that catches sellers out comes from MHRA Guidance Note 8, the MHRA’s own guidance on classifying products. Presentation alone can turn a product into a medicine. The MHRA looks at every claim made for it, explicit or implied, including those on websites, in testimonials and on social media. Even a product name can count as an implied claim. A peptide sold with a dosing chart or a promised effect in people can therefore be treated as an unlicensed medicine, regardless of any research-use label. At that point, regulation 46 applies, and offering it for sale becomes an offence.

Status varies between peptides. For the other common ones, are peptides legal in the UK lays out each case.

Can You Buy MOTS-c in the UK?

It’s available from UK research suppliers, sold under research-use-only terms. You won’t find it in pharmacies, because no licence exists for it. Buying from abroad brings its own problem, because customs officers check parcels for medicines: unlicensed medicines arriving at the UK border can be seized. Apexion’s sale terms appear in the Research Use Only notice.

Do You Need a Prescription for MOTS-c?

There’s no UK prescription route for MOTS-c, NHS or private. A prescription needs a licensed product, or at least a recognised unlicensed-medicine pathway, and MOTS-c has neither. UK clinics that offer it to clients as a service are operating outside that system, and the MHRA opened enquiries into peptide claims from clinics in April 2026. Research suppliers sell it to laboratories, and the people they deal with are researchers.

Is MOTS-c Banned in Sport?

WADA, the global anti-doping agency, names MOTS-c in section S4.4.1 of its Prohibited List, under metabolic modulators as an activator of AMPK. Everything in this section stays banned year-round, whether or not a competition is under way. MOTS-c first appeared there by name on the 2025 list, as the ISSF reported when the list was published, and AICAR is named in the same section.

The 2027 Prohibited List, approved in September 2026, keeps the same entry and comes into force on 1 January 2027. UK Anti-Doping (UKAD) applies the list across British sport. The US agency USADA also publishes a plain-English explainer on MOTS-c.

MOTS-c vs SS-31 and Other Mitochondrial Peptides

MOTS-c, SS-31 and humanin all appear in mitochondrial studies, yet they start in different places and do different jobs in lab models. Two are made by the cell’s own mitochondrial DNA. The third was designed by chemists. The quickest way to tell them apart is to ask where each one does its work: MOTS-c signals to the nucleus, SS-31 holds on to a membrane lipid, and humanin acts mostly from outside the cell.

	MOTS-c	SS-31	Humanin
Origin	Mitochondrial DNA, 12S rRNA	Synthetic (Szeto-Schiller series)	Mitochondrial DNA, 16S rRNA
Length	16 amino acids	4 amino acids	24 amino acids
Where it acts (lab models)	Cytoplasm and nucleus; AMPK signalling	Inner mitochondrial membrane; binds cardiolipin	Released from cells; binds cell-surface receptors
Human data	Natural levels measured; analogue Phase 1; Phase 2 recruiting	Several human trials, as elamipretide	Natural levels measured
Approval	None	US accelerated approval for one rare condition (2025)	None

The MOTS-c vs SS-31 vs NAD+ comparison on our blog goes deeper into each molecule. SS-31 also has its own UK research overview and the SS-31 specification page.

How to Verify Research-Grade MOTS-c

The certificate of analysis (COA) for the batch is the first thing to read. It should carry a lot code matching the label, an HPLC purity result alongside its method, and an LC-MS mass close to 2,174.6. It should also name the independent lab, give the test date and state the salt form.

The mass result is easier to read once you know what the raw spectrum looks like. Electrospray LC-MS gives a peptide several positive charges at once, so MOTS-c appears as a series of peaks. Divide the mass (plus the added protons) by the charge and you get the positions: about 725.9 for the 3+ ion and 544.7 for the 4+ ion. A COA that reports a deconvoluted mass of around 2,174.6 has done that maths for you.

For the HPLC result, look for the method behind the number. Reverse-phase HPLC on a C18 column, with UV detection around 214 to 220 nm, is the usual set-up for a peptide this size. A purity figure with no method attached is much harder to judge.

Check	What to look for
Lot number	Same code on certificate and label
HPLC purity	Purity %, with column type and detector stated
LC-MS identity	Mass near 2,174.6, or charge states near 725.9 (3+) and 544.7 (4+)
Lab and date	Testing lab named; report dated
Salt form	TFA or acetate, since the counter-ion adds weight to the powder

Red flags are easy to spot once you know them: dosing charts, body-weight or other outcome claims, and certificates with no lot number at all.

For a longer walkthrough, try how to read a peptide certificate of analysis and how to verify a research peptide batch. Lot codes can be looked up on our batch verification page. Since Apexion supplies MOTS-c as a pre-filled research pen, our peptide pen vs vial comparison explains how the two formats differ.

How Should MOTS-c Be Stored?

Dry powder keeps best cold, dry and dark, at −20 °C for long periods. Solutions and pre-filled pens go in the fridge, as the batch sheet directs. MOTS-c has a particular weak spot: its sequence includes methionine and tryptophan, two residues that oxidise readily when exposed to air and light. Oxidised methionine adds 16 to the mass, so it shows up on LC-MS as a small extra peak just above the main one. Fewer opening and closing cycles mean less oxidation, and a cleaner spectrum when the batch is retested. The full routine is covered by the storage and handling guide.

Frequently Asked Questions

The Bottom Line

In short, MOTS-c is a mitochondrial-DNA peptide whose research record is built mostly on cells and mice. Human research so far measures natural levels, with an analogue’s safety study behind it and a Phase 2 trial of the unmodified peptide still enrolling. In the UK, it’s an unlicensed, uncontrolled research material, and WADA prohibits it in sport. Apexion provides it to laboratories alone, for research and nothing else.

View MOTS-c 40mg specification and COA, or browse the mitochondria research range.

Disclaimer: This guide is educational and written for researchers. Apexion’s MOTS-c is a laboratory research material and doesn’t count as a medicine, supplement or food. It must not be given to humans or animals, and none of this guide counts as medical or legal advice. Regulatory details were checked in October 2026 and can change. See our Research Use Only notice.

Sources

Research

• Lee C, et al. Cell Metabolism, 2015. PMC4350682
• Kim KH, et al. Cell Metabolism, 2018. PMC6185997
• Reynolds JC, et al. Nature Communications, 2021. PMC7817689
• D’Souza RF, et al. Aging, 2020. PMC7138593
• Merry TL, et al. American Journal of Physiology: Endocrinology and Metabolism, 2020. PMC7750512
• Zheng Y, Wei Z, Wang T. Frontiers in Endocrinology, 2023. PMC9905433
• PubChem. MOTS-c, CID 146675088

Trials

• CB4211 Phase 1a/1b: NCT03998514
• MOTS-c Phase 2: NCT07505745

UK law

• Human Medicines Regulations 2012
• Misuse of Drugs Act 1971
• Psychoactive Substances Act 2016
• MHRA. Guidance Note 8: A guide to what is a medicinal product

Sport

• WADA Prohibited List (2026 and 2027)
• UK Anti-Doping: what’s banned in sport
• USADA: What is the MOTS-c peptide?

Quick answer

What is SS-31?

SS-31 (elamipretide) is a synthetic peptide made of four amino acids. It gathers in the inner mitochondrial membrane and binds a lipid called cardiolipin. It has been studied in cells, animals and human trials. In the US, a prescription form called Forzinity holds accelerated approval for Barth syndrome. In the UK it has no medicine licence and is sold only as a research material.

• Also known as elamipretide, Bendavia and MTP-131
• The bulk of the evidence is animal and cell work, and human trials have given mixed results
• UK status: research use only, with no MHRA licence

Type “SS-31 UK” into Google and you’ll get a wall of shop listings. Very few of them say what the peptide is, what its human trials found or what UK law says about it, and that’s the gap this guide fills.

We start with the molecule and its names, then cover how it binds its target in lab models and what the research shows, including the trials that missed. After that come its single US approval, UK law, sport rules and the checks a batch certificate should pass. Every finding is labelled with the model it came from, whether that’s cells, mice or people.

Apexion supplies SS-31 strictly for laboratory research. It’s sold for lab work alone, with no human or veterinary use, and nothing on this page is medical advice. Read our Research Use Only notice for the full terms.

What Is SS-31?

SS-31 is a synthetic tetrapeptide from the Szeto-Schiller family, named after its designers, the scientists Hazel Szeto and Peter Schiller. It dissolves in water and carries a positive charge. Even so, it crosses cell membranes and builds up in the inner mitochondrial membrane, the folded layer where cells make most of their ATP.

The series began as opioid-receptor research. Schiller had spent years building small peptides that bind opioid receptors, and a few of the designs turned up somewhere nobody expected: inside mitochondria. SS-31 was the one that stood out. Szeto went on to found the company now called Stealth BioTherapeutics, which developed the peptide under the drug name elamipretide. Stealth is now a subsidiary of Mighty Therapeutics.

Field	Detail
Names	SS-31, elamipretide, Bendavia, MTP-131 (US brand: Forzinity)
Sequence	D-Arg-Dmt-Lys-Phe-NH2
Class	Synthetic tetrapeptide (Szeto-Schiller series)
Formula	C32H49N9O5
Molecular weight	~639.8 g/mol (free base)
CAS number	736992-21-5
Research form	Lyophilised powder, commonly as an acetate salt (Forzinity uses the hydrochloride)
Target	Cardiolipin, inner mitochondrial membrane

Is SS-31 the Same as Elamipretide?

Yes, the two names describe one molecule. SS-31 is the laboratory code from the Szeto-Schiller series. Elamipretide is the INN, short for international nonproprietary name, which is the official generic name a drug carries worldwide. Bendavia and MTP-131 are development codes Stealth used in early trials, and Forzinity is the US brand.

Is Elamipretide a Peptide?

Yes. Elamipretide is a peptide of four amino acids joined in a chain. Two of them are modified: D-arginine, the mirror-image form of arginine, and 2′,6′-dimethyltyrosine (Dmt). Its full identity and batch details are on our SS-31 30mg specification and COA page.

How Does SS-31 Work?

In lab models, SS-31 binds cardiolipin, a lipid that is almost exclusive to the inner mitochondrial membrane. That binding is thought to steady the folded cristae and keep the electron transport chain working as a unit. In cell and animal models, it has been linked with lower reactive oxygen species (ROS), the reactive by-products of energy production.

Cardiolipin is an odd lipid. It has four fatty-acid tails where most lipids have two, which gives it a cone shape that helps the membrane fold tightly into cristae. It also acts as a kind of glue for the protein complexes of the electron transport chain, keeping them close enough to pass electrons along.

When cardiolipin is oxidised, that arrangement loosens. In cell and animal studies, the cristae lose their shape, electron flow becomes leaky and ROS output climbs. SS-31’s positive charges and aromatic rings are thought to let it dock on cardiolipin’s negatively charged head group and hold the structure in place.

A common misreading online calls SS-31 a free-radical scavenger. Its Dmt residue can neutralise some radicals in a test tube, but the Szeto 2014 review places its main action at the membrane, protecting cardiolipin before oxidation starts.

A 2020 study in PNAS by Chavez and colleagues added a protein-level picture. Using cross-linking mass spectrometry on mitochondria from mouse heart tissue, the team mapped which proteins lie closest to SS-31. Each partner they found was a protein already known to bind cardiolipin, many of them involved in ATP production.

What Is SS-31 Used For in Research?

SS-31 is a research tool for studying mitochondrial dysfunction. Labs use it in muscle, heart, kidney, eye and nerve models, and in rare mitochondrial diseases. Because it targets one lipid so precisely, it helps researchers test whether cardiolipin damage is behind a change they see in stressed cells or tissue.

Here’s how the main research areas break down by study type:

• Ageing muscle (animal): Campbell and colleagues studied aged mice and measured mitochondrial function and redox balance in skeletal muscle.
• Kidney (animal): Zhu and colleagues’ 2022 review gathered ischaemic, diabetic and drug-induced kidney injury models in rodents and cells.
• Heart (animal and human): mouse heart-failure models came first, followed by human trials in heart attack and heart failure.
• Dry AMD (human): trials in geographic atrophy, the advanced dry stage of age-related macular degeneration.
• Barth syndrome and primary mitochondrial myopathy (human): rare inherited conditions where mitochondria fail, and the setting for SS-31’s biggest trials.

Weight loss doesn’t appear among the conditions studied in its registered human trials.

What Does the Research on SS-31 Show?

The evidence is mixed. There are many animal studies, and most report positive changes within their own models. In people, several trials missed their primary endpoints, and the only approval anywhere is a US accelerated approval for Barth syndrome. The table below keeps each result tied to its study type.

Research area	Study type	What was reported	Status
Ageing muscle	Animal (aged mice)	Better mitochondrial function markers (Campbell 2019)	Preclinical
Kidney injury	Animal and cell	Fewer injury markers across models (Zhu 2022 review)	Preclinical
Heart	Animal; human (EMBRACE STEMI)	Positive in animal models; the human trial missed its infarct-size endpoint	Mixed
Primary mitochondrial myopathy	Human (MMPOWER-3, Phase 3)	Missed both primary endpoints	Negative
Barth syndrome	Human (TAZPOWER)	Randomised phase missed its primary endpoints; open-label extension data supported the US filing	US approval only
Dry AMD	Human (ReCLAIM-2, Phase 2)	Missed primary endpoints; Phase 3 ReNEW under way	In development

Why the gap between mice and people? Three causes keep surfacing. The human trials were small, which makes modest changes hard to detect. Several relied on surrogate endpoints, such as walking distance or muscle-strength scores, which stand in for clinical outcomes and don’t always track them. And a mouse model reproduces one slice of a human disease at best.

The approval itself came from Barth syndrome, a condition caused by faulty cardiolipin, the exact lipid SS-31 targets. That link between mechanism and disease is the clearest thread through the human data.

Reviewers still see room for more work. A 2025 review in the International Journal of Molecular Sciences by Tung and colleagues notes that “Elamipretide has a unique structure allowing for uptake in a variety of cell types,” and calls for further study of broader uses and long-term safety. The full register of trials is on ClinicalTrials.gov.

Is Elamipretide FDA Approved?

Yes, for one use only. On 19 September 2025 the FDA granted accelerated approval to Forzinity (elamipretide HCl) for Barth syndrome in people with a body weight of 30 kg or more. It isn’t approved for anything else, and keeping the approval depends on the results of a confirmatory trial.

The FDA label states the indication as improving muscle strength in Barth syndrome, approved “based on an improvement in knee extensor muscle strength.” That’s an intermediate endpoint, which is why a follow-up study is required. On 8 July 2026, Mighty Therapeutics dosed the first participant in 4TAZPower, a 72-week, placebo-controlled confirmatory trial.

For the patient community, the decision was a milestone. Emily Milligan, Executive Director of the Barth Syndrome Foundation, called approval day “a day to celebrate – although much work remains.”

Elamipretide also holds a US orphan drug designation for Friedreich’s ataxia, granted in 2022. Orphan status supports development for a rare disease, and it carries no approval.

	Research-grade SS-31	Forzinity (elamipretide HCl)
Purpose	Laboratory research only	Prescription medicine for Barth syndrome
Regulator	None as a medicine; sold under research-use terms	US FDA (accelerated approval)
Quality standard	Batch certificate of analysis (COA)	GMP drug manufacturing
UK availability	Sold to researchers	Not licensed in the UK

Is SS-31 Legal in the UK?

It is, as a research material. SS-31 appears on no schedule of the Misuse of Drugs Act 1971, and the MHRA has never licensed it as a medicine. UK suppliers may therefore offer it to laboratories for research, with sale for human use off the table and no NHS or private prescription route.

Three pieces of UK law set the boundaries (checked October 2026):

• Human Medicines Regulations 2012: any product sold with medicinal claims needs a marketing authorisation first. The MHRA has granted none for elamipretide.
• Misuse of Drugs Act 1971: SS-31 doesn’t appear in its schedules.
• Psychoactive Substances Act 2016: this covers substances that affect mental function, and SS-31 has no recorded psychoactive effect.

Europe looks similar. The EMA has given elamipretide an orphan designation for a mitochondrial DNA depletion syndrome, which is a development status with no authorisation behind it.

Are Peptides Legal to Buy in the UK?

For laboratory use, the large majority of research peptides can be bought legally in the UK. A peptide becomes restricted when it’s controlled under drug law, or when it’s sold as a medicine without an MHRA licence. Status varies from one compound to the next, so our guide are peptides legal in the UK goes through each case.

Can You Buy SS-31 Over the Counter?

No. SS-31 isn’t a pharmacy or over-the-counter medicine in the UK, and no UK pharmacy stocks it. UK suppliers sell it only as a research material for laboratories, under terms such as our Research Use Only notice.

Is SS-31 Banned in Sport?

SS-31 isn’t named on the 2026 WADA Prohibited List. WADA’s S0 class catches substances that no government health regulator has approved for therapeutic use in people, and elamipretide has held a US approval since September 2025. WADA approved its 2027 list on 10 September 2026, and it takes effect on 1 January 2027.

In the UK, UK Anti-Doping (UKAD) enforces the WADA list. The current text of each list is published on wada-ama.org, and UKAD sets out how the rules apply in UK sport at ukad.org.uk.

SS-31 vs MOTS-c: What’s the Difference?

SS-31 is a lab-made peptide with a structural job: it holds on to cardiolipin at the inner mitochondrial membrane. MOTS-c comes from the cell itself, coded by a stretch of mitochondrial DNA, and researchers study it as a messenger for metabolism. Both turn up in mitochondrial research, but they answer very different questions.

Three contrasts stand out:

• Origin: SS-31 came from a chemist’s design, while MOTS-c is read from a short open reading frame inside the 12S rRNA gene.
• Size: SS-31 has 4 amino acids and MOTS-c has 16.
• Site of action: SS-31 stays at the inner membrane in lab models, while MOTS-c is studied for signalling that reaches the cell nucleus under stress.

There are no published studies that combine the two. Our MOTS-c vs SS-31 vs NAD+ comparison covers both in detail, and the MOTS-c 40mg specification lists its identity data.

How to Verify Research-Grade SS-31

The first document to check is the batch certificate of analysis (COA). LC-MS should confirm a mass close to 640 Da, which shows up as a singly charged ion at about m/z 640.4. HPLC purity should be listed together with the method used, and every result should belong to the lot printed on the pen or vial label.

Run through this checklist when the COA arrives:

• Lot match: the COA’s lot code is identical to the one on the label.
• HPLC: the purity percentage, plus the column and detection method.
• LC-MS: the measured mass agrees with the expected value for SS-31.
• Named lab and date: the testing laboratory is identified and the report is dated.
• Salt form: acetate or TFA, because the counter-ion changes the weighed mass.
• Storage: sealed, cold and away from light, as the storage and handling guide explains.

Apexion supplies SS-31 as a pre-filled 30mg research pen, made up to order in the UK. Our pen vs vial comparison compares the two formats. For a full walkthrough of certificates, our guides cover how to read a peptide certificate of analysis and how to verify a research peptide batch. You can check a lot number on our batch verification page.

Frequently Asked Questions

The Bottom Line

SS-31 is one of the most studied mitochondria-targeting peptides. It has a deep animal literature, a mixed record in human trials and a single approval, which is US-only, accelerated and limited to Barth syndrome. UK law treats it as a research material, with no medicine licence behind it. Apexion supplies it strictly for laboratory research, with no human or veterinary use.

See the SS-31 30mg specification and COA, or browse the full mitochondria research range.

Disclaimer: This guide is educational content. Apexion Biolabs sells SS-31 to qualified researchers as a laboratory material only. In the UK it holds no MHRA authorisation and has no medicinal status, and it must never be used in humans or animals. The page offers no medical advice and no guidance on dosing or administration.

Sources

• Szeto HH, Birk AV. Serendipity and the discovery of novel compounds that restore mitochondrial plasticity. Clinical Pharmacology & Therapeutics, 2014. PMC4267688
• Tung C et al. Elamipretide: a review of its structure, mechanism of action, and therapeutic potential. International Journal of Molecular Sciences, 2025. PMC11816484
• Campbell MD et al. Free Radical Biology and Medicine, 2019. PMC6588449
• Zhu Y et al. Oxidative Medicine and Cellular Longevity, 2022. PMC9192202
• Chavez JD et al. PNAS, 2020. PMC7334473
• MMPOWER-3 (NCT03323749) and TAZPOWER (NCT03098797), ClinicalTrials.gov
• US FDA. Forzinity (elamipretide) prescribing information, 2025
• UK legislation: Human Medicines Regulations 2012 and Psychoactive Substances Act 2016
• WADA Prohibited List (2026 and 2027)
• UK Anti-Doping

Quick answer

What is Tesamorelin?

Tesamorelin is a synthetic, stabilised form of growth hormone-releasing hormone (GHRH). In the US, tesamorelin is an approved medicine (Egrifta) for one narrow use. UK regulators have never granted it a marketing authorisation, which leaves it outside the medicines system here. Buying it is legal only as a laboratory research material.

• A 44-amino-acid GHRH analogue that acts on the pituitary
• Not a controlled drug, but not licensed or available on the NHS in the UK
• Banned in sport under WADA S2

Search “tesamorelin UK” and page one is a wall of research shops. Click through to the US results and you’ll land on clinic pages talking about prescriptions, pharmacy collection and insurance cover. Both sets of pages describe the same 44-amino-acid molecule. Tesamorelin is a licensed drug in the United States and a research material in the UK, and most of the muddled claims online come from blending those two stories together.

Below, we pull them apart. You’ll get what tesamorelin is, how it acts on the pituitary, what UK law and anti-doping rules say about it, how it compares with ipamorelin and CJC-1295, and what to check on a batch certificate.

Apexion Biolabs supplies tesamorelin as a laboratory research material, covered by our Research Use Only policy. The page contains no medical advice.

What Is Tesamorelin?

Tesamorelin is a synthetic analogue of human growth hormone-releasing hormone, GHRH(1-44). It keeps all 44 amino acids of the natural hormone and adds a trans-3-hexenoyl group to the first one. That small cap helps the molecule survive the enzyme that strips natural GHRH apart within minutes, while the receptor-binding sequence stays untouched.

Theratechnologies, a Canadian drug developer, created it. The FDA approved it as Egrifta in November 2010, a date recorded in Adrian et al. (2018).

Structural Stabilization

Natural GHRH has a weak spot at its front end. An enzyme called dipeptidyl peptidase-4 (DPP-4) clips off the first two amino acids, tyrosine and alanine, and the shortened fragment loses most of its activity. Tesamorelin’s trans-3-hexenoyl group is fixed to that first tyrosine, which blocks the cut.

Everything after the cap matches the human hormone residue for residue. So researchers get a full-length GHRH sequence with a longer working window, and no change to the part that docks with the receptor.

Detail	Tesamorelin
Name	Tesamorelin (US brand name: Egrifta)
Class	Stabilised GHRH(1-44) analogue
Length	44 amino acids
Formula	C221H366N72O67S (PubChem)
Molecular weight	About 5,135.9 g/mol
CAS number	218949-48-5
Reference form	Lyophilised powder as the standard reference; our material comes as a pre-filled 20mg research pen
Storage	Chilled, kept dry and shielded from light, per the batch sheet
UK status	Research material with no marketing authorisation

What Is Tesamorelin Used For?

In the US, tesamorelin has one approved use: reducing excess abdominal fat in adults with HIV who have lipodystrophy, a condition that changes where fat is stored. It’s prescription-only and sold as Egrifta SV and, since 2025, Egrifta WR. The FDA label states it isn’t indicated for weight-loss management. In the UK, its only use is laboratory research. Lot details for our material are on the Tesamorelin 20mg specification and COA page.

How Does Tesamorelin Work?

Tesamorelin binds GHRH receptors on somatotrophs, the growth hormone-producing cells of the anterior pituitary. The receptor raises cAMP inside the cell, the cell releases stored growth hormone (GH) in pulses, and GH then prompts the liver to make IGF-1. Studies track IGF-1 because it’s steadier and easier to measure than GH pulses.

Here’s the chain, one step at a time:

1. Binding: tesamorelin docks with the GHRH receptor, a G-protein-coupled receptor on somatotroph cells.
2. Signal: cAMP rises and switches on protein kinase A.
3. Release: stored GH leaves the cell in bursts, keeping to the pituitary’s own rhythm.
4. Readout: circulating GH reaches the liver, which produces IGF-1.

The clearest picture of that pattern comes from Massachusetts General Hospital. Stanley and colleagues gave healthy men tesamorelin for two weeks and concluded that it “augments basal and pulsatile GH secretion” (JCEM, 2011). A companion study by Makimura et al. followed 13 men on the same schedule and found that it “increased endogenous GH release and IGF-1” (Growth Hormone & IGF Research, 2011).

The pulse detail is the reason GH-axis researchers treat releasing factors as their own category. Tesamorelin acts upstream, so the pituitary still sets the timing and the somatostatin and IGF-1 feedback loops stay in place. Recombinant growth hormone skips the pituitary entirely.

Tesamorelin in the US vs the UK: Approved Drug or Research Material?

The same molecule has very different statuses depending on the border. The US approved tesamorelin as a prescription medicine, Egrifta, in 2010. In the EU, the marketing authorisation application was withdrawn in 2012 before any decision. The UK has never licensed it, so tesamorelin can only be supplied here as a research material.

United States. Theratechnologies markets tesamorelin under the Egrifta name for its single approved indication. The original 1mg-vial product has since given way to newer formulations, the latest being Egrifta WR, approved in 2025 (FDA label, 2025).

European Union. The Spanish company Ferrer Internacional applied to the European Medicines Agency. Ferrer withdrew the application in June 2012 after the CHMP, the EMA’s medicines committee, said the data submitted did not yet let it conclude a positive benefit-risk balance (EMA).

United Kingdom. The MHRA grants UK marketing authorisations, and no company has ever held one for tesamorelin.

	US	EU	UK
Status	FDA-approved medicine (Egrifta), 2010	Application withdrawn (EMA)	No marketing authorisation
Use	One narrow approved indication	None	Laboratory research only
How it’s supplied	Prescription only	Not supplied as a medicine	Research material, not for human use

Is Tesamorelin Legal in the UK?

Yes, for laboratory work. The Misuse of Drugs Act 1971 doesn’t list tesamorelin in any class, which means possession isn’t a criminal offence. With no UK marketing authorisation, though, nobody may sell, supply or advertise it for human use. UK suppliers can only offer it for laboratory research.

Two laws set those limits:

• [Misuse of Drugs Act 1971]: sorts controlled drugs into Classes A, B and C. Tesamorelin appears in none of them, which answers “is it illegal to have tesamorelin?” with a clear no.
• [Human Medicines Regulations 2012]: regulation 46 bars anyone from selling or supplying a medicinal product without a marketing authorisation, and the MHRA enforces it.

The same two-law test applies to most research compounds, and our guide on whether are peptides legal in the UK runs through it compound by compound.

Do You Need a Prescription for Tesamorelin?

UK prescribers have no route to it. A prescription needs a licensed medicine behind it, and tesamorelin has no UK licence. Egrifta is a US product, and no UK version has ever been authorised.

Is Tesamorelin Available on the NHS?

No. NHS prescribers work from licensed medicines, and tesamorelin has never had a UK licence for any condition.

Can You Buy Tesamorelin Over the Counter?

No pharmacy stocks it, because it has no medicinal status here. UK research suppliers list it with research-use-only labels, for laboratory work. The MHRA and Border Force also seize unlicensed medicines at the border. Over two weeks in March 2026 they intercepted more than 2 million doses, valued at about £4.6m (The Pharmaceutical Journal).

Is Tesamorelin Banned in Sport?

Yes, and by name. WADA’s Prohibited List places tesamorelin under S2.2.4, growth hormone releasing factors, as an example of a GHRH analogue. Class S2 substances are prohibited year-round, during competition periods and outside them, with UK Anti-Doping (UKAD) handling enforcement in the UK.

The named examples are only part of the rule. S2 also covers “other substances with similar chemical structure or similar biological effect(s)”, so a GHRH analogue missing from the printed list is still prohibited. Sport bodies treat tesamorelin as a doping substance whatever its legal status for laboratories.

WADA’s Executive Committee signed off the 2027 Prohibited List on 10 September 2026, and it applies from 1 January 2027. Its headline changes cover other classes, such as cannabinoids, glucocorticoids and beta-blockers.

Tesamorelin vs Ipamorelin vs CJC-1295: What’s the Difference?

All three act on the growth hormone axis, but through different receptors. Tesamorelin and CJC-1295 are GHRH analogues, so they target the GHRH receptor. Ipamorelin is a ghrelin-receptor (GHSR-1a) agonist, which reaches the same pituitary cells through a second, separate receptor.

	Tesamorelin	CJC-1295	Ipamorelin
Class	GHRH(1-44) analogue	Modified GHRH(1-29) analogue	Ghrelin-receptor agonist (a pentapeptide)
Length	44 amino acids	29 amino acids	5 amino acids
Receptor	GHRH receptor	GHRH receptor	GHSR-1a
Regulatory status	US-approved (Egrifta)	Not approved anywhere	Not approved anywhere
UK status	Research material	Research material	Research material

CJC-1295 starts from GHRH(1-29), the shortest stretch of the hormone that still binds fully, and swaps four amino acids to toughen it. Tesamorelin keeps the whole 44-residue chain and protects only the front end. Ipamorelin belongs to a different family altogether, the growth hormone secretagogues, built to mimic ghrelin.

Can tesamorelin and ipamorelin be studied together? The receptor logic explains why labs pair the two classes. The GHRH receptor works through cAMP, while GHSR-1a signals mainly through calcium, so a combined design shows how two independent inputs to the same somatotroph interact. The CJC-1295 pairing follows the same reasoning, set out in CJC-1295 vs Ipamorelin and peptide stacks explained. Lot data is on the CJC-1295 + Ipamorelin specification page.

The three compounds share one more thing: WADA lists all of them in the same S2.2.4 clause.

What Is Tesamorelin Studied For?

Tesamorelin’s research record comes in three evidence levels. The strongest is the approved US indication, backed by phase 3 trials. Next are other clinical studies of the GH axis in defined groups. Laboratory work then uses tesamorelin as a stable GHRH-receptor tool in cell and tissue models.

Research area	Evidence level	What was studied
Abdominal fat accumulation in adults with HIV-associated lipodystrophy	Approved US indication	Phase 3 trial of 412 patients measuring visceral adipose tissue by CT scan over 26 weeks (Falutz et al., NEJM 2007)
GH pulsatility and IGF-1 output	Other clinical research	Short-term studies in healthy men at Massachusetts General Hospital (covered above)
GHRH receptor signalling	Preclinical and laboratory	Pituitary cell and receptor assays using tesamorelin as a protease-resistant GHRH reference

The labels count because claims online often borrow the weight of the first row for uses studied far less. The phase 3 evidence covers one defined patient group and one measured endpoint. Anything beyond that belongs in the lower rows.

How to Verify Research-Grade Tesamorelin

A tesamorelin certificate of analysis (COA) should prove three things. The lot number must match the pen label, the HPLC result must show purity, and the LC-MS (liquid chromatography-mass spectrometry) result must match the expected mass of about 5,135.9. For a peptide this size, look for a deconvoluted mass, because the raw spectrum shows several charge states.

Check	What to confirm
Product identity	The label reads “Tesamorelin” and matches the order
Lot number	Identical on the pen and the COA
HPLC purity	Result and method both stated
LC-MS identity	Deconvoluted mass close to 5,135.9
CAS number	218949-48-5 where listed

That mass point trips up a lot of first-time COA readers. A 44-residue peptide carries several protons at once, so the raw trace shows peaks near 1,028 (5+) and 857 (6+). Software then converts those peaks back into one mass of about 5,136. The guide to how to read a peptide certificate of analysis walks through those charge states. Lot-matching steps are set out in how to verify a research peptide batch, and our own process is described under Apexion batch verification.

How Should Tesamorelin Be Stored?

Does tesamorelin peptide need refrigeration? Lyophilised powder keeps best chilled, dry and in the dark, and freezer storage at around −20 °C is usual for the long term. Solutions and pre-filled pens should be refrigerated according to the batch guidance supplied with them.

• Leave the pack closed until the lab needs it, since moisture speeds up breakdown.
• Limit freeze-thaw cycles, which can damage a long peptide chain.
• Shield it from light and keep it in its original packaging.

Formulation changes the rules, which is why the batch sheet always wins. The US medicine Egrifta WR, for example, is labelled for room-temperature storage at 20 to 25 °C before and after mixing (FDA label, 2025). Research material is a different preparation, so it follows its own instructions. Our guide to reconstituted peptide storage and handling for research covers temperatures and receipt checks, and peptide pens vs vials compares the two formats.

Frequently Asked Questions

Conclusion

Tesamorelin is a US-approved molecule with a very different status in the UK. Here it’s an unlicensed, uncontrolled laboratory material, unavailable on prescription or the NHS and banned in sport under WADA S2. For laboratory work, a batch earns trust through its COA: a matching lot number, a stated HPLC purity and a deconvoluted mass near 5,135.9. Every compound we cover gets the same documentation-first treatment, from this guide to our GHK-Cu research overview.

[View Tesamorelin 20mg specification and COA]

Disclaimer: This guide is educational content. Apexion Biolabs sells tesamorelin to qualified researchers as a laboratory material only. In the UK it holds no MHRA authorisation and has no medicinal status, and it must never be used in humans or animals. The page offers no medical advice and no guidance on dosing or administration.

Sources

• FDA: Egrifta SV prescribing information (2024) and Egrifta WR label (2025)
• EMA: Ferrer Internacional withdraws its application for Egrifta (2012)
• Adrian et al., J Frailty Aging, 2018 (PMC6766405)
• Falutz et al., NEJM, 2007 (PubMed 18057338)
• Stanley et al., JCEM, 2011 (PubMed 20943777) and Makimura et al., GH & IGF Research, 2011 (PubMed 21531600)
• MHRA on gov.uk and Human Medicines Regulations 2012, regulation 46
• legislation.gov.uk: Misuse of Drugs Act 1971
• WADA 2026 Prohibited List and WADA 2027 Prohibited List

Quick answer

What is KPV peptide?

KPV is a tripeptide (lysine-proline-valine) taken from the end of alpha-melanocyte-stimulating hormone (α-MSH). It’s studied mainly for its effect on inflammatory signalling in gut and skin cell models. UK law allows its purchase as research material. No regulator has licensed it as a medicine, and no controlled clinical trial exists.

• Three amino acids: Lys-Pro-Val (α-MSH residues 11 to 13)
• The evidence comes mostly from mouse colitis and cell studies
• One of the four peptides in the KLOW blend

Three amino acids rarely make the news. KPV did in late July 2026, when a US Food and Drug Administration advisory panel backed it, by 8 votes to 6, for the American pharmacy compounding list. Search for KPV peptide in the UK, though, and you’ll mostly find shop listings and US consumer articles.

This guide follows the research trail: what KPV is, how it relates to α-MSH, what the evidence shows, why oral and vial forms both exist, its UK legal status, and what a batch certificate should show.

Apexion supplies KPV strictly for laboratory research. It is not for human or veterinary use. This is general information, not medical or legal advice.

What Is KPV Peptide?

KPV is a three-amino-acid peptide, lysine-proline-valine, that matches positions 11 to 13 of α-MSH, a 13-amino-acid hormone. Researchers study it as a pared-down version of α-MSH’s anti-inflammatory activity, mostly in gut and skin cell models and in mice.

The parent hormone comes from a bigger precursor protein called POMC. Its first 13 residues line up with the start of another hormone, ACTH, which is why chemical databases such as PubChem also file KPV under the name ACTH-(11-13).

Interest in the fragment grew out of 1990s work by Anna Catania, James Lipton and colleagues, who reported that α-MSH could damp down inflammatory signalling. Thomas Luger’s University of Münster group summed it up in a 2007 review: “Most of the anti-inflammatory activities of α-MSH can be attributed to its C-terminal tripeptide KPV.”

Property	Detail
Full name	Lysyl-prolyl-valine (KPV)
Sequence	Lys-Pro-Val
Class	Tripeptide, α-MSH fragment
Also listed as	α-MSH (11-13), ACTH (11-13)
Molecular formula	C16H30N4O4
Molecular weight	~342.4 g/mol
CAS number	67727-97-3
Research form	Lyophilised (freeze-dried) powder; Apexion supplies a pre-filled 10mg research pen
Storage	Cold, dry and dark

Apexion’s product details are on the KPV 10mg specification and COA page.

How Does KPV Work?

The mechanism isn’t fully settled. Two lines of research stand out: KPV entering cells through the PepT1 transporter and quietening inflammatory signalling inside them, and the open question of whether it acts on melanocortin receptors such as MC1R the way full α-MSH does. Both rest on mouse and cell models.

PepT1 transport. PepT1 is a membrane transporter whose usual job is moving small two- and three-residue peptides out of the gut and into lining cells. In a 2007 Gastroenterology study, Guillaume Dalmasso, Didier Merlin and colleagues at Emory University showed that PepT1 also carries KPV into intestinal epithelial cells and T cells. Once inside those cultured cells, nanomolar amounts of KPV blocked NF-κB and MAP-kinase signalling, two of the main switches that turn on inflammatory genes.

The team also noted that PepT1 is “induced in colon during inflammatory bowel disease,” which made the inflamed mouse colon the obvious next test.

Melanocortin receptors. α-MSH acts through a family of melanocortin receptors, and MC1R is the best known of them. Whether KPV uses the same receptors is still debated. Luger’s review notes that “KPV seems not to bind to MC-1R,” and a 2008 mouse study by Kerstin Kannengiesser and colleagues found the peptide’s effects held up in mice with a non-working MC1R. The authors described them as “at least partially independent of MC1R signaling.”

KPV vs Alpha-MSH: What’s the Difference?

α-MSH is a 13-amino-acid hormone with roles in pigment, appetite and immune signalling. KPV is its final three residues, studied only for the anti-inflammatory part. The Münster group’s 2008 follow-up review described the fragment as keeping that activity with a “lack of pigmentary action.”

	α-MSH	KPV
Length	13 amino acids	3 amino acids
Origin	Made from POMC in the pituitary and skin	C-terminal fragment of α-MSH
Receptors	Melanocortin receptors (MC1R to MC5R)	Debated; studied largely via PepT1 uptake
Pigment role	Yes	No pigment activity reported
Research focus	Pigment, appetite, inflammation	Inflammatory signalling in gut and skin models

The short length is what drew researchers in. A three-residue peptide is cheap to make, simple to modify and small enough for PepT1 to carry.

What Does the Research on KPV Show?

Almost all KPV data is preclinical, mostly from mouse colitis models and cell studies, and no human trial has been run. The work keeps circling one question: how a tiny peptide behaves in inflamed gut tissue, and how to get more of it there.

Research area	Model	Evidence level
Intestinal inflammation (colitis)	Mouse (DSS and TNBS models), intestinal cells	Preclinical: the most studied area
Oral and nanoparticle delivery to the colon	Mouse	Preclinical (delivery research)
Skin and keratinocytes	Cell culture	Preclinical
Wound models	Animal, cell	Limited
Humans	None	No controlled clinical trials

The colitis work leans on two chemical models, DSS and TNBS, which each inflame the mouse colon in a predictable way. Dalmasso’s team gave KPV in the animals’ drinking water and tracked cytokine levels, and Kannengiesser’s group added a third model based on transferred immune cells.

Skin research is smaller and cell-based, mostly measuring inflammatory and oxidative-stress markers in keratinocytes, the main cells of the skin’s outer layer. In 2026, KPV also appeared in liver and fat-cell culture studies on lipid signalling.

Oral vs Lyophilised KPV: Why Are There Two Forms?

Research has looked at oral delivery because PepT1 carries KPV across the gut lining, while lyophilised powder is the standard research form for lab handling. A capsule or tablet listing is only as checkable as its paperwork, and without a batch COA there’s no way to confirm what’s inside.

Getting a peptide through the stomach intact is hard, so most oral KPV research is delivery research. Merlin’s group packed KPV into nanoparticles wrapped in a gel that releases them in the colon. In their 2010 mouse study, Hamed Laroui and colleagues reported a similar effect at a concentration “12,000-fold lower than that of KPV in free solution.” A January 2026 mouse study took the idea further with a KPV conjugate built to survive the gut and release its cargo where inflammation is present.

In papers, oral KPV means engineered carriers tested in mice. In shop listings, it usually means capsules or tablets, which need the same batch testing as any vial.

Apexion supplies KPV as a pre-filled 10mg research pen, which it prepares to order in the UK. The peptide pens vs vials comparison shows how that format differs from a traditional vial.

Is KPV Legal in the UK?

Yes. KPV can be bought in the UK as research material. No UK drug schedule controls it, and the MHRA has never licensed it as a medicine, so there’s no prescription route and no lawful sale for human use. Its status comes down to how it’s presented and supplied.

MHRA Guidance Note 8 sets two tests for a medicine. One asks whether a product is presented as treating or preventing disease. The other asks whether it’s used to modify physiological functions. Research material supplied for laboratory work, with no human-use claims, meets neither.

For the wider picture across compounds, read are peptides legal in the UK. Apexion sets out its supply terms in our Research Use Only policy.

Do You Need a Prescription for KPV?

No prescription route exists, because there’s no licensed KPV medicine in the UK to prescribe. A clinic offering KPV isn’t supplying an MHRA-licensed product. The MHRA’s guidance adds that “where unauthorised products are marketed for a medical purpose MHRA will take appropriate action.” The same reasoning answers the over-the-counter question: pharmacy counters stock licensed medicines, and KPV holds no licence.

Is KPV Banned in Sport?

WADA doesn’t list KPV by name on its 2026 Prohibited List, and the 2027 list, published in September 2026, doesn’t name it either. KPV still falls under S0, the always-prohibited class for substances with no approval for human therapeutic use. Once the 2027 wording takes effect on 1 January, S0 spells this out by including “peptides” in its examples.

What Are the Risks and Unknowns of KPV?

There’s no controlled human safety data on KPV, so nobody knows what side effects it has in people. Every observation so far comes from mice and cultured cells. Questions such as “who shouldn’t take KPV” have no evidence-based answer, because no clinical trial has ever addressed them.

Three unknowns stand out:

• Identity and purity: untested products may contain less KPV than labelled, a different form of it, or impurities
• Long-term exposure: published studies run for days or weeks in mice
• Combinations: blends add compounds that have never been studied together in people

Searches pairing KPV with cancer trace back to a 2016 mouse study from Merlin’s lab on colitis-linked tumours. That’s early animal work with no clinical evidence behind it.

KPV in Research Blends: KLOW

KLOW combines 50mg of GHK-Cu with BPC-157, TB-500 and KPV at 10mg apiece, 80mg in all. KPV is what separates it from GLOW, the three-peptide blend it builds on. Apexion supplies it as one pre-filled 80mg research pen.

Within the blend, KPV contributes the PepT1 and NF-κB line of research. Our KLOW vs GLOW comparison sets the two blends side by side, and the KLOW 80mg specification and COA page lists the components. The largest ingredient has its own GHK-Cu UK guide, and peptide stacks explained covers blend design in general.

How to Verify Research-Grade KPV

Check the batch-specific COA first. KPV’s small mass, about 342 g/mol, makes the LC-MS result a quick identity check. One detail deserves a look: free-acid KPV and the C-amidated version found at the end of α-MSH differ by about 1 g/mol, so the COA should name the form it tested.

• ☐ Lot numbers on the COA and the pen label agree
• ☐ HPLC purity is reported alongside its method
• ☐ The LC-MS mass is about 342 for free-acid KPV, or about 341 for the amidated form, with the form named
• ☐ The report gives the testing lab’s name and the test date
• ☐ Storage guidance comes with the batch

Two guides go line by line: how to read a peptide COA and verify a research peptide batch. Apexion batch verification explains how each pen’s QR code leads to its documentation.

Frequently Asked Questions

The Bottom Line

KPV is the three-residue tail of α-MSH, studied mainly in mouse models of gut inflammation and in cell cultures. No human trials exist. UK law treats it as a research material, it isn’t a medicine, and it’s the extra ingredient that turns GLOW into KLOW.

View the KPV 10mg specification and COA.

Apexion supplies KPV strictly for laboratory research. It is not for human or veterinary use. This is general information, not medical or legal advice.

Sources

• Dalmasso G et al. Gastroenterology, 2008; 134(1): 166-178 (online October 2007). PMID 18061177.
• Kannengiesser K et al. Inflammatory Bowel Diseases, 2008; 14(3): 324-331. PMID 18092346.
• Laroui H et al. Gastroenterology, 2010; 138(3): 843-853. PMID 19909746.
• Luger TA, Brzoska T. Annals of the Rheumatic Diseases, 2007; 66 Suppl 3: iii52-55. PMID 17934097.
• Brzoska T et al. Endocrine Reviews, 2008; 29(5): 581-602. PMID 18612139.
• Viennois E et al. Cellular and Molecular Gastroenterology and Hepatology, 2016; 2(3): 340-357. PMID 27458604.
• Cheng J et al. Science Advances, 2026; 12(3): eaea2989. PMID 41533788.
• MHRA. Guidance Note 8: A guide to what is a medicinal product.
• WADA. 2027 Prohibited List (September 2026).
• PubChem CID 125672.

Quick answer

What is a peptide stack?

A peptide stack is a combination of two or more peptides studied together, either as separate vials in one protocol or as a single pre-mixed blend. Researchers pair peptides that act on different pathways to study complementary mechanisms. Very few combinations have been tested as combinations, and none is licensed for human use in the UK.

• Common research stacks: BPC-157 + TB-500, and CJC-1295 + ipamorelin
• A blend needs a COA that confirms every component
• Legal as research materials, but most of the components are banned in sport

Updated October 2026

“Stacking” has gone mainstream. Vogue covered it in November 2025, Women’s Health picked it up in April 2026, and Reddit threads swap stack cheat sheets by the hundred. Almost all of that coverage is written for personal use, so anyone wanting the lab-bench version has had to piece it together.

This guide puts it in one place: what peptide stacks are, the common research combinations, the named blends (Wolverine, KLOW and GLOW), pre-mixed blends vs separate vials, UK legal status, and how to check a blend’s paperwork.

Apexion’s blends are supplied strictly for laboratory research. They are not for human or veterinary use. This page is general information, not medical or legal advice.

What Is a Peptide Stack?

A peptide stack is two or more peptides used together in one research protocol. Some labs keep each compound in its own vial or single-compound research pen and combine them at the bench. Others work from a pre-mixed blend, where fixed amounts of each peptide come together in a single vial or pen. Both count as peptide stacking.

So what are peptide stacks in practice? They come in two formats:

• Separate vials: each peptide is supplied on its own, and the researcher decides how to combine them.
• Pre-mixed blend: the combination is fixed at the point of manufacture, with one label and one batch number.

The word itself is gym slang. Scientific papers say “combination” or “co-administration”, which is why a literature search for “Wolverine stack” comes back nearly empty while “BPC-157 and thymosin beta-4” turns up real studies.

The logic behind combining is simple enough. Each peptide binds its own receptor or nudges its own pathway, so two compounds can reach the same system from different directions. The textbook case pairs a GHRH analogue (CJC-1295) with a ghrelin-receptor agonist (ipamorelin), two separate routes into pituitary growth-hormone signalling.

Peptides themselves are familiar ground for medicine. “A peptide is a legitimate molecule made from things we know about and already use,” Jeremy Korman, MD, told Cedars-Sinai in July 2026.

Why Are Peptides Studied Together?

Researchers study peptides together to compare complementary mechanisms inside one model. The working idea is that two compounds with different targets might reveal something neither shows alone. For most popular stacks, that idea comes from each peptide’s individual mechanism, and the combination itself has rarely been put to a direct test.

Three reasons come up again and again:

1. Different receptor targets. Two peptides hitting two receptors give a cleaner comparison than two peptides competing for one.
2. Different pathways in the same tissue model. A tendon or skin model lets a lab watch cell migration, collagen and blood-vessel signals side by side.
3. One blend, one batch. A fixed mix keeps the ratio identical from run to run and cuts down on bench handling.

Most synergy claims are built on paper, from what each compound does alone. The first direct test of the best-known pair only appeared in July 2026, when a team in Istanbul published a rat Achilles-tendon study with four groups: control, BPC-157, TB-500 and the two combined.

Both peptides improved tendon structure on their own, and TB-500 also raised the load the repaired tendon could take before failing. The combined group showed no extra gain over either peptide alone. The authors suggest the two may converge “on shared downstream pathways” and concluded that “both peptides warrant further investigation.”

That result gives a useful way to size up any stack. We call it the Pathway, Proof, Paperwork check:

Question	What to look for
Pathway	Do the components act on different receptors or pathways?
Proof	Has anyone studied the combination itself, or only each part?
Paperwork	Does the COA identify and measure every component?

What Is the Most Common Peptide Stack?

The two most common peptide stacks in the UK are BPC-157 + TB-500, known as the “Wolverine” stack, and CJC-1295 + ipamorelin. They’re the most searched and most sold combinations, and each pairs compounds with clearly different targets. GHK-Cu blends such as GLOW and KLOW come next.

BPC-157 + TB-500 brings together two peptides studied in tissue repair models, each from a different starting point. CJC-1295 + ipamorelin pairs two compounds that act on separate receptors in the same pituitary signalling system.

The copper-peptide blends are catching up quickly. “Peptide stacks KLOW” now has its own related search on Google, a sign of where interest in popular peptide stacks is heading.

Common Research Peptide Stacks at a Glance

The table below covers the combinations UK researchers look for most, what each component is studied for, and how much evidence exists for the combination itself. It doubles as a quick peptide stacking chart. In every row, the bulk of the published work looks at the peptides one at a time.

Stack	Components	What each component is studied for	Evidence for the combination
Wolverine	BPC-157 + TB-500	Gut, tendon and blood-vessel models; actin and cell migration	One 2026 rat tendon study; otherwise each peptide alone
KLOW	GHK-Cu + BPC-157 + TB-500 + KPV	As above, plus copper-peptide collagen research and KPV anti-inflammatory pathway models	Studies of each peptide on its own only
GLOW	GHK-Cu + BPC-157 + TB-500	Collagen, tissue and cell-migration models	Studies of each peptide on its own only
CJC-1295 + Ipamorelin	GHRH analogue + ghrelin-receptor agonist	Pituitary growth-hormone signalling via two receptors	Studies of each peptide on its own, plus a class-level mechanistic rationale

BPC-157 + TB-500 (the “Wolverine” Stack)

BPC-157 is a 15-amino-acid peptide based on a fragment of a gastric protein, studied mostly in rat models of gut, tendon and blood-vessel biology. TB-500 is a synthetic peptide based on thymosin β4, a protein best known for binding actin, the scaffolding inside cells. The pair is a classic two-pathway combination, and the 2026 tendon study above is the first to test them side by side. Our BPC-157 vs TB-500 guide compares them in detail, and the Wolverine blend specification and COA lists the 10mg + 10mg contents.

CJC-1295 + Ipamorelin

CJC-1295 mimics GHRH, the hypothalamic signal that tells the pituitary to release growth hormone. Ipamorelin binds the ghrelin receptor, a separate switch on the same cells. The precedent comes from the drug class: a 1990 study led by Cyril Bowers found that a GHRP and GHRH acted synergistically through independent mechanisms. Here’s why CJC-1295 and Ipamorelin are studied together, and the CJC-1295 + Ipamorelin specification (no DAC, 5mg + 5mg).

KLOW and GLOW

Both blends add GHK-Cu, a copper-binding tripeptide. A 2018 gene-data review by Loren Pickart reported that GHK changes the expression of 31.2% of human genes by 50% or more. KLOW then adds KPV, a three-amino-acid fragment of alpha-MSH. See the KLOW vs GLOW key differences and our GHK-Cu research overview.

Wolverine vs KLOW vs GLOW: What’s in Each Stack?

All three blends contain BPC-157 and TB-500 at 10mg each. GLOW adds 50mg of GHK-Cu, and KLOW adds the same GHK-Cu plus 10mg of KPV. Wolverine is the two-peptide base, GLOW is the three-peptide version, and KLOW is the four-peptide version with the largest total mass.

	Wolverine	GLOW	KLOW
BPC-157	10mg	10mg	10mg
TB-500	10mg	10mg	10mg
GHK-Cu	None	50mg	50mg
KPV	None	None	10mg
Total	20mg	70mg	80mg

GHK-Cu makes up most of the mass in GLOW and KLOW, so the copper peptide is the main thing separating them from Wolverine. The peptide stack names themselves are branding. Wolverine borrows from the Marvel character, while GLOW and KLOW are trade names you won’t find in a single paper.

Apexion supplies all three as pre-filled research pens, prepared to order in the UK. Full details are on the Wolverine blend specification and COA, GLOW 70mg specification and COA and KLOW 80mg specification and COA pages.

Pre-Mixed Blend vs Separate Vials: What’s the Difference?

A pre-mixed blend puts fixed amounts of each peptide into one vial or pen, so the ratio is set before it reaches the lab. Separate vials let a researcher change the ratio between experiments, but every extra vial adds handling steps, documents to file and chances for error at the bench.

Factor	Pre-mixed blend	Separate vials
Ratio flexibility	Fixed by the manufacturer	Set by the researcher
Handling steps	One item to prepare and log	One per peptide
Consistency between runs	Same ratio every batch	Depends on bench technique
Documentation	One COA covering every component	One COA per vial
Storage	One set of conditions	Each peptide on its own label guidance

Each format suits a different design. A study that tests different ratios needs separate vials, while one that repeats a fixed combination many times gains from a blend, because the ratio can’t drift.

Apexion’s blends come as pre-filled research pens, which keep the fixed ratio in a sealed, measured format for laboratory handling. Our guide to peptide pens vs vials covers how the two compare.

Which Peptides Should Not Be Stacked Together?

There’s no validated list of peptides that shouldn’t be stacked, because almost no combinations have been formally studied. From a research-quality view, though, some pairings are much harder to justify than others. The weak spots are redundant targets, clashing chemistry and blends too crowded to verify.

• Two compounds on the same receptor. Pairing ipamorelin with another ghrelin-receptor agonist, or two GHRH analogues, gives no mechanistic reason to combine them. Any result becomes hard to pin on either one.
• Peptides with different stability or solvent needs. A blend has to suit every component at once. Copper-bound GHK-Cu, for example, brings metal-binding chemistry that the other peptides in a mix don’t share.
• Large blends with many components. Each extra peptide is another identity to confirm and another peak to measure on the COA.

All three points come back to the Pathway and Paperwork questions in the check above. If either one fails, the combination is a weak research tool. For an example of three compounds often grouped together but acting on different targets, see MOTS-c, SS-31 and NAD+ compared. For the individual compounds, see the MOTS-c Peptide UK guide, the MOTS-c 40mg specification and COA and the SS-31 30mg specification.

How Many Peptides Can You Stack at Once?

There’s no set limit on how many peptides can be stacked. Each added component makes results harder to attribute and the product harder to verify, so good research design usually favours the fewest variables that answer the question.

The arithmetic gets steep fast. Testing two peptides properly took the 2026 tendon study four groups. A full test of a four-peptide blend, covering every on-off combination, would need 16.

Is Peptide Stacking Legal in the UK?

Peptide stacking follows the same UK rules as single peptides. Research blends are legal to buy and sell as laboratory materials, but they can’t be sold or advertised for human use. Most of the individual components are also banned in sport under the WADA Prohibited List, which UKAD enforces in the UK.

Regulatory Status

The MHRA regulates medicines under the Human Medicines Regulations 2012. A licensed medicine holds a marketing authorisation, and research peptides hold none. The MHRA’s Guidance Note 8, amended in March 2026, decides whether something counts as a medicine by its presentation and function, including implicit claims on websites and social media. Our guide on are peptides legal in the UK goes further.

Sport

BPC-157 is named under S0 (non-approved substances) on the WADA list. TB-500, CJC-1295 and ipamorelin fall under S2 (peptide hormones, growth factors and related substances). All are banned at all times, in and out of competition. More detail is in our BPC-157 UK guide and TB-500 Peptide UK guide.

How to Verify a Peptide Blend

A blend’s certificate of analysis (COA) should identify and measure every component separately. A single overall purity figure can’t tell you whether one peptide in the mix is short or missing. Look for a separate HPLC result and LC-MS mass for each peptide, matched to the lot on the label.

Run through this checklist with the COA in hand:

1. The lot number on the vial or pen matches the COA.
2. Each peptide is listed with its own HPLC peak and purity.
3. There’s an LC-MS mass for each component.
4. The amount of each component is stated (for example, 10mg + 10mg).
5. The testing lab, method and test date are named.

Apexion prepares each blend to order, so the batch is tested after it’s made and the certificate follows that batch. Scan the QR code on the product or enter the batch number to pull it up. Our guides explain how to read a peptide COA, how to verify a research peptide batch and how to evaluate a research peptide supplier. The Apexion batch verification page shows the process step by step.

Frequently Asked Questions

The Bottom Line

Peptide stacks combine compounds with different mechanisms, and that logic is sound. The evidence, though, still comes mostly from studies of each peptide alone, with the first direct test of a popular pair arriving in 2026. The same UK rules apply to blends as to single peptides, and every component should appear separately on the COA.

Apexion’s blends are supplied strictly for laboratory research and are not for human or veterinary use. To compare specifications, browse Apexion research stacks.

Sources

• Biçer O, Adanir O, et al. Effects of BPC-157 and TB-500 on Achilles tendon healing in rats. Jt Dis Relat Surg, July 2026. PubMed
• Bowers CY, et al. GH-releasing peptide stimulates GH release and acts synergistically with GHRH. J Clin Endocrinol Metab, 1990. Oxford Academic
• Pickart L, Margolina A. Regenerative and protective actions of the GHK-Cu peptide in the light of the new gene data. Int J Mol Sci, 2018. PMC
• Cedars-Sinai. Peptide Therapy: What the Science Shows About BPC-157, TB-500 and Wolverine Stacks. July 2026. Cedars-Sinai
• MHRA. Guidance Note 8: A guide to what is a medicinal product (amended March 2026). GOV.UK
• WADA Prohibited List 2026 and UK Anti-Doping. UKAD

Quick answer

What is BPC-157?

BPC-157 (Body Protection Compound-157) is a synthetic 15-amino-acid peptide based on a fragment of a protein found in human gastric juice. Researchers have studied it mainly in animal and cell models of gut, tendon and blood-vessel biology. In the UK it’s legal to buy as a research material, though it isn’t a licensed medicine.

• Synthetic pentadecapeptide, supplied for research use only
• The evidence is mostly preclinical, and human data is very limited
• Banned in sport under the WADA Prohibited List (S0)

BPC-157 has had a busy 2026. In April, a Guardian investigation led the MHRA to look into UK clinics making claims about it. In July, the BBC reported on a US FDA panel vote to ease restrictions on it. All that attention has landed on a small peptide that started life in a Croatian university lab.

Below you’ll find what BPC-157 is, where it stands under UK law, what the studies show so far, why it’s banned in sport, and how to check a batch before it reaches the bench.

We supply BPC-157 strictly for laboratory research. It is not a medicine and is not for human or veterinary use. This page is general information, not medical or legal advice.

What Is BPC-157?

BPC-157 is a pentadecapeptide, a chain of 15 amino acids, made in the lab to match part of a larger protein found in human gastric juice. The name stands for Body Protection Compound-157. Most of what’s known about it comes from rat and cell studies published since the early 1990s.

The story starts with Predrag Sikirić at the University of Zagreb School of Medicine. His team collected gastric juice from hospital clinics, isolated a parent protein and, in 1990, named its active 15-residue stretch BPC-157. According to a 2026 Undark investigation, the Croatian drugmaker PLIVA later ran two early human trials in ulcerative colitis, and the rights returned to Sikirić in 2009.

Sikirić, who has worked on the idea since his student days in 1975, summed up his view of drug research to Undark in one line: “What is the essential purpose of the drug? To be useful for the people.”

One property turns up again and again in the Zagreb papers. BPC-157 is described as stable in human gastric juice, an acidic, enzyme-rich environment that breaks most peptides apart. That stability is why oral and capsule forms appear in the animal research alongside dissolved ones.

BPC-157 fact sheet
Full name	Body Protection Compound-157
Class	Synthetic pentadecapeptide (15 amino acids)
Sequence	Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val (GEPPPGKPADDAGLV)
Molecular formula	C62H98N16O22
Molecular weight	~1419.5 g/mol
CAS number	137525-51-0
Half-life (animal data)	Under 30 minutes
Standard research form	Lyophilised (freeze-dried) powder
Storage	Cold, dry and dark; long-term storage is typically at −20 °C

The BPC-157 20mg specification and COA page shows these values alongside the current batch’s test data.

How Does BPC-157 Work?

The mechanism of BPC-157 isn’t fully established, and no single receptor for it has been identified. Lab studies have traced its activity through several overlapping signalling pathways linked to blood-vessel growth, cell movement and tissue structure. Nearly all of that work is preclinical.

The pathways that come up most often are:

• Angiogenesis and VEGFR2 signalling. Rat studies have looked at BPC-157 alongside VEGFR2, the receptor that drives new blood-vessel formation. A 2025 narrative review by McGuire and colleagues names it among the best-documented pathways.
• The nitric oxide pathway. The same review points to nitric oxide production through the Akt-eNOS axis, the signal that relaxes and widens blood vessels.
• Growth-hormone-receptor expression. Cultured tendon fibroblasts exposed to BPC-157 have shown more growth-hormone receptors on their surface.
• FAK-paxillin signalling. Cell-migration studies have examined BPC-157’s effect on FAK and paxillin, two proteins that help cells crawl, spread and anchor.

A common thread runs through these studies. Much of the tendon research focuses on tissue with a poor blood supply, which is why angiogenesis became the pathway researchers keep returning to.

Is BPC-157 a Growth Hormone?

No. BPC-157 is a short peptide and isn’t a hormone or a growth-hormone secretagogue (a compound that prompts the pituitary gland to release GH). The confusion traces back to one line of research on tendon cells, where BPC-157 was studied for its effect on growth-hormone-receptor numbers.

A 2025 systematic review in the HSS Journal reported that BPC-157 “enhances growth hormone receptor expression”. Receptor expression describes how ready a cell is to respond to growth hormone already in circulation. Secretagogues such as ipamorelin act at the pituitary, whereas BPC-157 research has stayed at the level of local tissue signalling.

What Does the Research on BPC-157 Actually Show?

Most BPC-157 research has been carried out in rats and cell cultures, across gut, tendon, muscle, bone and blood-vessel models. Human data comes from a handful of small pilot and retrospective reports. A randomised, placebo-controlled Phase 2 trial began in 2026 and is due to report in 2027.

On the preclinical side, the picture is encouraging. The McGuire review describes BPC-157 as “a potentially valuable tool in musculoskeletal medicine” and calls for well-designed human trials to test it properly. The same authors counted three published human pilot studies, covering knee pain, interstitial cystitis and an intravenous safety study.

Research area	Model	Evidence level
Gastrointestinal (ulcer and IBD models)	Rat	Preclinical: many studies, mostly from one research group
Tendon and ligament	Rat, cell culture	Preclinical
Muscle and bone	Rat	Preclinical
Blood vessels (angiogenesis)	Rat, cell culture	Preclinical
Human	Small pilot and retrospective reports	Very limited, with no large controlled trials published

Much of the published work comes from Sikirić’s group in Zagreb, and replication by independent labs is still thin. Reviewers treat that as the main gap to close, since findings carry more weight once a separate team can reproduce them.

That independent test is now running. In February 2026, Hudson Biotech began a randomised, double-blind, placebo-controlled Phase 2 trial at Peking University Shenzhen Hospital, enrolling 120 adults with MRI-confirmed hamstring strains, according to its ClinicalTrials.gov record (NCT07437547). Primary completion is estimated for February 2027, which makes it the trial to watch.

Is BPC-157 Legal in the UK?

Yes, as a research material. BPC-157 isn’t a controlled drug under the Misuse of Drugs Act 1971, so buying and holding it for laboratory work is lawful. It has no MHRA marketing authorisation, though, so it can’t legally be sold, supplied or advertised for human use.

UK law draws its line at how a product is presented. Under the Human Medicines Regulations 2012, anything offered to treat or prevent a condition counts as a medicine, whatever its label says. For the wider rules on other compounds, see our guide: are peptides legal in the UK.

Can You Buy BPC-157 in the UK?

Yes. UK research suppliers stock BPC-157 labelled for research use only, as lyophilised powder, pre-mixed solution or pre-filled research pens. Suppliers working within the rules describe identity, purity and storage, and make no claims about effects in people. Our Research Use Only policy sets out how Apexion applies this to every order.

Is BPC-157 Available on the NHS?

No. There’s no licensed BPC-157 product in the UK, and it has no place in NHS treatment pathways, so GPs and hospital doctors don’t offer it. Anyone searching “BPC-157 UK NHS” will find it only through private clinics and research suppliers, and that’s where the regulator has turned its attention.

What Has the MHRA Said?

In April 2026, a Guardian investigation found UK clinics claiming BPC-157 helps with recovery from injuries. The MHRA confirmed these were medicinal claims, which clinics aren’t allowed to make.

Once a clinic makes medicinal claims, the MHRA said, its peptide products “will be considered medicines”. At least one clinic deleted its claims after the Guardian got in touch. The MHRA also said it will take action against clinics found breaching the rules, and a “research only” label gives no cover to a seller who markets health outcomes.

What Is the FDA’s Position on BPC-157?

BPC-157 isn’t FDA-approved. In 2023, the FDA placed it in Category 2, its list of substances with safety concerns for compounding. It came off that list in April 2026, and on 23 July an FDA advisory panel voted 8 to 6 to recommend it for US compounding pharmacies. The FDA’s final decision is still pending.

The BBC’s coverage of the vote, published on 24 July 2026, noted that the FDA doesn’t have to follow the panel but often does. For UK readers, the vote changes nothing on the ground. US compounding rules have no bearing on MHRA licensing, so BPC-157’s UK status stays the same whichever way the FDA rules. We’ll update this page when that decision lands.

Why Is BPC-157 a Banned Substance in Sport?

WADA lists BPC-157 under S0, non-approved substances, because no health authority anywhere has approved it for human therapeutic use. It has been named on the Prohibited List since 2022 and is banned at all times, in and out of competition. In the UK, UKAD enforces the ban.

S0 works as a catch-all category. Any substance without human approval falls under it, named or not, and a search of the WADA Prohibited List for BPC-157 returns S0 with the status “all times”.

Anti-doping rules run on strict liability. Athletes in UKAD’s testing pool are responsible for anything found in their sample, including traces from a mislabelled supplement, and a supplement marketed as a “BPC-157 complex” puts them in exactly that position.

What Are the Known Risks and Side Effects of BPC-157?

Human safety data on BPC-157 is very limited, so its side effects in people aren’t established. The three human pilot studies were small and short, and no long-term follow-up exists. Regulators want long-term safety data before they’ll approve a medicine, and for BPC-157 that data hasn’t been gathered yet.

The open questions researchers discuss fall into three groups:

• Long-term data. No study has followed people over months or years, so any late or cumulative effects remain unknown.
• Angiogenesis. Reviews note a theoretical question: a compound studied for new blood-vessel growth could, in principle, act on tissue where extra blood supply is unwanted, such as tumours. No study has shown this; it remains a question for future trials.
• Product identity. Unverified products may be mislabelled, underfilled or contaminated. That risk comes from the supply chain, and a batch COA is the way to rule it out.

Is BPC-157 Bad for the Heart?

There’s no reliable human evidence either way. Sikirić’s group has published rat studies in cardiovascular models, including heart-muscle and heart-rhythm models, but no human cardiac data has been published. For now, the effect of BPC-157 on the human heart is unknown.

BPC-157 Capsules vs Lyophilised Vials: What’s the Difference?

Research-grade BPC-157 normally comes as freeze-dried powder in a sealed vial, backed by a batch COA. Many “BPC-157 capsules” or “BPC-157 amino complex” products sold as supplements on Amazon UK are amino-acid blends, and they may contain little or no verified BPC-157.

	Lyophilised vial	Pre-filled research pen	Supplement capsule or tablet
What’s inside	Freeze-dried BPC-157 powder	BPC-157 prepared to order	Often an amino-acid blend
Batch COA	Expected	Expected	Rarely supplied
Identity tested	HPLC, often LC-MS	HPLC	Seldom stated
UK status	Research material	Research material	Sold as a food supplement

Searches for “BPC-157 capsules UK”, “BPC-157 tablets” and “BPC-157 Holland and Barrett” usually lead to this third column. We’re not aware of any authorised BPC-157 food supplement in the UK, so a capsule’s label claim is only as good as the lab data behind it.

Apexion supplies BPC-157 in pre-filled research pens, prepared to order in the UK, each with its own batch COA. Our comparison of peptide pens vs vials covers how the two formats differ for lab handling.

BPC-157 vs TB-500

BPC-157 and TB-500 are different peptides with different research areas. BPC-157 is a 15-amino-acid fragment based on a gastric protein. TB-500 is a synthetic fragment of thymosin beta-4, a protein found in most cells and studied for its role in cell migration.

Researchers often study the two side by side in tendon and muscle models. Our BPC-157 vs TB-500 research comparison goes through each one, and the BPC-157 + TB-500 blend specification lists our combined format for research. Both peptides also appear in the multi-peptide blends compared in KLOW vs GLOW.

How to Check the Quality of Research-Grade BPC-157

A reliable batch of BPC-157 comes with a certificate of analysis that ties the product in your hand to named lab data. Before any BPC-157 goes into an experiment, check the COA for these five points:

1. A batch-specific COA. The lot number on the certificate should match the one on the product. A generic, undated certificate proves nothing about your batch.
2. HPLC purity, with the method stated. Look for the percentage purity plus the column, wavelength or gradient used.
3. An LC-MS observed mass near 1419.5 Da. Many reports show the doubly charged ion instead, at around 710 m/z, which confirms the same molecule.
4. The testing lab and test date. A named lab and a recent date make the result traceable.
5. Storage guidance. The COA or product sheet should state storage conditions for that specific batch.

Our guide on how to read a peptide COA goes through a real certificate line by line, and you can verify a research peptide batch with the same checks. For conditions after delivery, see peptide storage and handling.

Our BPC-157 is third-party tested, typically ≥98% HPLC-verified, and each batch links to its COA through a QR code or batch number. Our batch verification shows how to look one up.

Frequently Asked Questions

The Bottom Line

BPC-157 is a legal UK research material and not a licensed medicine. Its evidence base is mostly animal and cell studies, and a controlled human trial is due to report in 2027. It’s banned in sport at all times, and the MHRA is watching clinics that make claims about it.

For laboratory work, choose a supplier with batch-matched documentation. Apexion supplies BPC-157 for research use only, never for human or veterinary use.

View BPC-157 20mg specification and COA

Sources

• McGuire FP et al. “Regeneration or Risk? A Narrative Review of BPC-157 for Musculoskeletal Healing.” Current Reviews in Musculoskeletal Medicine, 2025. PMC12446177
• Vasireddi N et al. “Emerging Use of BPC-157 in Orthopaedic Sports Medicine: A Systematic Review.” HSS Journal, 2025. PMC12313605
• ClinicalTrials.gov. NCT07437547, BPC 157 for Acute Hamstring Muscle Strain Repair. Record
• Undark. “A Peptide, a Secretive Scientist, and a Debate Over Evidence”, 29 May 2026. Article
• The Guardian. “Medicines watchdog to investigate UK peptide clinics over health claims”, 4 April 2026. Article
• BBC News. “FDA panel votes to loosen restrictions for controversial peptides”, 24 July 2026. Article
• World Anti-Doping Agency. The Prohibited List. wada-ama.org

Peptides spent much of 2026 in the headlines. The BBC ran a feature on the “wellness peptide craze” in March, and The Guardian followed in April by asking what the evidence says. One question got far less airtime than the science: are peptides legal in the UK, and who’s allowed to buy, sell or own them?

The answer depends on the peptide and on how it’s sold. This guide covers buying, selling, possession, importing, sport and drug testing, then runs eight well-known compounds past each rule.

This article is general information, not legal advice. Apexion products are supplied strictly for laboratory research use only and are Research Use Only.

Quick answer: are peptides legal in the UK? Most research peptides are legal to buy, sell and possess in the UK as laboratory research materials. They aren’t licensed medicines, so nobody can legally sell, supply or advertise them for human use. A few peptide hormones, including somatropin (HGH) and HCG, are Class C controlled drugs, and many peptides are banned in sport.

Key facts

1. Research peptides aren’t banned in the UK, though most have no MHRA licence as a medicine.
2. Selling or advertising a peptide for human use without a marketing authorisation breaks the Human Medicines Regulations 2012.
3. “Research use only” means laboratory work and doesn’t cover personal use.
4. Somatropin (HGH), somatrem and HCG are Class C drugs under the Misuse of Drugs Act 1971.
5. The WADA Prohibited List bans many peptides at all times, and UK Anti-Doping (UKAD) enforces it here.

What Counts as a “Peptide” Under UK Law?

UK law has no single rule for “peptides”. A peptide is a short chain of amino acids, and the same molecule can be regulated as a medicine, a cosmetic ingredient or a research chemical. Which law applies depends on how the product is presented and what it’s for.

Category	Examples	Rules that apply
Licensed medicine	Insulin, semaglutide (Wegovy), tirzepatide (Mounjaro)	MHRA marketing authorisation; most are prescription-only
Cosmetic ingredient	Copper tripeptide-1 (GHK-Cu) in face serums or other topicals	UK cosmetics rules; for use on the skin
Research material	BPC-157, TB-500 and MOTS-c supplied to labs	Sold for laboratory work, with no claims about human use

The dividing line is written into the Human Medicines Regulations 2012. Regulation 2 treats a product as a medicine if it’s “presented as having properties of preventing or treating disease in human beings”, or if people use it to change how the body works.

In practice, a product page or a social media caption can turn a research chemical into an unlicensed medicine overnight. The chemistry stays the same, but the legal category changes.

Which UK Laws Apply to Peptides?

Four UK frameworks cover peptides. The Human Medicines Regulations 2012 govern medicines, the Misuse of Drugs Act 1971 controls a short list of peptide hormones, the Psychoactive Substances Act 2016 covers mind-altering products, and UK cosmetics law covers skincare. The MHRA enforces medicines law, and WADA and UKAD set the rules for sport.

To check any single compound, run it through four questions. We call this the Four-Checkpoint Test:

1. Licensed? Does it hold a UK marketing authorisation as a medicine?
2. Controlled? Is it listed under the Misuse of Drugs Act 1971?
3. Claims? Is anyone selling it with health, dosing or body-change promises?
4. Sport? Is it on the WADA Prohibited List?

Human Medicines Regulations 2012

These regulations (SI 2012/1916) are the main UK law for anything sold as a medicine. Three rules do most of the work:

• Regulation 46: nobody may sell or supply a medicinal product without a marketing authorisation.
• Prescription-only medicines: these can only be supplied against a valid prescription.
• Regulations 279 and 284: no advertising a medicine that has no authorisation, and no advertising prescription-only medicines to the public.

Regulation 46 reaches stockholders too. Keeping an unauthorised medicine is an offence when the person knows, or has reason to believe, it’s meant to be sold or supplied to someone else.

Misuse of Drugs Act 1971

Most research peptides aren’t controlled substances. The exceptions are a handful of peptide hormones listed in Class C alongside anabolic steroids. Schedule 2, Part III of the Act names chorionic gonadotrophin (HCG), non-human chorionic gonadotrophin, somatotropin, somatrem and somatropin.

Supplying these hormones without authority is an offence, and so is importing them without a Home Office licence. The Misuse of Drugs Regulations 2001 exempt possession when they’re in the form of a medicinal product. As a result, the law treats owning one very differently from selling it.

Psychoactive Substances Act 2016

The 2016 Act bans producing or supplying substances for their mind-altering effects, the products once sold as “legal highs”. It rarely touches research peptides. Schedule 1 exempts controlled drugs and medicinal products outright, so a peptide sold with health claims falls under medicines law, and a Class C hormone falls under the Misuse of Drugs Act.

UK Cosmetics Regulation

Peptide skincare follows its own route. Copper peptide serums, usually listed as copper tripeptide-1 on the label, are cosmetics under UK law. Before sale, the brand needs a UK Responsible Person, a product safety report and a notification through the government’s cosmetics portal. For the lab science behind the molecule, see our GHK-Cu research overview.

The MHRA’s Role

The Medicines and Healthcare products Regulatory Agency (MHRA) licenses medicines and acts against unlicensed ones. None of the research peptides in this guide are MHRA-approved.

The MHRA’s Criminal Enforcement Unit works with Border Force, the police and internet companies. In 2025, it seized almost 20 million doses of illegally traded medicines, valued at nearly £45 million, and disrupted more than 1,500 websites and social media accounts. In April 2026, it opened inquiries into UK clinics making medical claims about peptide injections.

Is It Legal to Buy Peptides in the UK?

Yes, you can legally buy most peptides in the UK as research materials, and owning them isn’t a criminal offence. The Class C peptide hormones, such as somatropin and HCG, are the exception, because the law controls how they’re supplied and imported. Buying a peptide legally doesn’t make it approved for human use.

The BBC’s March report called this a legal and regulatory grey area. Anyone can own a vial of BPC-157, yet no one can legally market it as a treatment.

The MHRA warns people against using unlicensed products, because nobody has assessed them for safety, quality or effectiveness.

Is It Legal to Sell Peptides in the UK?

Yes, selling peptides for laboratory research is legal in the UK. Selling, supplying or advertising them for human use without a marketing authorisation breaks the Human Medicines Regulations 2012, because the product then counts as an unlicensed medicine. So the same vial can be a lawful research sale or an illegal medicine sale, depending on how it’s marketed.

Things that make a sale unlawful:

• Health, healing, anti-ageing or weight-loss claims
• Dosing instructions or “how to use” guides
• Before-and-after photos or results stories
• Marketing aimed at consumers for self-use

Things a compliant research supplier does:

• Labels products research use only (RUO) and keeps every description to identity, purity and storage.
• Makes no therapeutic claims anywhere, including on social media.
• Publishes batch documents, such as a certificate of analysis for each lot.
• Age-gates the website and asks buyers to confirm a research purpose.
• Applies written terms of sale that set out permitted use.

You can see how we apply this in our Research Use Only policy and our terms of sale. The same rules apply to pre-filled pens: see are peptide pens legal in the UK.

What Does “Research Use Only” Mean on Peptides?

“Research use only” (RUO) means a product is supplied for laboratory research, such as in-vitro, analytical or preclinical work. It isn’t approved or intended for use in people or animals, or for diagnosing or treating anything. The label tells you who the product is for and how the supplier may sell it.

An RUO label only protects a sale when the marketing matches it. The MHRA’s Lynda Scammell said in April 2026, “We disregard claims that products are for ‘research purposes'” when they’re used to dodge medicines regulations.

New medicines begin with research-grade peptides. Stanford Medicine counts about 100 peptide therapeutics approved by the FDA, and Professor Katrin Svensson says peptides for conditions such as Alzheimer’s disease are now a realistic possibility. A 2021 review in Nature Reviews Drug Discovery counted hundreds more candidates in preclinical and clinical testing.

A good research reagent supplier gives you:

• A batch or lot number on every product
• A certificate of analysis (COA) for that batch
• The testing method, usually HPLC and sometimes LC-MS
• Storage guidance for the material

Every Apexion batch comes with a COA confirming identity and purity, which you can open by scanning the QR code or entering the batch number on our Apexion batch verification page. Our guides explain how to read a peptide certificate of analysis and how to verify a research peptide batch.

Can You Import Peptides Into the UK?

Yes, research peptides can be imported into the UK for genuine research. Border Force can stop, hold or seize parcels that look like unlicensed medicines or controlled drugs. Class C peptide hormones such as somatropin need a Home Office licence to import.

Ordering from overseas brings three common problems:

• Customs delays or seizure, which can hold up a research project for weeks
• No UK accountability if the order is wrong, damaged or never arrives
• Certificates you can’t check, with no way to link the document to the vial in your hand

Our guide on how to evaluate a UK research peptide supplier covers the checks that separate a traceable supplier from a risky one.

Are Peptides Prescription-Only in the UK?

Licensed peptide medicines such as semaglutide (Wegovy, Ozempic) and tirzepatide (Mounjaro) are prescription-only medicines in the UK. Research peptides aren’t medicines, so no prescription route exists for them, and they can’t replace prescribed treatment. Your GP or a registered pharmacy is the route to licensed care.

A few compounds sold as research peptides have been approved abroad but hold no UK licence:

• Tesamorelin: approved by the US FDA as Egrifta in 2010. Read more in our Tesamorelin research overview.
• Bremelanotide: approved by the FDA as Vyleesi in 2019.

Licensed peptide medicines are available on the NHS. The NHS began offering Mounjaro through GP practices for weight management in 2025, subject to clinical eligibility. Research peptides have no NHS route at all.

UK Legal Status of Common Research Peptides

None of the research peptides below holds a UK marketing authorisation, and none is a controlled drug. Sport is where the rules tighten: seven of the eight are named on, or covered by, the 2026 WADA Prohibited List. Somatropin is included at the bottom for comparison.

Peptide	UK marketing authorisation?	Controlled drug?	Banned by WADA (2026)?
BPC-157	No	No	Yes, S0 (named as a non-approved substance)
TB-500	No	No	Yes, S2 (thymosin-β4 derivative)
GHK-Cu	No (allowed in topical cosmetics)	No	Not named on the list
CJC-1295	No	No	Yes, S2 (GHRH analogue)
Ipamorelin	No	No	Yes, S2 (GH secretagogue)
Tesamorelin	No (approved in the US)	No	Yes, S2 (GHRH analogue)
MOTS-c	No	No	Yes, S4.4 (named as an AMPK activator)
Retatrutide	No (Phase 3 complete; Eli Lilly plans a US filing in early 2027)	No	Covered by S0 while unapproved
Somatropin (HGH), for comparison	Yes, as licensed brands	Yes, Class C	Yes, S2

Statuses checked against legislation.gov.uk and the WADA list on 26 September 2026.

Batch documents: BPC-157 20mg specification & COA · TB-500 10mg specification & COA · GHK-Cu 50mg specification & COA · CJC-1295/Ipamorelin 10mg specification & COA · MOTS-c 40mg specification & COA

Is BPC-157 legal in the UK?

Yes. BPC-157 is legal to buy and possess in the UK as a research material. It isn’t a controlled drug and holds no marketing authorisation, so it can’t be sold for human use. WADA names it in section S0, which bans it for athletes at all times. Our BPC-157 vs TB-500 research overview compares the two in the lab. For its full legal status, the research and how to check a batch, see our full BPC-157 UK guide.

Is CJC-1295 legal in the UK?

Yes, as a research material. CJC-1295 is an analogue of growth hormone-releasing hormone (GHRH), and it isn’t listed under the Misuse of Drugs Act. It holds no UK licence and is banned in sport under WADA’s S2. Researchers often study it alongside ipamorelin, and our CJC-1295 vs Ipamorelin guide explains why.

Are Peptides Banned in Sport?

Yes, many are. The WADA Prohibited List bans peptide hormones, growth factors and growth hormone secretagogues under section S2, and unapproved substances such as BPC-157 under S0. Both bans apply in and out of competition. UK Anti-Doping (UKAD) enforces the list for athletes in the UK.

Three sections of the 2026 list catch most research peptides:

• S0, non-approved substances: any drug with no human approval anywhere, including compounds still in clinical trials. BPC-157 is named here.
• S2, peptide hormones and growth factors: TB-500, CJC-1295, ipamorelin, tesamorelin and somatropin. The 2026 list added pegmolesatide as a new example.
• S4.4, metabolic modulators: MOTS-c is named as an AMPK activator.

Anti-doping works on strict liability. An athlete is responsible for anything found in their sample, however it got there.

Will Peptides Show Up on a Drug Test?

A standard workplace drug test usually won’t screen for peptides. Those panels look for drugs such as cannabis, cocaine, opiates and amphetamines. Anti-doping tests run by WADA-accredited laboratories use targeted methods, including mass spectrometry, that can detect many banned peptides and their breakdown products.

WADA funds ongoing research into detecting small peptide hormones, so the range of detectable compounds grows each year. The British Army runs its own Compulsory Drug Testing programme, covered in the FAQ below.

Are Peptides the Same as Steroids?

No. Peptides are short chains of amino acids, the same building blocks that make up proteins. Anabolic steroids are synthetic relatives of testosterone, built on a four-ring carbon structure. UK law treats them differently too: anabolic steroids are Class C drugs, while most research peptides aren’t controlled.

	Peptides	Anabolic steroids
Structure	Short amino-acid chains	Four fused carbon rings
Examples	BPC-157, GHK-Cu, insulin	Nandrolone, stanozolol
UK legal status	Mostly uncontrolled; a few hormones are Class C	Class C

How to Stay Compliant When Buying Research Peptides in the UK

A compliant purchase comes down to buying from the right supplier and keeping your paperwork in order. Run through this checklist before you order:

1. Buy from a UK supplier that labels every product research use only.
2. Check for a batch-specific COA that shows the testing method (HPLC or LC-MS) and names the lab.
3. Match the batch number on the product to the COA. Our guide shows how to verify a research peptide batch.
4. Avoid sellers making health, weight-loss or dosing claims. A seller willing to break medicines law gives you little reason to trust its testing.
5. Store and handle materials to lab guidance. See our notes on peptide storage and handling and on pre-filled pens vs vials.

For a deeper supplier check, read how to evaluate a UK research peptide supplier, or browse UK research peptides with batch documents attached.

Frequently Asked Questions

The Bottom Line

Most peptides are legal to buy, own and sell in the UK as research materials. None of the research compounds in this guide is licensed for human use, a handful of peptide hormones are Class C drugs, and many peptides are banned in sport. The safest purchase comes from a supplier that publishes its batch testing and makes no health claims.

Browse Apexion’s batch-verified research range or see how Apexion batch verification works.

Apexion products are supplied strictly for laboratory research use only and are Research Use Only.