group
Healing and recovery peptides
Six compounds people research for repair, taken one at a time: what each one is, what the published work measured, in which species, and what the agency record says as of August 2026.
Six compounds are grouped here because people research them for the same thing: repair. KPV is the last three amino acids of a hormone the body makes. BPC-157 is a fifteen amino acid sequence derived from a protein found in human gastric juice. TB-500 is a short synthetic fragment sold under the name of a much larger protein. GHK-Cu is a three amino acid peptide bound to a copper ion, which occurs naturally in blood plasma. Larazotide is an eight amino acid peptide taken by mouth. ARA-290 is an eleven amino acid piece of erythropoietin, engineered to leave the red-blood-cell effect behind.
The tissues split them. BPC-157 and TB-500 are researched for tendon, muscle and joint injury. GHK-Cu is researched for skin and connective tissue, and it is sold in two forms whose legal position is not the same: a listed cosmetic ingredient applied to skin, and an unapproved drug in a vial. KPV and larazotide are researched for the lining of the gut. ARA-290 was built for nerve, and is marketed well past that.
Each entry below names the species, the model and the design behind every result, and carries the tier of the strongest source that tested that compound for the use it is sold for. Evidence about a parent molecule sets no tier for a fragment, which matters most for TB-500. The reference list runs to 24 numbered sources: 19 primary papers and reviews, and five agency and registry documents. Identifiers were checked on 2 August 2026, and the GHK-Cu entry was rechecked on 8 August 2026 when its own review published.
Not medical advice
This page reports what has been documented about a compound. It is not medical advice, not a diagnosis, not a dosing protocol, and not a recommendation to obtain or use anything described here. Talk to a licensed clinician about anything concerning your health. Read the full disclaimer.
Reviewed against editorial standards Updated
The compounds in this group
Each row names what the compound is and what its published work covers. The evidence level is the strongest tier of evidence about that compound for the use it is sold for. It is a single figure for a whole entry rather than a claim by claim grading, so an entry may also describe work that is weaker, or that tested a different route or a different molecule, and each of those carries its own citation in the text. Where a compound's own review has been run, its page grades every claim area separately.
| Compound | Also known as | What the published work covers | Where it stands | Evidence level |
|---|---|---|---|---|
| KPV | Lysine-proline-valine, alpha-MSH (11-13) | Seven rodent colitis studies, a rabbit corneal wound model, a diabetic mouse wound model and human cell lines. Zero human studies on any route. Reviewed in full on its own page | Not on the FDA 503A Bulks List. Reviewed by the compounding advisory committee on 23 July 2026 | [Animal] |
| BPC-157 | Body Protection Compound-157, PL 14736, pentadecapeptide BPC | Rodent tendon, muscle, ligament and bone models, plus one published retrospective report of 16 people given an injection into the knee. Two registrations, neither reported | Was placed in FDA 503A Category 2 in 2023. Named on the face of the WADA S0 class | [Human open-label] |
| TB-500 | Thymosin beta-4 fragment, TB4 | One rat tendon study and rat metabolism work on the fragment itself. The eighteen registrations usually counted for it tested thymosin beta-4, a different molecule, in the eye and in skin ulcers | Unapproved. Named on the WADA list at S2 | [Animal] |
| GHK-Cu | Copper tripeptide-1, glycyl-L-histidyl-L-lysine copper | A rat knee-ligament model using injections into the joint, decades of cell work, and two randomized human trials of topical products, in 1992 and 2006, neither of which separated from its control on an objective measure. Reviewed in full on its own page | In FDA 503A category 1 for non-injectable routes. The injectable nomination was withdrawn from category 2 | [Human RCT] |
| Larazotide | AT-1001, INN-202 | Ten registered trials in coeliac disease taken by mouth, including a phase 2 in 342 people and a phase 3 in 307 that was terminated. Nothing tested the gut-health use it is now sold for | Unapproved. The phase 3 programme was discontinued in 2022 | [Human RCT] |
| ARA-290 | Cibinetide, Helix B surface peptide | Four registrations, all small: nerve fibre and pain endpoints in sarcoidosis and in type 2 diabetes, a cognition study, and a terminated eye study | Unapproved, and it never progressed beyond phase 2 | [Human RCT] |
Three of these six are fragments, and that is where the trial counts go wrong
TB-500 is a fragment of thymosin beta-4. KPV is a fragment of alpha-melanocyte-stimulating hormone. ARA-290 is a fragment of erythropoietin, deliberately redesigned. A fragment does not inherit the parent's trials, and this is the commonest way a compound in this category acquires a research record it never earned.
The clearest case is TB-500. Analysis of the product itself identified Ac-LKKTETQ, the acetylated 17 to 23 fragment of a 43 residue protein [7]. Thymosin beta-4 has eighteen registrations behind it. TB-500 has one, and it is not about tendons [22].
ARA-290 shows the same split running the other way, and honestly. It was engineered so that it would not do what its parent does, which is raise red cell counts, and its trials are its own [17] [18].
Where the registered trials in this group actually sit
Counting registrations on ClinicalTrials.gov for these six on 2 August 2026 gives a lopsided picture [22]. Larazotide has by a wide margin the most: ten studies of larazotide itself, in coeliac disease, by mouth. A free-text search returns 29, and the difference is a name collision worth knowing about, because AT-1001 is also the development code for migalastat, an approved Fabry disease drug that has nothing to do with this molecule.
ARA-290 has four registrations. BPC-157 has two, one of which was first posted in December 2015 and carries a status of unknown. TB-500 has one, first posted in March 2026, whose primary outcomes are counts of adverse events rather than any measure of repair. GHK-Cu returns three records to a free-text search and only one of them is a trial of the compound itself: a phase 2 split-wound study of a topical gel, recruiting since 2 February 2026. Of the other two, one is a completed open-label device study that applied a multi-ingredient serum containing the compound to all 27 participants with no control arm, and the other measures circulating GHK levels rather than administering anything. KPV has none.
Registered is not the same as completed, and completed is not the same as published. Where a trial has read out, the entry below says what it measured and what it found, including where it found nothing.
The six compounds, one at a time
KPV
Also known as Lysine-proline-valine, Lys-Pro-Val, alpha-MSH (11-13), MSH 11-13
Plain-English version: The last three amino acids of a hormone the body makes, studied as an anti-inflammatory agent in rodents and in cell culture.
Strongest evidence, and what it covers [Animal] Gut and skin inflammation [1] [19] [20] [22]
KPV is lysine, proline and valine: residues 11 to 13 of alpha-melanocyte-stimulating hormone, and nothing else. It has a finished evidence review on this site running to 32 numbered sources, so this entry is a pointer rather than a summary that could drift from it.
What has been studied is rodent and cell work. Seven rodent colitis studies sit behind the gut claim, five of them delivering KPV inside an engineered carrier rather than as free peptide, and uptake into the intestinal lining runs through the PepT1 transporter in human cell lines and in mice, where deleting the transporter removed the effect entirely [1]. Beyond the gut there is a rabbit corneal wound study, a diabetic mouse wound study that delivered a growth factor alongside, and cell work in human intestinal, bronchial and skin lines. The hub records zero human studies on any route, confirmed four separate ways, and grades the compound D.
Where it stands KPV is not on the FDA 503A Bulks List. The Pharmacy Compounding Advisory Committee took it up on 23 July 2026, in the same morning session as BPC-157, on two separate voting questions covering the free base and the acetate salt [20]. The use FDA evaluated was wound healing and inflammatory conditions [19].
Our takeThe only compound in this group with a finished review on this site, and that review is exactly why it carries the lowest grade available.
BPC-157
Also known as Body Protection Compound-157, PL 14736, Pentadecapeptide BPC
Plain-English version: A fifteen amino acid sequence derived from a protein found in human gastric juice, researched in rodent injury models and sold for injury recovery.
Strongest evidence, and what it covers [Human open-label] Tendon, muscle and joint recovery [2] [3] [4] [5] [6] [9] [22]
BPC-157 is a fifteen residue sequence, GEPPPGKPADDAGLV, taken from a protein found in human gastric juice. It is the highest-volume compound here outside the metabolic group, and its record is almost entirely rodent.
In rats whose Achilles tendon was cut through, animals given the peptide into the abdominal cavity showed a higher load to failure and smaller tendon defects than saline controls over 14 days [2]. A crushed calf muscle model reported differences in repair and in enzyme markers [3]. In rat tendon fibroblasts, growth hormone receptor expression rose at the messenger RNA and protein level [4]. A 2025 systematic review counted 36 studies from 1993 to 2024, 35 of them preclinical [6].
One human report is published: a retrospective chart review at a single Florida clinic, covering injection into the knee for knee pain. Seventeen patients, 16 reached by telephone, 12 of them on BPC-157 alone, pain rated from memory, no measurement instrument and no control arm [5]. Two registrations exist, neither reported: a phase 1 in 42 people, first posted December 2015, status unknown; and a randomized phase 2 in acute hamstring strain, 120 people, recruiting since 27 February 2026, primary completion estimated February 2027 [22].
Where it stands The use FDA evaluated for BPC-157 was ulcerative colitis, per its Federal Register notice of 16 April 2026 under Docket No. FDA-2025-N-6895 [19], and the advisory committee took it up on 23 July 2026 on two voting questions [20]. It is named on the face of the S0 class of the WADA 2026 Prohibited List, which is prohibited at all times, in and out of competition [21].
Our takeThe distance between what was measured, cut rat tendons over 14 days, and what is claimed, human injury recovery, is the widest in this group. The hamstring trial recruiting now is the first thing capable of closing it.
TB-500
Also known as Thymosin beta-4 fragment, TB4
Plain-English version: A short synthetic fragment of thymosin beta-4, an actin-binding protein, sold under the parent protein's reputation.
Strongest evidence, and what it covers [Animal] Tendon and muscle recovery, and the parent molecule [7] [8] [9] [10] [11] [22]
TB-500 and thymosin beta-4 are different molecules. Thymosin beta-4 is a 43 residue protein. A doping-control laboratory that analysed the product sold as TB-500 identified Ac-LKKTETQ, the acetylated 17 to 23 fragment, seven residues long [7]. The registrations split the same way: eighteen name the parent, one TB-500 [22].
Those eighteen tested the parent, in the eye and in skin, not tendon or muscle. A phase 2 in severe dry eye covered nine patients [10]. A phase 3 in neurotrophic keratopathy reported closure of epithelial defects in 6 of 10 treated patients against 1 of 8 on placebo, short of significance [11].
Work on the fragment itself is thin. In 32 rats with a cut and repaired Achilles tendon, the eight given TB-500 into the abdominal cavity over four weeks reached a higher maximum load to failure than controls and lower degeneration scores; adding BPC-157 changed nothing [9]. A 2024 study tracked TB-500 in rats and found that in a fibroblast scratch assay the metabolite Ac-LKKTE, not the parent fragment, separated from control [8]. The one registration naming TB-500 is a phase 1/2 in 80 people, first posted March 2026, with counts of adverse events as its primary outcomes [22].
Where it stands The use FDA evaluated for TB-500 was wound healing, per the Federal Register notice of 16 April 2026 [19], and the advisory committee took it up on the afternoon of 23 July 2026 on two voting questions [20]. TB-500 is named on the WADA 2026 Prohibited List in class S2.3, growth factors and growth factor modulators, in the entry reading thymosin beta-4 and its derivatives, and that class is prohibited at all times [21].
Our takeEvery trial count published for this compound is really a count for a molecule seven times its length, tested in an eye. That substitution is the single most useful thing to know about it.
GHK-Cu
Also known as Copper tripeptide-1, Glycyl-L-histidyl-L-lysine copper, Copper peptide
Plain-English version: A three amino acid peptide bound to a copper ion, present in blood plasma, sold both as a cosmetic ingredient and as an injectable.
Strongest evidence, and what it covers [Human RCT] Connective tissue repair from injected GHK-Cu. The topical route is covered separately [12] [13] [14] [20] [22] [23] [24]
GHK-Cu is glycine, histidine and lysine holding a copper ion. It occurs naturally in plasma, the observation the marketing rests on. Two products carry the name: a topical form sold as a cosmetic ingredient, and a vial that is an unapproved drug. It has a finished evidence review on this site running to 29 numbered sources, so this entry is a pointer rather than a summary that could drift from it.
Two randomized human trials have read out, both topical, and neither separated from its control on a measure an assessor or an instrument made. The 1992 trial ran to 86 evaluable patients with venous stasis ulcers and found no difference between a tripeptide copper complex cream and an inert vehicle, in a trial where a third arm did beat both [23]. The 2006 trial ran to 13 patients after carbon dioxide laser resurfacing and found no difference in erythema, wrinkles or skin quality on the blinded and computer-assisted assessments; the one measure that separated was the patients' own questionnaire [12].
The mechanism writing behind the topical claim is mostly review articles rather than measurements, and the most-cited of them is a 2015 review from a company research and development department [14]. The closest animal work to the injected form is a rat knee study. Seventy-two rats had their anterior cruciate ligament reconstructed, then weekly injections into the joint for four weeks. At six weeks the treated groups had a smaller side to side difference in knee laxity than saline. At twelve weeks, after treatment stopped, no difference remained [13]. No published study has given GHK-Cu by injection to a person for a systemic purpose [22]. The hub sets out the rest, including the two ex vivo skin-permeation studies that contradict each other, and grades the compound B.
Where it stands FDA's compounding record splits by route. GHK-Cu for routes other than injection sits in 503A category 1, the category for nominated substances the agency is still evaluating, having come off the list on 22 April 2026 when the nominations were withdrawn and gone back on after a nominator clarified on 5 May 2026 that it meant to withdraw only the injectable route. GHK-Cu for injectable routes had been in category 2 for significant safety risks and its nomination was withdrawn. FDA states it intends to consult the Pharmacy Compounding Advisory Committee about the compound before the end of February 2027; it was not on that committee's agenda of 23 and 24 July 2026 [20] [24]. The hub carries the documents.
Our takeThe only compound in this group that has been tested against a control in people, twice. Both trials came back the same way on their objective measures, and that is a different situation from having no evidence at all.
Larazotide
Also known as AT-1001, INN-202
Plain-English version: An eight amino acid peptide taken by mouth, developed for coeliac disease and now sold as a gut-health compound.
Strongest evidence, and what it covers [Human RCT] Coeliac disease symptoms, taken by mouth [15] [16] [22]
Larazotide is the most conventionally developed compound in this group. It is taken by mouth, it acts on the junctions between the cells lining the intestine, and it has ten registered trials of its own, all in coeliac disease [22].
The largest published trial randomized 342 adults with coeliac disease who still had symptoms on a gluten-free diet, across three amounts and placebo, with a placebo run-in and run-out. The primary endpoint, a gastrointestinal symptom rating score, separated from placebo in the lowest of the three arms; the two higher arms did not differ from placebo on any endpoint [15]. A 2022 systematic review and meta-analysis pooled the randomized trials [16]. The phase 3 that followed, covering 307 people, is recorded on the registry as terminated, with the reason given as terminated by the sponsor [22].
Every one of those trials tested coeliac disease, in people already on a gluten-free diet, taking the peptide by mouth. Intestinal permeability, leaky gut and general gut repair are the claims it is sold under now, and no trial on the registry tested any of them.
Where it stands Larazotide has no marketing approval in the United States or elsewhere, and the phase 3 programme in coeliac disease ended in termination on the registry rather than in a filing [22].
Our takeA real drug programme with a real, mostly negative answer, now sold for something the programme never studied. The dose-response pattern in the phase 2, where only the lowest arm separated, is the part that gets left out.
ARA-290
Also known as Cibinetide, Helix B surface peptide
Plain-English version: An eleven amino acid piece of erythropoietin, engineered to keep the tissue-protective activity while leaving out the effect on red blood cells.
Strongest evidence, and what it covers [Human RCT] Nerve fibre repair and neuropathic pain [17] [18] [22]
ARA-290 has an unusually clear rationale. Erythropoietin protects tissue in laboratory models and also raises red cell counts, which makes it unusable at the amounts that protection would need. ARA-290 is the surface of helix B of that protein, chosen because it engages a different receptor complex. Whether it raises red cell counts is a question its own trials measured rather than something this page can assert, and those trials are described below.
Four trials are registered and all of them are small [22]. A randomized trial in 64 people with sarcoidosis-associated small nerve fibre loss and neuropathic pain measured corneal nerve fibre abundance by confocal microscopy and reported an increase against placebo, alongside changes in pain scores [17]. A phase 2 in 24 people with type 2 diabetes and prediabetes reported changes in metabolic measures and in neuropathic symptom scores [18]. A cognition study in depression and an eye study terminated after nine participants complete the set.
What is marketed reaches past that. Nerve regeneration, chronic inflammation, autoimmune conditions and general tissue repair are attached to it in vendor and community writing. The registered trials cover two neuropathy populations, one cognition endpoint and one eye condition, in fewer than 140 people in total.
Where it stands ARA-290 has no marketing approval anywhere and no registered trial beyond phase 2. It was not among the substances the Pharmacy Compounding Advisory Committee considered on 23 and 24 July 2026 [20].
Our takeThe best-designed molecule in this group and the smallest evidence base to match a marketing claim. Two positive phase 2 readouts in narrow neurological populations do not reach the general repair claim it is sold under.
What we do not know about this group
Only one compound in this group has a completed, published, randomized human trial of the use it is actually sold for, and it has two. Both GHK-Cu trials tested topical products, in 1992 and 2006, and neither separated from its control on a measure an assessor or an instrument made [12] [23]. Larazotide and ARA-290 have randomized trials, in coeliac disease and in neuropathy, which are not the uses being marketed. BPC-157, TB-500 and KPV have none at all.
Exposure in a person is unknown for all six. No pharmacokinetic measurement in a human being has been published for BPC-157, TB-500, GHK-Cu or KPV on any route, so nothing converts a rodent figure into a human one. The rat metabolism work on TB-500 is the closest anything comes, and it raises a further question rather than settling one, because the wound-closure activity in that study belonged to a metabolite rather than to the parent fragment [8].
Long-term exposure has been characterized for none of them. The rodent studies ran for days to a few weeks: 14 days in the transected tendon model, four weeks in the 2026 Achilles study, four weeks of injections in the rat knee study with follow-up to twelve. Nothing in this group has been given to any species for a period comparable to how it is used.
Product identity is its own gap. TB-500 is the clearest case, because what a laboratory found in the product was a seven residue acetylated fragment rather than the protein the name implies [7], but the same question applies to every vial in this group, and it is a certificate-of-analysis question rather than a research question.
What this evidence can and cannot show
These results come from rats and mice in surgically transected tendons, crushed muscle, reconstructed knee ligaments and chemically induced colitis, not from people. An animal model is a deliberate simplification: the injury is created on purpose, the animal is young and healthy, the dose is scaled to body weight in a way that does not translate directly, and the outcome is measured at a fixed point rather than lived with. Cell and tissue work is a further step removed, because the concentrations that produce an effect in a dish are often far above anything a body reaches. Mechanism is a reason to run a trial. It is not a substitute for one, and compounds that looked mechanistically convincing have failed in people many times.
Frequently asked questions
Which compound in this group has the strongest human evidence?
Larazotide, and it is not close. It has ten registered trials of its own, a published phase 2 in 342 people, and a meta-analysis of the randomized set [15] [16] [22]. All of that tested coeliac disease in people taking it by mouth, so it is strong evidence about a question other than the one it is now sold for.
Is TB-500 the same thing as thymosin beta-4?
No. Thymosin beta-4 is a 43 residue protein. Analysis of the product sold as TB-500 identified Ac-LKKTETQ, a seven residue acetylated fragment of it [7]. The eighteen registrations people count for TB-500 tested the parent protein, mostly in dry eye and corneal wound healing, and one registration names TB-500 itself [22].
Has BPC-157 been tested in people?
One report is published: a retrospective chart review of 16 people given an injection into the knee at a single clinic, with pain rated by telephone from memory and no control arm [5]. Two trials are registered, neither reported, and one of them is recruiting now in acute hamstring strain [22].
Why does the same rat tendon result keep appearing in different articles?
Because the preclinical literature is concentrated. A 2025 systematic review found 36 studies of BPC-157 across three decades, 35 of them preclinical [6], and two of the rodent papers cited on this page come from the same Zagreb pharmacology group. The reference list here prints full author lists so that overlap is checkable.
Does the copper peptide research apply to the injectable form?
The published work is topical or applied directly to cells, with one rat study using injections into a knee joint [13]. Both randomized human trials tested topical products: a cream in venous stasis ulcers in 1992 [23] and a skin care regimen after laser resurfacing in 2006 [12]. Neither separated from its control on an objective measure, and neither says anything about an injected route. No published study has given GHK-Cu by injection to a person for a systemic purpose, and FDA treats the two routes separately in its own compounding record [24].
What did the FDA advisory committee do on 23 July 2026?
It considered whether certain bulk drug substances should go on the 503A Bulks List. BPC-157 and KPV were the morning session, TB-500 and MOTS-c the afternoon, with two voting questions each, one for the free base and one for the acetate salt [20]. A committee recommendation is advisory: the agency still has to decide, publish a proposed rule, take comment and issue a final rule.
Are any of these prohibited in sport?
BPC-157 is named on the face of the S0 class of the WADA 2026 Prohibited List, and TB-500 is named in S2.3 under growth factors, in the entry for thymosin beta-4 and its derivatives. Both classes are prohibited at all times, in and out of competition [21]. KPV is not named anywhere on the list and is reached only by the S0 catch-all definition, which the KPV review sets out in full.
Why does larazotide return 29 registrations in some counts and ten here?
A name collision. AT-1001 is larazotide's development code and it is also the development code for migalastat, an approved drug for Fabry disease. A free-text search returns both sets. Ten of the 29 studies are larazotide, and the remainder are the Fabry programme, which has nothing to do with this molecule [22].
What would change any of these grades?
A completed, published, randomized trial of the compound itself, in people, for the use it is sold for. The BPC-157 hamstring trial has primary completion estimated for February 2027 and is the nearest candidate in this group [22]. A tier moves here only when such a study is published and added to the reference list in the same edit.
References
- Dalmasso G, Charrier-Hisamuddin L, Nguyen HT, Yan Y, Sitaraman S, Merlin D. PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation. Gastroenterology. 2008. PMID 18061177 DOI 10.1053/j.gastro.2007.10.026
- Staresinic M, Sebecic B, Patrlj L, Jadrijevic S, Suknaic S, Perovic D, Aralica G, Zarkovic N, Borovic S, Srdjak M, Hajdarevic K, Kopljar M, Batelja L, Boban-Blagaic A, Turcic I, Anic T, Seiwerth S, Sikiric P. Gastric pentadecapeptide BPC 157 accelerates healing of transected rat Achilles tendon and in vitro stimulates tendocytes growth. J Orthop Res. 2003. PMID 14554208 DOI 10.1016/S0736-0266(03)00110-4
- Novinscak T, Brcic L, Staresinic M, Jukic I, Radic B, Pevec D, Mise S, Tomasovic S, Brcic I, Banic T, Jakir A, Buljat G, Anic T, Zoricic I, Romic Z, Seiwerth S, Sikiric P. Gastric pentadecapeptide BPC 157 as an effective therapy for muscle crush injury in the rat. Surg Today. 2008. PMID 18668315 DOI 10.1007/s00595-007-3706-2
- Chang CH, Tsai WC, Hsu YH, Pang JH. Pentadecapeptide BPC 157 enhances the growth hormone receptor expression in tendon fibroblasts. Molecules. 2014. PMID 25415472 DOI 10.3390/molecules191119066
- Lee E, Padgett B. Intra-Articular Injection of BPC 157 for Multiple Types of Knee Pain. Altern Ther Health Med. 2021. PMID 34324435
- Vasireddi N, Hahamyan H, Salata MJ, Karns M, Calcei JG, Voos JE, Apostolakos JM. Emerging Use of BPC-157 in Orthopaedic Sports Medicine: A Systematic Review. HSS J. 2025. PMID 40756949 DOI 10.1177/15563316251355551
- Esposito S, Deventer K, Goeman J, Van der Eycken J, Van Eenoo P. Synthesis and characterization of the N-terminal acetylated 17-23 fragment of thymosin beta 4 identified in TB-500, a product suspected to possess doping potential. Drug Test Anal. 2012. PMID 22962027 DOI 10.1002/dta.1402
- Rahaman KA, Muresan AR, Min H, Son J, Han HS, Kang MJ, Kwon OS. Simultaneous quantification of TB-500 and its metabolites in in-vitro experiments and rats by UHPLC-Q-Exactive orbitrap MS/MS and their screening by wound healing activities in-vitro. J Chromatogr B Analyt Technol Biomed Life Sci. 2024. PMID 38382158 DOI 10.1016/j.jchromb.2024.124033
- Biçer O, Adanir O, Güleryüz Y, Balci EC, Dinçel YM, Yenigün MY, Aydin C, Bayrak BY. Effects of BPC-157 and TB-500 on Achilles tendon healing in rats: A histopathological and biomechanical study. Jt Dis Relat Surg. 2026. PMID 42542926 DOI 10.52312/jdrs.2026.2951
- Sosne G, Dunn SP, Kim C. Thymosin β4 significantly improves signs and symptoms of severe dry eye in a phase 2 randomized trial. Cornea. 2015. PMID 25826322 DOI 10.1097/ICO.0000000000000379
- Sosne G, Kleinman HK, Springs C, Gross RH, Sung J, Kang S. 0.1% RGN-259 (Thymosin ß4) Ophthalmic Solution Promotes Healing and Improves Comfort in Neurotrophic Keratopathy Patients in a Randomized, Placebo-Controlled, Double-Masked Phase III Clinical Trial. Int J Mol Sci. 2022. PMID 36613994 DOI 10.3390/ijms24010554
- Miller TR, Wagner JD, Baack BR, Eisbach KJ. Effects of topical copper tripeptide complex on CO2 laser-resurfaced skin. Arch Facial Plast Surg. 2006. PMID 16847171 DOI 10.1001/archfaci.8.4.252
- Fu SC, Cheuk YC, Chiu WY, Yung SH, Rolf CG, Chan KM. Tripeptide-copper complex GHK-Cu (II) transiently improved healing outcome in a rat model of ACL reconstruction. J Orthop Res. 2015. PMID 25731775 DOI 10.1002/jor.22831
- Pickart L, Vasquez-Soltero JM, Margolina A. GHK Peptide as a Natural Modulator of Multiple Cellular Pathways in Skin Regeneration. Biomed Res Int. 2015. PMID 26236730 DOI 10.1155/2015/648108
- Leffler DA, Kelly CP, Green PH, Fedorak RN, DiMarino A, Perrow W, Rasmussen H, Wang C, Bercik P, Bachir NM, Murray JA. Larazotide acetate for persistent symptoms of celiac disease despite a gluten-free diet: a randomized controlled trial. Gastroenterology. 2015. PMID 25683116 DOI 10.1053/j.gastro.2015.02.008
- Hoilat GJ, Altowairqi AK, Ayas MF, Alhaddab NT, Alnujaidi RA, Alharbi HA, Alyahyawi N, Kamal A, Alhabeeb H, Albazee E, Almustanyir S, Abu-Zaid A. Larazotide acetate for treatment of celiac disease: A systematic review and meta-analysis of randomized controlled trials. Clin Res Hepatol Gastroenterol. 2022. PMID 34339872 DOI 10.1016/j.clinre.2021.101782
- Culver DA, Dahan A, Bajorunas D, Jeziorska M, van Velzen M, Aarts LPHJ, Tavee J, Tannemaat MR, Dunne AN, Kirk RI, Petropoulos IN, Cerami A, Malik RA, Brines M. Cibinetide Improves Corneal Nerve Fiber Abundance in Patients With Sarcoidosis-Associated Small Nerve Fiber Loss and Neuropathic Pain. Invest Ophthalmol Vis Sci. 2017. PMID 28475703 DOI 10.1167/iovs.16-21291
- Brines M, Dunne AN, van Velzen M, Proto PL, Ostenson CG, Kirk RI, Petropoulos IN, Javed S, Malik RA, Cerami A, Dahan A. ARA 290, a nonerythropoietic peptide engineered from erythropoietin, improves metabolic control and neuropathic symptoms in patients with type 2 diabetes. Mol Med. 2015. PMID 25387363 DOI 10.2119/molmed.2014.00215
- US Food and Drug Administration. Pharmacy Compounding Advisory Committee; notice of meeting; establishment of a public docket; request for comments. Docket No. FDA-2025-N-6895. The notice carries the chart of uses FDA evaluated: ulcerative colitis for BPC-157, wound healing for TB-500, wound healing and inflammatory conditions for KPV. Federal Register, document 2026-07361. 2026. Source document
- US Food and Drug Administration. Questions for PCAC regarding whether FDA should include certain bulk drug substances on the 503A Bulks List, Pharmacy Compounding Advisory Committee, 23 and 24 July 2026. Two voting questions each on seven substances across four sessions: BPC-157 and KPV on the morning of 23 July, TB-500 and MOTS-c that afternoon, emideltide and epitalon on the morning of 24 July, and semax that afternoon. FDA advisory committee materials. 2026. Source document
- World Anti-Doping Agency. The 2026 Prohibited List, international standard, effective 1 January 2026. WADA. 2026. Source document
- US National Library of Medicine. ClinicalTrials.gov registry, queried through API v2 on 2 August 2026 for each compound on this page. A free-text search returned two registrations for BPC-157, one naming TB-500 and eighteen naming thymosin beta-4, three for GHK-Cu and copper tripeptide, four for ARA-290 and cibinetide, and 29 for larazotide and AT-1001 of which ten are larazotide. The three GHK-Cu records were re-read in full on 8 August 2026, and only one of them has GHK-Cu itself as its intervention. ClinicalTrials.gov. 2026. Source document
- Bishop JB, Phillips LG, Mustoe TA, VanderZee AJ, Wiersema L, Roach DE, Heggers JP, Hill DP Jr, Taylor EL, Robson MC. A prospective randomized evaluator-blinded trial of two potential wound healing agents for the treatment of venous stasis ulcers. J Vasc Surg. 1992. PMID 1495150 DOI 10.1067/mva.1992.37086
- US Food and Drug Administration. Bulk Drug Substances Nominated for Use in Compounding Under Section 503A of the Federal Food, Drug, and Cosmetic Act. Document updated 14 May 2026, carrying the category 1 list and the GHK-Cu withdrawal and clarification history. FDA human drug compounding. 2026. Source document