BRAK LABS Peptide research, plainly written

group

Healing and recovery peptides

Seven 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.

Last Reviewed Editorial policy Methodology

Seven 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. Thymosin beta-4 is the 43 amino acid parent protein TB-500 is a fragment of.

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 27 numbered sources: 21 primary papers and reviews, and six agency and registry documents. Identifiers were checked on 2 August 2026, the GHK-Cu and BPC-157 entries were rechecked on 8 August 2026 and the TB-500 entry on 9 August 2026 as each compound's own review published, and the registry note was re-read on 30 August 2026.

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.

Compounds covered on this page, what each one is, and what the published record on it covers
CompoundAlso known asWhat the published work coversWhere it standsEvidence level
KPVLysine-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 pageNot on the FDA 503A Bulks List. Reviewed by the compounding advisory committee on 23 July 2026[Animal]
BPC-157Body Protection Compound-157, PL 14736, pentadecapeptide BPCRodent tendon, muscle, ligament and gut models, plus five human studies: two randomized against placebo and unpublished beyond an abstract, and three uncontrolled. Reviewed in full on its own pageNomination withdrawn from the FDA 503A process. Named on the face of the WADA S0 class[Human RCT]
TB-500Thymosin beta-4 fragment, TB4One rat tendon study, rat and equine metabolism work, and two further animal studies in which the fragment was not administered on its own. Of the nineteen registrations usually counted for it, eighteen tested thymosin beta-4, a different molecule, in the eye and in skin ulcers. Reviewed in full on its own pageUnapproved, and in FDA 503A category 2. Named on the face of the WADA list at S2.3[Animal]
GHK-CuCopper tripeptide-1, glycyl-L-histidyl-L-lysine copperA 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 pageIn FDA 503A category 1 for non-injectable routes. The injectable nomination was withdrawn from category 2[Human RCT]
LarazotideAT-1001, INN-202Ten 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 forUnapproved. The phase 3 programme was discontinued in 2022[Human RCT]
ARA-290Cibinetide, Helix B surface peptideFour registrations, all small: nerve fibre and pain endpoints in sarcoidosis and in type 2 diabetes, a cognition study, and a terminated eye studyUnapproved, and it never progressed beyond phase 2[Human RCT]
Thymosin beta-4Tbeta4, TB4, RGN-259, NL005Five Phase 3 registrations in the eye, of which the only published one was terminated early and missed its primary endpoint, and one published randomised cardiac trial in 96 patients that was null on its overall comparison. Both US registrations of an injected form were withdrawn before enrolling anyone. Reviewed in full on its own pageUnapproved in every indication. Named on the face of the WADA list at S2.3, prohibited at all times, non-Specified[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]. Of the eighteen registrations a term search returns, seventeen belong to the parent protein and none of those is about tendons. The eighteenth is the one record naming TB-500, and its own registered summary states that it is a fictional example of a registry-style record [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].

How few laboratories these files come from

Counting studies is the easy part. Counting independent studies is what a reader actually needs, and this site treats concentration of authorship as a quality signal rather than an accusation, because a small field is small and a group that builds an assay keeps using it.

Two of the three BPC-157 rodent papers cited here come from the same Zagreb pharmacology group, with Sikiric P and Staresinic M on both [2] [3], and the BPC-157 review counted the corpus it cites: 17 of its 25 preclinical and identity papers carry the same senior author, and all three published human studies share a first author. The two thymosin beta-4 eye trials cited for TB-500's parent share their first author [10] [11]. Both ARA-290 papers share an author group that includes the two people named on the molecule's design [17] [18].

Full author lists are stored in the reference list below for exactly this reason. A truncated list ending in et al. cannot be used to check whether two studies came from one laboratory, so nothing here is truncated.

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 three as of 8 August 2026: one first posted in December 2015 that carries a status of unknown, one completed single-arm supplement study first posted nine months after it finished, and one phase 2 registration whose sponsor account the BPC-157 review reads in full. TB-500 has one, first posted in March 2026, whose primary outcomes are counts of adverse events rather than any measure of repair, and which states in its own registered summary that it is a fictional example record rather than a study. It belongs to the same sponsor account. GHK-Cu returns three records to a free-text search and only one of them names the compound as its intervention: a split-wound study of a topical gel, registered as a phase 2 and as recruiting since 2 February 2026. It belongs to the same sponsor account as the TB-500 record, so the GHK-Cu review reads that account in full and counts no trial in progress from it. 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 RCT] Tendon, muscle and joint recovery [2] [3] [4] [5] [6] [22] [25]

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 it has a finished evidence review on this site running to 43 numbered sources, so this entry is a pointer rather than a summary that could drift from it.

The preclinical file is rats. In animals whose Achilles tendon was cut through, those 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, from two different routes [3]. In rat tendon fibroblasts, growth hormone receptor expression rose at the messenger RNA and protein level, and proliferation rose only once growth hormone was added [4]. A 2025 systematic review counted 36 studies from 1993 to 2024, 35 of them preclinical [6].

Five human studies exist and the hub sets out all five. Two were randomized against placebo in the early 2000s and neither was published beyond a conference abstract; the one that measured effectiveness, in 53 patients with ulcerative colitis, reported a between-group difference whose confidence interval crossed zero [25]. Three are published and all three are uncontrolled, including the retrospective chart review at a single Florida clinic covering injection into the knee: 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]. That randomized readout is what puts the compound at grade B on the hub, and the grade records how much research exists rather than which way it came out.

Three registry records exist and none has posted results [22]. One is a phase 1 in 42 people, first posted December 2015, status unknown. One is a completed single-arm supplement study, first posted nine months after it finished. The third is a phase 2 registration in acute hamstring strain, and the hub reads it alongside the sponsor account it sits in, three of whose eight records describe themselves in their own registered text as examples rather than studies. Nothing verifiably controlled is running.

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]. FDA's reviewers proposed against adding either form, writing that a balancing of the criteria weighs against both, and the substance now sits in FDA's table of bulk drug substances nominated but withdrawn rather than in the active category 2 table [25]. 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 one time anyone randomized it against a placebo, in a different condition by a different route, it did not separate.

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] [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]. 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.

The registrations split by molecule and the split is the whole story. A term search returns eighteen; seventeen registered the parent protein, in eyes and in skin rather than tendon or muscle, and the eighteenth is the single record naming TB-500, which states in its own registered brief summary that it is a fictional example of a ClinicalTrials.gov-style record [22]. On the fragment itself the published work is one rat Achilles tendon study at eight animals per group [9], rat and equine metabolism work [8], and two further animal studies in which it was given inside an engineered gel or alongside a second peptide rather than on its own.

The hub sets out the rest, including a second identity split FDA draws between the acetylated fragment and the plain heptapeptide most of the wound-healing reputation rests on, and it grades the compound D.

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]. FDA separately lists the substance in 503A category 2, for nominated substances that may present significant safety risks, citing immunogenicity and aggregation. TB-500 is named on the face of the WADA 2026 Prohibited List in class S2.3, growth factors and growth factor modulators, as the example given in the entry for thymosin beta-4 and its derivatives; that class is prohibited at all times and all of its substances are non-Specified [21]. The hub carries the documents.

Our takeEvery trial count published for this compound is really a count for a molecule six 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 30 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 whose control-arm evidence was ever published, and it was published twice. Both trials came back the same way on their objective measures, and that is a different situation from having no evidence at all. BPC-157 was also randomized against placebo twice, but neither of those studies was published beyond a conference abstract, which is the distinction the tiers on this page are drawing.

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.

Thymosin beta-4

Also known as Tbeta4, TB4, TMSB4X, RGN-259, NL005

Plain-English version: A 43 amino acid protein the body makes that holds on to actin, developed as an eye drop and as an injected recombinant drug.

Strongest evidence, and what it covers [Human RCT] Repair in the eye and the heart [26] [27]

Thymosin beta-4 is the protein TB-500 is a fragment of, and it has a finished evidence review on this site running to 30 numbered sources, so this entry is a pointer rather than a summary that could drift from it.

It is the one compound in this group with published randomised human trials, and reading them is the reason the page exists. The Phase 3 in neurotrophic keratopathy was terminated early at 18 of 46 planned participants and its pre-specified primary endpoint returned p=0.0656. The randomised cardiac trial in 96 patients after a heart attack reported no significant difference in infarct size overall, with a difference confined to the 43 participants dosed within eight hours. Both are cited elsewhere as successes.

The route with the evidence is not the route that is sold. Three Phase 3 trials have been run on an eye drop, and the two US registrations for an injected form were both withdrawn before enrolling anyone.

Where it stands Not approved in any indication. Named on the WADA 2026 Prohibited List under S2.3 as Thymosin-ss4 and its derivatives e.g. TB-500, prohibited at all times, non-Specified.

Our takeThe full review is on the compound page, including the registry count and why a search on the molecule name alone undercounts it.

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 has two randomized placebo-controlled studies that were never published beyond a conference abstract, one of them an efficacy study in ulcerative colitis whose between-group difference crossed zero, so it has been randomized without ever having a published randomized trial. TB-500 and KPV have none at all.

Exposure in a person is unknown for all six. No human pharmacokinetic profile 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. For BPC-157 the measurement was attempted: the two unpublished rectal studies looked for it in plasma and did not detect it, which is a null result rather than an absence of data. The rat metabolism work on TB-500 is the closest anything comes, and it raises a further question rather than settling one: in that study's own scratch assay TB-500 did not separate from control at the concentration tested, while the metabolite Ac-LKKTE did [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]. Of the eighteen registrations people count for TB-500, seventeen tested the parent protein, mostly in dry eye and corneal wound healing, and the eighteenth is the one record naming TB-500 itself, which states in its own registered summary that it is a fictional example record [22]. The TB-500 review sets both halves out in full.

Has BPC-157 been tested in people?

Yes, in five studies covering about 80 people, and the review sets out all five. Two were randomized against placebo in the early 2000s and neither was published beyond a conference abstract, the efficacy one reporting a between-group difference whose confidence interval crossed zero. Three are published and all three are uncontrolled, including the 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]. Three registry records exist and none has posted results [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 the BPC-157 review counted the authorship directly: 17 of the 25 preclinical and identity papers it cites carry the same senior author. 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 on the face of S2.3 under growth factors, by its own name, as the example given in the entry for thymosin beta-4 and its derivatives. Both classes are prohibited at all times, in and out of competition [21]. The two differ in sanctioning category: every S0 substance is a Specified Substance, while every substance in class S2 is non-Specified. 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, reporting whether it met its primary endpoint. Nothing verifiably controlled is running for any compound in this group. The nearest completed BPC-157 registration is a single-arm supplement study with no control arm and no results posted [22], and the phase 2 registration often named as the coming answer sits in the sponsor account the BPC-157 review reads in full. A tier moves here only when a qualifying study is published and added to the reference list in the same edit.

References

  1. 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
  2. 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
  3. 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
  4. 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
  5. Lee E, Padgett B. Intra-Articular Injection of BPC 157 for Multiple Types of Knee Pain. Altern Ther Health Med. 2021. PMID 34324435
  6. 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
  7. 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
  8. 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
  9. 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
  10. 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
  11. 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
  12. 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
  13. 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
  14. 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
  15. 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
  16. 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
  17. 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
  18. 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
  19. 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
  20. 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
  21. World Anti-Doping Agency. The 2026 Prohibited List, international standard, effective 1 January 2026. WADA. 2026. Source document
  22. 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 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. A term search for thymosin beta 4 returned eighteen records; seventeen of those registered the parent protein and the eighteenth is the single record naming TB-500, matched because its registered title carries both names. 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. BPC-157 was re-queried on 8 August 2026 and returns three records rather than the two this note previously recorded: NCT02637284, NCT07437547 and NCT07752381, the last first posted 7 August 2026, none with results posted. The thymosin beta-4 set and the TB-500 record were re-read in full on 9 August 2026, and the TB-500 record's registered brief summary states that it is a fictional study and an example of a ClinicalTrials.gov-style record. A sponsor search on that record, run on 30 August 2026, returns eight records including the BPC-157 registration NCT07437547 and the GHK-Cu registration NCT07437586. Three of the eight state in their own registered text that they are an example record, a mock study or a fictional study, and two carry Eli Lilly protocol identifiers for Lilly molecules. All eight are recruiting, single-site at Peking University Shenzhen Hospital, first posted between 27 February and 1 April 2026, never amended since, and list the same central contact at an email domain that does not match the sponsor name. ClinicalTrials.gov. 2026. Source document
  23. 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
  24. 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
  25. US Food and Drug Administration. FDA briefing document for BPC-157-related bulk drug substances, Pharmacy Compounding Advisory Committee, 23 and 24 July 2026. 68 pages. Carries FDA's reprinting of the Ruenzi 2005 randomized ulcerative colitis abstract with its numbers, and the recommendation that neither BPC-157 form be added to the 503A Bulks List. FDA advisory committee materials. 2026. Source document
  26. 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 Registration NCT02600429. Terminated early at 18 of 46 planned participants; the pre-specified primary endpoint of complete healing by day 29 returned p=0.0656.
  27. Zhang Y, Dong Q, Bian X, Qiao Z, Cui C, Yang N, Liu J, Fu R, Zhang J, Jia L, Wu C, Guo J, Lin W, Wang J, Fan J, Li Y, Liu F, Yang B, Jia X, Gao C, Bai M, He Y, Han C, Yin D, Dou K. Recombinant human thymosin beta 4 improves ischemic cardiac dysfunction in mice and patients with acute ST-segment elevation myocardial infarction after reperfusion. Cardiovasc Res. 2025. PMID 41229390 DOI 10.1093/cvr/cvaf223 The randomised trial in 96 patients reported no significant overall difference in infarcted areas against placebo; the significant result is confined to 43 participants dosed within 8 hours. Three authors are employed by Beijing Northland Biotech.