compound
BPC-157
A fifteen residue peptide described from gastric juice and sold for injury recovery, covered claim by claim: what the rodent work measured, what the five human studies contain, and where the agency and anti-doping record stands.
BPC-157 is a peptide fifteen amino acids long, written GEPPPGKPADDAGLV. It is described in the primary literature as a partial sequence of a larger peptide the originating laboratory reported isolating from human gastric juice, and the fragment has been studied since the early 1990s, first for stomach and gut injury and later for tendon, muscle and ligament repair [2] [3] [32]. It is the highest-volume compound in this category outside the metabolic peptides, and it has the largest research file of anything on this site.
What people research it for tracks the way that file grew. Tendon and muscle recovery is the dominant interest and the reason most readers arrive: the underlying work is rat models in which a tendon was cut through or a muscle crushed, measured by load to failure, walking recovery and histology [4] [7] [8]. Gut inflammation is the older interest and the one the compound was actually developed for, and it is the only use a regulator has ever formally evaluated [32]. Joint pain, gut health and general recovery circulate in community and vendor sources, and every one of those claims is graded below.
The human record is small, specific, and worth reading before anything else on this page. Three studies are published in journals, all uncontrolled, all from one clinician's Florida practices, covering 31 patients in total [26] [27] [28]. Two more exist that were randomized against placebo, both from the original commercial development programme, neither published beyond a conference abstract, and the efficacy one did not separate from placebo [32]. The reference list runs to 43 numbered sources, every PubMed identifier fetched from its live NCBI record and every agency, registry and anti-doping document opened and read. The regulatory section is current to 8 August 2026.
| Property | Value | Source |
|---|---|---|
| Category | Pentadecapeptide fragment, studied as a cytoprotective and repair agent | PMID 17186181 |
| Also known as | Body Protection Compound-157, pentadecapeptide BPC, PL 14736, PL-10, PLD-116, BPC15, Bepecin | FDA briefing document, 2026 |
| Sequence | GEPPPGKPADDAGLV, written residue by residue in FDA's review as H-Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val-OH | FDA briefing document, 2026 |
| Molecular formula | C62H98N16O22, giving 1419.5 g/mol for the free base | FDA briefing document, 2026 |
| CAS number | 137525-51-0 for the free base, 216441-37-1 for the acetate. UNII 8ED8NXK95P and PAR2FC72XP | FDA briefing document, 2026 |
| Naming | A common name rather than a USAN, INN or IUPAC name, which is one of the reasons FDA evaluated the free base and the acetate salt as two separate substances | FDA briefing document, 2026 |
| The parent peptide | Described in 1992 as a newly and partially characterized gastric juice peptide, and FDA records that it has never been fully characterized since | PMID 1345210 |
| Molecular target | Not identified. FDA: the molecular targets for BPC-157 have not been identified, and the mechanisms of action of BPC-157 are unknown | FDA presentation, July 2026 |
| Half-life | Measured in animals only, and short. A single intravenous dose gave a plasma half-life of minutes rather than hours in dogs and in rats. No half-life in a person has been reported on any route | PMID 36588717 |
| Measured in human plasma | Attempted twice, in the two unpublished rectal studies FDA reviewed, and not detected in either | FDA briefing document, 2026 |
| Routes with published human exposure | Rectal, intra-articular, intravesical and intravenous. FDA found no study administering BPC-157 to humans by the oral, subcutaneous, nasal or transdermal route | FDA presentation, July 2026 |
| Published human studies | 3, all uncontrolled, plus 2 randomized studies that exist only as conference abstracts | FDA briefing document, 2026 |
| Registry records | 3 as of 8 August 2026: a 2015 phase 1 with status unknown, a completed single-arm supplement study, and a phase 2 registration discussed in the trials table below. None has posted results | ClinicalTrials.gov |
| FDA 503A Bulks List | Not on the list. BPC-157 sits in FDA's table of bulk drug substances nominated but withdrawn, with the agency's safety text retained beside it, on a page whose content is current as of 22 April 2026 | FDA bulk drug substances page |
| WADA 2026 | One of only four examples the S0 class names on its own face, rather than reaching by definition. Two of the other three are classes rather than single substances. S0 is Non-Approved Substances and it applies in competition and out of it | WADA 2026 list |
| US Department of Defense | On the DoD Prohibited Dietary Supplement Ingredients list. Its Operation Supplement Safety status label reads Prohibited | OPSS ingredient index |
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
Key takeaways
- BPC-157 has been randomized against placebo in people, twice, and both studies come from the original commercial programme in the early 2000s. The efficacy one, in 53 patients with ulcerative colitis, reported a between-group difference whose confidence interval crossed zero, and neither has ever been published in full. [Human RCT] [32]
- Everything published about BPC-157 in a journal in people is uncontrolled: a retrospective knee-pain chart review, a single-arm bladder study, and an infusion report in two patients. All three share a first author and all three appeared in the same journal. [Human open-label] [26] [27] [28]
- Subcutaneous injection is how the retail market sells this compound, and FDA reported finding no study administering BPC-157 to a person by that route. No published animal efficacy study used it either. [Anecdote] [33]
- The tendon, muscle and ligament results come from rats in which the tissue was cut through, detached from bone or crushed on purpose, measured over 14 to 90 days by load to failure, walking recovery and histology. [Animal] [4] [5] [7] [8] [9] [10] [11]
- FDA's own reviewers proposed that BPC-157 free base and BPC-157 acetate not be added to the 503A Bulks List, and wrote that a balancing of the criteria weighs against both. The advisory committee took the question up on 23 July 2026, and FDA has published no minutes, transcript or vote record.
- BPC-157 is named on the face of the WADA S0 class, so it is prohibited at all times for a tested athlete, and the Department of Defense lists it as a prohibited dietary supplement ingredient for Service Members.
- The plasma half-life measured in rats and dogs is under half an hour, and a 2026 review names the gap between that figure and the effect durations reported for the compound as an unexplained pharmacokinetic and pharmacodynamic mismatch. [Animal] [24] [31]
- Twenty-eight days of intramuscular dosing in rats and dogs produced changes in clotting time in both species and in triglycerides, liver enzymes and glucose in female rats, and FDA records that no longer study exists to say whether those signals persist. [Animal] [25] [33]
- Of the 25 preclinical and identity papers cited here, 17 carry the same senior author, and a second author appears on every one of those 17. This is a fact about how the literature was produced, not a judgement about any of it.
- SEQUENCE
- GEPPPGKPADDAGLV
- PUBLISHED HUMAN STUDIES
- 3
- NUMBERED SOURCES
- 43
- EVIDENCE GRADE
- B
Who researches BPC-157?
Four groups arrive at this compound from different directions, and the published work meets them very unevenly.
The largest is reading about a musculoskeletal injury: a strained hamstring, a sore Achilles, a shoulder that has not come back. The rodent work speaks to that interest more directly than most compounds in this catalog manage, and the distance is still large. Every tendon and ligament study on this page created the injury with a scalpel, in a young healthy rat, and read the answer out at a fixed day.
The second is reading about the gut, usually after a diagnosis of inflammatory bowel disease or after encountering the intestinal-permeability literature. This is the oldest interest and the one with the only randomized human result in the whole file, which is set out in the human record section below.
The third is reading about a joint, most often a knee, and often after finding the one published account of injection into a knee. That account is a retrospective chart review, and what it did and did not measure is worth knowing before it is weighed.
The fourth is reading about recovery in general: training volume, soft-tissue niggles, getting back sooner. Nothing in the published record was built to answer that question in a person, and the matrix below grades those claims as what they are.
What is BPC-157?
Plain-English version: a chain of fifteen amino acids, cut from a larger peptide that one laboratory reported finding in human gastric juice.
In 1992 a group in Zagreb described what it called body protection compound, or BPC, as a newly and partially characterized gastric juice peptide [2]. Two years later the same group reported a fifteen residue fragment of it, coded BPC 157, and tested it against restraint stress, cysteamine and ethanol lesions in rats alongside famotidine, cimetidine, somatostatin and half a dozen other reference agents [3]. That is the origin of the compound and of its name.
Two facts follow from that origin and they matter more than they look. The parent peptide has never been fully characterized: the 1992 paper says partially characterized, and FDA said the same in 2026 [2] [32]. And BPC-157 is a common name rather than a USAN, INN or IUPAC name, which is why the agency had to evaluate a free base and an acetate salt as two separate substances, and why it recorded that inconsistent naming contributes to the substance being not well-characterized [32].
The sequence itself is not in dispute. GEPPPGKPADDAGLV, fifteen residues, C62H98N16O22, 1419.5 g/mol for the free base, and FDA writes it out residue by residue in its own review [1] [32]. What sits under the name is where the ambiguity lives, and the aliases in the record show the history: PL-10, PLD-116, PL 14736 and Bepecin are all development codes from the commercial programmes that carried it, and BPC15 and Body Protection Compound-157 are the older forms of the name itself.
GEPPPGKPADDAGLV · C62H98N16O22, 1419.5 g/mol
How strong is the evidence, claim by claim?
Every claim area this compound is discussed for gets a row, including the ones with the weakest support. The tier records what the row rests on, and the last column states what that work can and cannot show. Each tier links to its definition on the methodology page.
| Evidence Area | What Has Been Studied | Evidence Level | What It Can and Cannot Show |
|---|---|---|---|
| Gut inflammation, colitis and inflammatory bowel disease | One randomized, double-blind, placebo-controlled study in people, reported in 2005 as a conference abstract and never published in full. 53 patients with mild to moderate ulcerative colitis were randomized 1:1 to a two-week rectal course of BPC-157 or placebo, with 46 completing. The primary endpoint was change in a Disease Activity Index the abstract defines only as a composite of clinical, laboratory, endoscopic and pathohistological findings. FDA obtained the abstract, read it and reprinted its numbers, which is where they are recoverable from. Behind it sit rodent colitis and anastomosis models: TNBS colonic injury with the route split reported separately, cysteamine colitis with colon-to-colon anastomosis, and ileoileal anastomosis leak pressure [32] [12] [13] [14] | [Human RCT] | Supports the finding that a two-week rectal course did not separate from placebo on the index that trial measured. The index fell in both arms, by a mean of 3.2 points with the compound and 1.6 with placebo, and the estimated between-group difference of 1.6 points carried a 95 percent confidence interval running from minus 4.84 to 1.62, which crosses zero. Does not settle the question at 53 patients, and the abstract omits the inclusion criteria, the statistical methods and the follow-up. FDA's own reading is that the data presented are inadequate to support efficacy or safety for this use, and that there is a lack of evidence to make a conclusion on effectiveness. |
| Tolerability of administration | Three sources with human exposure and one with animal exposure. A published report of intravenous infusion in two patients on two consecutive days, with fasting blood work and vital signs before and after. A placebo-controlled phase 1 tolerability and pharmacokinetic study in 32 healthy volunteers randomized across four ascending levels of a rectal course, 24 of them receiving the compound, existing only as two conference abstracts read through FDA's review. And a 28-day repeat-dose toxicology study by intramuscular injection in rats and dogs [28] [32] [33] [25] | [Human RCT] | Supports a description of what was measured and reported in roughly 26 people and two animal species. Does not characterize tolerability in a person: two patients is a case report by this site's own definition, the phase 1 exists only as an abstract, and the toxicology found changes in clotting time in both species and in triglycerides, liver enzymes and glucose in female rats. FDA's conclusion travels with all of it: there is insufficient clinical safety information to characterize the safety profile, and longer repeat-dose studies were unavailable to show whether the animal signals persist. |
| Knee and joint pain | One retrospective chart review at a single Florida clinic covering 2019 and 2020. 17 patients were identified and 16 reached by telephone, 12 of whom had received BPC-157 alone by injection into the knee and 4 the same with thymosin beta-4. Patients were asked to rate their pain before the injection from memory, months to a year afterwards. The authors state that no specific tools were used to measure improvement in function, quality of life, stiffness or activities of daily living. There was no control arm [26] | [Human open-label] | Supports the statement that a clinic recorded improvement in most of the patients it reached, in a series whose only instrument was a recalled pain rating. Does not show an effect of the compound, because a recalled baseline, an unblinded patient and no comparison group cannot separate a change in a joint from a change in expectation or from the ordinary course of the complaint. A 2025 systematic review characterizes this same study by duration rather than by improvement, reporting 7 of 12 patients with relief beyond six months, so two different figures for it are in circulation and they are not the same measure. |
| Bladder pain and interstitial cystitis | One single-arm pilot study at a private Florida clinic in 12 women aged 39 to 76, all of whom had previously failed pentosan polysulfate. Each had a cystoscopy followed by injection around the area of bladder inflammation in a single procedure. The outcome instrument was the Global Response Assessment questionnaire, and there was no control arm [27] | [Human open-label] | Supports the statement that 12 patients rated the procedure highly on a single questionnaire, with no dropouts reported. Does not show an effect on interstitial cystitis, because a one-arm study with a subjective instrument and a cystoscopy in the same visit has nothing to separate the compound from the procedure or from the ordinary variation of the condition. |
| Tendon injury and repair | Three rat studies with a surgical injury and a mechanical readout. An Achilles tendon transected 5 mm above its insertion, measured by load to failure, load per area, Young's modulus, the Achilles functional index, histology and defect size over 14 days. An Achilles sharply detached from the calcaneal bone, followed to day 21 with collagen type I immunohistochemistry and run alongside methylprednisolone. And a 2026 four-arm study in 32 rats comparing BPC-157, TB-500, the combination and control after transection and repair over four weeks [4] [5] [6] | [Animal] | Supports a measurable difference in how a surgically cut or detached rat tendon heals under laboratory conditions, on mechanical and histological measures, in the first two studies. Does not show an effect on a human tendon injury by any route. The third study is the least favourable result in the set and the only one with a comparator peptide: BPC-157 was numerically better than control and did not reach statistical significance on the total histopathology scores, while TB-500 did, and adding the two together added nothing. Every model here is a scalpel injury rather than the tendinopathy or partial tear the compound is sold into. |
| Muscle strain, tear and crush injury | Four rat studies across four different injuries. A quadriceps completely transected above the patella and followed for 72 days by load to failure, walking recovery, extensor postural thrust and myofibril diameter. A crushed gastrocnemius followed 14 days by haematoma, oedema, contracture, function and the enzymes CK, LDH, AST and ALT, run by two different routes. A quadriceps dissected off at the myotendinous junction and followed to day 42, including by two routes and with eNOS and COX-2 messenger RNA. And a quadriceps detached from bone, complete and partial, followed to 90 days with ultrasound, MRI, biomechanics and histology of new bone at the muscle interface [7] [8] [9] [10] | [Animal] | Supports a measurable difference in recovery from four created muscle injuries in rats, on mechanical, functional and histological measures, and the crush model is the closest published analogue to the strain injury the compound is marketed for. Does not show an effect on a human muscle strain. A complete transection and a surgical detachment from bone are not athletic injuries, and no study in this set used the route the compound is sold by. |
| Ligament sprain and tear | One rat study with a transected medial collateral ligament followed for 90 days, measuring function, biomechanics and macroscopic and histological healing, and comparing three different routes of administration against control [11] | [Animal] | Supports a difference in how a surgically transected rat knee ligament recovers over three months, by each of the three routes tested. Does not show an effect on a sprain, which is a stretch injury to an intact ligament rather than a clean division of one, and does not show anything in a person. |
| Skin wound healing | Two studies from the developer's own laboratory, both against becaplermin, the recombinant PDGF-BB product, as an active comparator. Full-thickness excisional wounds in healthy and alloxan-hyperglycaemic rats, measured by planimetry, macroscopic score and histology to day 7. And a sponge granuloma model in normoglycaemic rats plus excisional wounds in diabetic mice, measuring granulation tissue and collagen organization [18] [17] | [Animal] | Supports a dose-dependent acceleration of wound closure in hyperglycaemic rats that matched the active comparator at the highest concentrations, and a similar selectivity for granulation tissue with more activity on early collagen organization. Does not show anything in a person, and carries two negatives from inside the same papers: there was no significant effect on wound contraction by planimetry, and healing in the healthy rats was too fast for either agent to show a difference. |
| What the body does with it | One formal study in Sprague-Dawley rats and beagle dogs, using single intravenous, single intramuscular at three ascending levels, and repeated intramuscular dosing, with a tritium label for distribution and excretion. It reports a plasma half-life for the parent peptide under 30 minutes, linear kinetics at every level tested, intramuscular bioavailability far below complete in both species, excretion by urine and bile, and rapid cleavage to short fragments and then to free amino acids [24] [33] [31] | [Animal] | Supports a description of how quickly the intact peptide leaves the plasma of two animal species and where it goes. Does not describe what happens in a person: no human pharmacokinetic profile exists on any route, and the only human attempts, in the two unpublished rectal studies, did not detect the compound in plasma. A 2026 review names the mismatch between a half-life of minutes and the effect durations reported for the compound as a pharmacokinetic and pharmacodynamic disconnect with no established explanation. |
| Blood vessels, clotting and bleeding | Three rat studies. An abdominal aorta clamped, transected and rejoined, measuring clot volume at the join and function at 24 hours. A Budd-Chiari model made by ligating the suprahepatic inferior caval vein, with venography of bypass pathways, pressures, ECG and tissue markers. And tail amputation in animals given heparin, warfarin or aspirin, measuring bleeding time and volume, platelet count, aPTT, thrombin time and anti-Xa activity [19] [20] [21] | [Animal] | Supports a set of vascular readouts in rats going in the same direction across three different insults, including reduced bleeding time under three different anticoagulants without a change in heparin's anti-Xa activity. Does not show anything in a person, and this is the row that belongs beside FDA's reading of the 28-day toxicology, which found clotting-time changes in both species tested. |
| Brain and spinal cord injury | Two studies. Traumatic brain injury in mice by falling weight at graded force, scoring consciousness, haemorrhage, laceration extent and brain oedema at 24 hours. And spinal cord compression in rats after laminectomy, followed for 360 days by tail motor function, spasticity, autotomy, white and grey matter histology, myelinated axon counts and EMG [22] [23] | [Animal] | Supports improvement on those measures in two created central nervous system injuries, and the spinal study is the longest follow-up anywhere in this file. Does not show anything about a person, and neither model resembles anything the compound is marketed for. Their presence in the file is the breadth problem in one line: a compound reported to improve outcomes in this many unrelated injuries is either doing something very general or is being measured very generously. |
| How it is thought to work | Cell and tissue work, mostly from one Taiwanese group. Rat tendon explants and isolated fibroblasts, measuring outgrowth, proliferation by MTT, survival under hydrogen peroxide, migration in a transwell, F-actin organization and phosphorylation of FAK and paxillin. A cDNA microarray in rat Achilles tendon fibroblasts followed by growth hormone receptor messenger RNA and protein and JAK2 activation. And egr-1 and nab2 expression in Caco-2 cells alongside the granulation work [15] [16] [17] [33] | [In-vitro] | Supports specific changes in cultured cells: outgrowth, survival and migration rose, growth hormone receptor expression rose, and an early-response transcription factor was induced. Does not identify a target or a pathway. Direct proliferation was not affected in the explant work, and the growth hormone receptor finding only produced more proliferation when growth hormone was added. FDA states in its own presentation that the molecular targets have not been identified and the mechanisms of action are unknown. |
| Injury recovery by subcutaneous injection, the route it is sold by | Community forum accounts, vendor product copy and podcast discussion, which is the entire source set for this claim. FDA searched the literature and reported finding no study that administered BPC-157 to humans by the oral, subcutaneous, nasal or transdermal route. A 2025 systematic review of the orthopaedic sports medicine literature included 36 studies from 1993 to 2024, of which 35 were preclinical and one was clinical, and none of the preclinical efficacy work used the subcutaneous route either [33] [29] | [Anecdote] | Records that the highest-volume claim in this category, made for the route almost every buyer uses, rests on report rather than on measurement. Shows nothing about what subcutaneous injection does in either direction, because no study of any design in any species has tested it. This is the row every competitor page omits, and on the site's own scale it is the weakest tier available. |
Rolled up, that puts BPC-157 at evidence grade B Human data, endpoint missed . Human evidence for the marketed use has read out, and it did not separate from control: the one randomized trial that tested it missed the primary endpoint. The grade describes how much and how good the research is, not which way it came out, so a compound that has been tested and beaten grades above one nobody has tested at all. A grade describes the quality of the research, not whether something works and not whether anyone should use it. The derivation is published.
How BPC-157 is thought to work
Mechanism work on BPC-157 has an unusual shape. There is a large and internally consistent body of reported effects, and there is no identified target. Those two facts are usually presented together in a way that lets the first stand in for the second, so the subsections below run in order of how well each one is supported and say plainly where each stops.
1. What it changes in cultured cells, how tendon cells move, survive and grow when the peptide is in the dish (best-supported, and it is cell work)
A group at Chang Gung ran the two most specific cell experiments in the file. In rat tendon explants and isolated fibroblasts, outgrowth from the explant rose, survival under oxidative stress rose, and migration across a transwell rose, with F-actin reorganized and FAK and paxillin more heavily phosphorylated [15]. Those are the signatures of a cell that is moving and adhering differently rather than dividing faster, and the same paper reports that direct proliferation was not affected.
The second experiment started from a cDNA microarray of treated tendon fibroblasts and followed the strongest hit. Growth hormone receptor expression rose at both the messenger RNA and the protein level, with JAK2 activation downstream [16]. The detail that travels with it is that proliferation only rose once growth hormone was added, so the finding is a change in what the cell is listening for rather than a growth signal in itself. [In-vitro] [15] [16]
Our takeTwo careful papers from one laboratory, pointing at cell motility and receptor expression rather than at a receptor of its own. It is the most concrete thing anyone has shown, and it is in a dish.
2. The nitric oxide account, the signal that makes blood vessels widen and new ones form (proposed across many papers, tested directly in few)
Most of the Zagreb papers attribute their results to the nitric oxide system, and several measure it. The Budd-Chiari study reports counteracted pressure and thrombosis changes alongside tissue nitric oxide and malondialdehyde measurements [20]. The aortic anastomosis study reports reduced clot volume at the join with recovered function within 24 hours [19]. The colitis and anastomosis paper reports the same direction across models that have little else in common [13].
The pattern to notice is that the nitric oxide account is offered as the explanation for effects in the stomach, the colon, the tendon, the aorta, the caval vein, the spinal cord and the brain. A single mediator that general is either a real upstream control point or a description of the measurement that was available, and no published work distinguishes those two readings. [Animal] [20] [19] [13]
Our takeA hypothesis carried across two decades of papers from largely one group, measured indirectly, and never isolated. It is the reason the compound is described as a vascular agent, and it is not a target.
3. No identified molecular target, nobody has found what it binds to (the agency's own reading of the whole literature)
FDA reviewed the pharmacology for the July 2026 advisory committee and recorded three limitations in its own words: dose-response relationships for the gastrointestinal effects have not been established, the pharmacological studies have been limited to rodent models, and the molecular targets for BPC-157 have not been identified with the mechanisms of action unknown [33].
What exists instead of a target is a list of downstream observations. Egr-1, an early-response transcription factor, is induced in Caco-2 cells alongside the granulation findings [17]. Growth factor expression, inflammatory factor release and angiogenesis (the growth of new blood vessels) are all offered as candidate routes in the primary papers. None of them is a binding partner, and a downstream change measured after the fact cannot become one.
A 2026 review of the compound's development barriers states the problem from the formulation side and adds a second one: a plasma half-life measured in minutes has no published reconciliation with reported effects lasting hours to days [31]. [In-vitro] [33] [31] [17]
Our takeThirty years of reported effects and no answer to what the molecule touches first. That is unusual for a compound with this much preclinical literature, and it is the single most useful thing to hold in mind while reading any of it.
What we do not know
The target is the largest gap and it is not narrowing. FDA states that the molecular targets have not been identified and the mechanisms of action are unknown, which is a reading of the whole published corpus rather than of any one paper [33].
Exposure in a person is unknown on every route. The only human plasma measurements ever attempted are the two unpublished rectal studies, and the compound was not detected in either [32]. Nothing converts a rodent figure into a human one, and the rodent figure itself is a half-life of minutes [24].
Whether the compound survives to act is genuinely open. The rat and dog work reports rapid cleavage to short fragments and then to free amino acids, which is what a fifteen residue peptide would be expected to do, and the reported durations of effect are much longer than that clearance allows [24] [31].
Route makes a difference and the literature says so from inside its own experiments. In the 1995 colitis study the intraperitoneal arm reduced necrosis and colonic myeloperoxidase in a dose-dependent way while the intracolonic arm did not significantly reduce either [12]. A compound whose effect depends on how it arrives cannot have its route treated as an incidental detail.
What this evidence can and cannot show
These results come from rats, mice and dogs in surgically transected tendons, crushed and detached muscle, transected ligaments, chemically induced colitis, and vascular occlusion, 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.
Has BPC-157 been tested in humans?
Five studies have given BPC-157 to a person under a written protocol, and the table below carries all five with the design, the number of people and what was reported. Three are published in journals and two are not.
The table also carries the three registry records a search returns and one row about a limit on this page's own sourcing. Counting only the arms that received the compound, about 80 people have been given BPC-157 in those five studies, and 40 more took a supplement stated to contain it in the completed registration below. A table is the only honest way to show how they divide.
| Study | People | What was done | Result | Evidence level |
|---|---|---|---|---|
| Ruenzi 2005, ulcerative colitis. Conference abstract only [32] | 53 randomized, 46 completed | Multicentre, randomized, double blind, placebo-controlled, 1:1 to a two-week rectal course or placebo. The primary endpoint was a Disease Activity Index the abstract never fully defines, and FDA lists the inclusion criteria, the statistical methods and the follow-up among the things it omits. No registry identifier exists for it: the study predates the registration norm and no NCT number or equivalent has ever been attached to it, so the citation here is the FDA document that reprints the abstract | The index fell in both arms: a mean change of minus 3.2 points with the compound and minus 1.6 with placebo, with an estimated between-group difference of 1.6 points whose 95 percent confidence interval ran from minus 4.84 to 1.62 and therefore crossed zero. Three withdrawals in the active arm and two in placebo for adverse events, described by the authors as mainly progression of the disease, and one loss to follow-up in each arm. Never published in full in the twenty-one years since. These numbers are recoverable only because FDA obtained the abstract and reprinted them | [Human RCT] |
| Veljaca 2002 and 2003, healthy volunteers. Conference abstracts only [32] | 32 randomized, 24 receiving the compound | Placebo-controlled phase 1 tolerability and pharmacokinetic study across four ascending levels of a rectal course, run in two stages with a washout between them. Reported as two meeting abstracts and read here through FDA's review of them | The authors report no significant adverse events attributable to single or repeated dosing, with headache and flatulence most frequent and no obvious difference in frequency or severity against placebo. BPC-157 was not detected in plasma: most concentrations fell below the limit of quantification of the assay. This is the only human pharmacokinetic measurement that exists, and its result is a null | [Human RCT] |
| Lee and Padgett 2021, knee pain [26] | 17 identified, 16 reached | Retrospective chart review at one Florida clinic covering 2019 and 2020, injection into the knee. 12 patients had the compound alone and 4 had it with thymosin beta-4. Pain before injection was rated by telephone from memory, months to a year later. The authors state that no specific tools were used to measure function, quality of life, stiffness or activities of daily living. No control arm | 11 of 12 on the compound alone and 3 of 4 on the combination were recorded as significantly improved, 14 of 16 overall. The material was compounded by a named Kentucky pharmacy. A 2025 systematic review reports this study differently, as 7 of 12 patients with relief beyond six months, which is a duration measure rather than the paper's improvement figure. Both are in the record and they are not the same number | [Human open-label] |
| Lee 2024, interstitial cystitis [27] | 12 | Single-arm pilot study at a private Florida clinic in women aged 39 to 76, all of whom had failed pentosan polysulfate. Cystoscopy, then injection around the area of bladder inflammation in a single procedure. Outcome instrument was the Global Response Assessment questionnaire. No control arm | 10 of 12 rated success at 100 percent and the other 2 at 80 percent, with no dropouts and no adverse events reported. The material came from an unnamed 503A compounding pharmacy. Every element of the result is a patient rating collected in the same visit as a procedure, with nothing to compare it against | [Human open-label] |
| Lee and Burgess 2025, intravenous infusion [28] | 2 | A 58-year-old man and a 68-year-old woman, both of whom had received intravenous BPC-157 before the study. One infusion on each of two consecutive days, with fasting blood work and vital signs before and after | No measurable change in the cardiac, hepatic, renal, thyroid or glucose markers tested, and the authors record nothing else observed across the two days. Two patients is a case report on this site's own definitions. The authors' own conclusion generalizes from those two people to a statement about humans, which is the step this page does not repeat | [Human open-label] |
| NCT02637284, registered phase 1 [38] | 42 estimated | Randomized, quadruple-masked, placebo-controlled study of an oral tablet in healthy volunteers aged 18 to 35, sponsored by PharmaCotherapia d.o.o. with Hospital Angeles Tijuana. Single site in Tijuana, Mexico. The intervention is named Bepecin with PCO-02 and BPC-157 as other names. Primary outcome is adverse events, with Cmax, Tmax, AUC and half-life secondary | Status listed as unknown. Start October 2015, primary completion estimated February 2016. First posted and last updated on the same day, 22 December 2015, and nothing has been added since. No results posted. The sponsor holds exactly one registration | not a claim about effect |
| NCT07752381, completed single-arm [40] | 40 actual | Open-label, no randomization and no masking, in physically active adults aged 18 to 65. Sponsor Parlay Wellness with Citruslabs, site in Las Vegas, Nevada. The intervention is a dietary-supplement gummy stated to contain BPC-157. Co-primary outcomes are hs-CRP, interleukin-6 and a self-reported swelling questionnaire over eight weeks | Completed 1 November 2025, and first posted on 7 August 2026, which is nine months after the study finished. No results posted. This is the only completed registration in the set, and a single-arm supplement study with no control arm cannot attribute a change to anything. Citruslabs holds around thirty registrations, all single-arm consumer-supplement studies, and this record carries no disclaimer of its own | not a claim about effect |
| NCT07437547, and the sponsor account it sits in [39] [41] | 120 estimated | Registered as a randomized 1:1, quadruple-masked, placebo-controlled phase 2 in MRI-confirmed acute grade II hamstring strain, ages 18 to 45, sponsored by Hudson Biotech. Co-primary outcomes are time to unrestricted sport and change in MRI injury volume at day 14. Actual start 2 February 2026, primary completion estimated 14 February 2027 | Read the sponsor account before weighing the record. Querying the registry for that sponsor on 8 August 2026 returns eight records. Three say in their own registered text that they are not studies: one begins This example interventional study record describes, one is titled with the words Mock Study, and one begins This fictional study is an example of a ClinicalTrials.gov-style record. Two more carry a large manufacturer's own internal protocol identifiers for its own molecules, one of them registered under the title of that manufacturer's published phase 3. All eight share the status recruiting, a first-posted window of five weeks, the same single site at Peking University Shenzhen Hospital, the same central contact on an email domain that does not match the sponsor name, and an oversight block recording the study as not FDA-regulated, and six of the eight including this one share the identical actual start date of 2 February 2026. This record itself carries no disclaimer and reads as an ordinary protocol synopsis. It has posted no results. This page therefore states no forward-looking expectation from it and counts no trial in progress from it | not a claim about effect |
| Full-text access for the two randomized studies, checked 8 August 2026 | Not applicable | PubMed, Europe PMC and author-plus-drug searches for both the 2005 and the 2002 and 2003 abstracts | Neither is indexed in PubMed and neither returns to a search. Everything this page reports about them comes from FDA's briefing document, which obtained both, quoted them directly and reprinted their numbers. This page attributes them that way rather than implying the abstracts were read at source | not a claim about effect |
Why we are not calling this proof
Two randomized placebo-controlled studies is more human testing than most compounds in this catalog have had, and being exact about what that buys is the whole point of the table above.
It buys one efficacy answer, in a condition almost nobody buys this compound for, from a study nobody can read. The 2005 abstract reports a between-group difference whose confidence interval runs through zero, and twenty-one years later there is no full paper behind it. FDA read it and wrote that the data presented are inadequate to support efficacy or safety for that use. A result nobody can check, which did not separate, is neither a verdict against the compound nor evidence for it.
It buys a tolerability description in 24 healthy volunteers and a null pharmacokinetic result, both from abstracts. The null is the more interesting half: the only two attempts to measure this compound in human plasma did not find it.
The three published studies buy something narrower again. 31 patients, no control arm anywhere, one recalled baseline, one single-visit questionnaire, and one report in two people. Each is a record of what a clinic observed. None of them is designed to tell a change caused by the compound apart from a change that would have happened anyway.
One structural fact belongs beside the count rather than inside it. All three published human studies share a first author, all three were conducted at Florida clinics, and all three appeared in the same journal. Both randomized studies come from the same commercial development programme. That is not an accusation about anyone's work and it is not evidence that any of it is wrong. It means the five human studies come from two origins rather than five, and a reader weighing them is entitled to know that before deciding how much weight to give them.
The FTC sets the substantiation bar for a health claim at randomized controlled human trials and says animal work, laboratory work and observational data are generally not enough on their own. BPC-157 has two randomized studies, one of which measured efficacy, and it did not separate from placebo. That is the whole human picture as of August 2026.
Benefits: what the research shows
Each heading below is a claim people make about BPC-157, not a finding. Under each one is what was measured, in what, and by whom, with the detail the matrix rows above could not carry.
One review is worth naming here because it is cited as though it held data of its own. A 2025 systematic review in orthopaedic sports medicine screened 544 articles from 1993 to 2024 and included 36, of which 35 were preclinical and one was clinical [29]. It is a count of the literature rather than a new measurement, and it is cited on this page for that count.
Tendon injury and repair
The matrix gives the study set. What it cannot carry is the shape of the 2026 result, and that result is the most informative thing in this claim area because it is the only one with an active comparator and the only one from outside the group that produced the rest [6].
Thirty-two rats, a transected and repaired Achilles, four arms: control, BPC-157, TB-500, and both together. Maximum load to failure, Bonar and Movin histopathology scores, Sirius red birefringence and collagen I and III H-scores. BPC-157 came out numerically better than control and short of statistical significance on the total scores. TB-500 reached significance. The combination added nothing over either alone.
That is one study and it does not overturn the two older ones, which measured real mechanical differences in cut rat tendons and did so carefully [4] [5]. It does mean the newest and most independent tendon experiment in the file is the least favourable one, and a page reporting the first two without the third would be selecting. [Animal] [4] [5] [6]
Our takeThe claim area with the most rodent work behind it, and the newest rodent work is the weakest result in it. Both of those facts are the file.
Muscle strain, tear and crush injury
Four injuries, four studies, and only one of them resembles what readers arrive asking about [8]. A crushed gastrocnemius is a blunt-force injury to intact muscle, which is the nearest published model to a strain, and it was followed 14 days by haematoma, oedema, contracture, function and four enzyme markers, with the peptide given by two different routes.
The other three are surgical. A quadriceps cut completely across is not a pulled hamstring, and neither is a quadriceps dissected off at the myotendinous junction or detached from bone [7] [9] [10]. Their value is duration and instrumentation rather than realism: the transection study ran 72 days, the detachment study ran 90 and added ultrasound and MRI, and the myotendinous study measured eNOS and COX-2 messenger RNA alongside the mechanical work.
Two of these four gave the peptide by mouth or in drinking water as one of their arms and reported the same direction as the injected arm [9] [10]. That is a route observation worth carrying, because it runs against the assumption that the compound has to be injected to do anything, and it has never been tested in a person by any route. [Animal] [7] [8] [9] [10]
Our takeOne model close to the marketed injury and three that are surgery. The oral arms are the underreported part of this file and nobody selling injectable vials mentions them.
Gut inflammation, colitis and gut health
This is the oldest claim, the one the compound was developed for, and the only one with a randomized human result. The result is in the human record section above and it did not separate from placebo.
The rodent work underneath it is more interesting than the usual summary allows. The 1995 TNBS colitis study is the one that split by route: intraperitoneal administration reduced necrosis area and colonic myeloperoxidase in a dose-dependent way, and intracolonic administration significantly reduced neither [12]. A page that reports this study as positive without the route split has reported half of it.
The other two are surgical repairs rather than inflammation models. Ileoileal anastomosis measured leak volume and pressure, adhesions, oedema, granulocytes and collagen [14]. The cysteamine colitis paper also carried a colon-to-colon anastomosis arm, and in the same paper a cuprizone demyelination model in the brain [13]. That last combination is the breadth problem stated in one figure set: colitis and multiple sclerosis in the same experiment, from the same laboratory, in the same direction.
Nothing in the record addresses the leaky-gut and gut-health framing the compound is sold under. Every gastrointestinal model here is a chemically or surgically injured animal, and no study of any design has given the compound to an uninjured gut and measured anything. [Human RCT] [32] [12] [13] [14]
Our takeThe one claim area that has been randomized in people, and the answer it gave was no. Everything sold under the gut-health heading is a different question that nobody has asked.
Knee and joint pain
The 2021 chart review is the single most-cited human source for this compound and it is worth reading closely rather than counting [26]. Its design is a telephone call to former patients, asking each to recall a pain level from before an injection they received months to a year earlier, with no instrument, no baseline record and no comparison group.
The authors state the limitation themselves: no specific tools were used to measure improvement in function, quality of life, stiffness or activities of daily living. Their Clinical Implications section then makes several statements this site does not repeat in any form, because they are conclusions about what the compound does drawn from a series that cannot support one.
One more thing belongs beside it. The 2025 systematic review characterizes this study as 7 of 12 patients reporting relief beyond six months [29], which is a different measure from the paper's own 11 of 12 improvement figure. Neither is wrong. A page quoting one should not let it read as the other. [Human open-label] [26]
Our takeThe most-cited human study on this compound is a recalled pain rating with no control arm, and its two circulating figures measure two different things.
General recovery, and the route almost every buyer uses
Subcutaneous injection is how BPC-157 is sold, discussed and used. It is also the one route with nothing behind it at all. FDA searched PubMed and Embase and reported finding no study administering the compound to humans by the oral, subcutaneous, nasal or transdermal route [33]. Every published human exposure is rectal, intra-articular, intravesical or intravenous.
The animal side does not fill the gap either. The rodent efficacy work is intraperitoneal, oral, intragastric, topical or a local bath on exposed tissue. Not one published animal efficacy study in this file used subcutaneous injection, and the 2025 systematic review of the whole orthopaedic literature does not identify one [29].
The recovery claim itself has the same shape. There is no model anywhere in the record of a healthy animal recovering faster, returning to activity sooner, or performing better. Every model created an injury first. [Anecdote] [33] [29]
Our takeThe best-selling compound in this category is sold for a route that has never been studied in anything, for an outcome no study has ever measured. That is the honest centre of this page.
Skin wounds and scarring
The two skin studies are the only work in the file with an approved product as the comparator, which makes them the most interpretable results here [18] [17]. Both come from the developer's own laboratory, and both ran the compound head to head against becaplermin, the recombinant PDGF-BB wound product.
In alloxan-hyperglycaemic rats the topical gel accelerated healing in a dose-dependent way and matched the comparator at the highest concentrations. Two negatives sit in the same paper: there was no significant effect on wound contraction by planimetry, and in healthy rats both agents were indistinguishable because healing was already too fast to separate [18]. The second study reported similar selectivity for granulation tissue and more activity on early collagen organization, in a sponge granuloma model and in diabetic mice [17].
Nobody markets BPC-157 as a topical wound product, so this claim area is smaller commercially than it is scientifically. It is on the page because a comparator-controlled result is worth more than an uncontrolled one, whichever way it comes out. [Animal] [18] [17]
Our takeThe best-designed preclinical work on this compound is in a tissue almost nobody buys it for, and it came from the company developing it.
Blood vessels, clotting and bleeding
This claim area rarely reaches marketing copy and it is the one with the clearest safety implication, which is why it is here rather than only in the safety section.
In rats given heparin, warfarin or aspirin and then subjected to tail amputation, the reported result is reduced bleeding time and reduced thrombocytopenia, with no change in heparin's anti-Xa activity [21]. In two other models the reported result runs the other way, towards less clot: reduced clot volume at an aortic join [19] and resolved occlusion in a Budd-Chiari model [20].
A compound reported to reduce bleeding in one setting and clotting in another is being described as a regulator rather than as an agonist or an antagonist, and no published work tests that description directly. What makes it worth publishing is the pairing in the safety section below: the formal 28-day toxicology found clotting-time changes in both species it tested, in opposite directions [25]. [Animal] [19] [20] [21]
Our takeThree rat studies pointing at haemostasis, and a toxicology package that found clotting signals independently. Neither says what happens in a person, and together they are the part of this file least discussed anywhere else.
Brain, spinal cord and nerve
Two studies, both created injuries, both reporting improvement [22] [23]. The spinal cord compression study is the longest experiment anywhere in this file at 360 days, with motor function, spasticity, histology, myelinated axon counts and EMG.
They are on this page for the reason the tumour and vascular rows are on the KPV and GHK-Cu pages: a claim area with real published work in it gets a row whether or not it helps. Nobody sells BPC-157 for spinal cord injury, and these two studies are frequently reproduced in secondary writing as evidence of general repair.
The reading that fits the record is narrower than that. A compound reported to improve outcomes in a cut tendon, a crushed muscle, a chemically inflamed colon, an occluded vein, a compressed spinal cord and a weight-drop brain injury has either found a very general control point or has been measured in a very consistent way by a very consistent group. The file does not distinguish those. [Animal] [22] [23]
Our takeThe breadth of this literature is usually presented as its strength. It is at least as reasonable to read it as the thing most in need of independent replication.
The honest bottom line on benefits
Of the claim areas above, one has a randomized human result and it did not separate from placebo. Two more have uncontrolled human reports. The rest is rodent and cell work, and the single highest-volume claim, recovery by subcutaneous injection, has nothing at all.
There is a second thing to say about the count, and it does not cut the way counts usually do. This site checked the author lists of every paper it cites here against their live PubMed records. Of the 25 preclinical and identity papers cited here, 17 carry the same senior author, and a second author appears on every one of those 17. The remaining eight split across a Taiwanese cell-biology group with two papers, the original developer's own laboratory with two, an industry pharmacology group with one, a Chinese pharmacokinetics and toxicology group with two, and a Turkish orthopaedic group with one.
The human side is more concentrated still, and it is the more important number. All three published human studies share a first author and a journal. Both randomized studies come from the same commercial development programme, with one investigator on both.
Overlapping authorship is not proof of anything and it is not an accusation. Small fields are small, and a group that builds a model keeps using it. But this site treats concentration of authorship as a quality signal when it reads every other compound, and a reader weighing thirty years of consistent results should know they are closer to a handful of independent lines than to thirty.
What anyone does with that is a judgement rather than a fact, and it belongs to the reader. This site reports what has been documented. It does not prescribe what should be done.
How long BPC-157 stays in the body
BPC-157 has been measured properly in two animal species and never in a person. The one formal study gave single intravenous, single intramuscular at three ascending levels and repeated intramuscular doses to Sprague-Dawley rats and beagle dogs, with a tritium label to follow distribution and excretion [24]. The parent peptide's plasma half-life came out under 30 minutes in both species, kinetics were linear at every level tested, intramuscular bioavailability was well short of complete, excretion ran through urine and bile, and the peptide was rapidly cleaved to short fragments and then to free amino acids.
Two sets of figures for that study are in circulation and this page carries neither as the number. The paper's own abstract reports bioavailability as a range for each species, and FDA's presentation reports single point estimates for both half-life and bioavailability, reading them out of the same paper [24] [33]. The divergence is a reading difference rather than a disagreement, and quoting either as the figure would imply a precision the record does not have.
In a person, nothing has been established on any route. The only attempts to measure the compound in human plasma are the two unpublished rectal studies, and in both the compound was not detected, with most concentrations below the limit of quantification of the assay used [32]. That is a measurement with a null result rather than an absence of measurement, and the distinction matters: something was looked for and was not found.
The consequence is the open problem in this compound's file, and a 2026 review names it directly [31]. A plasma half-life of minutes sits against reported biological effects lasting hours to days, and no published work reconciles the two. Every explanation offered for it, a local depot, an active metabolite, an upstream signalling event that outlasts the molecule, is a hypothesis nobody has tested.
Measured in rats and dogs: a plasma half-life under 30 minutes for the parent peptide, linear kinetics, incomplete intramuscular bioavailability, urinary and biliary excretion, and rapid cleavage to amino acids. In people, no profile exists on any route, and the only two attempts to detect the compound in plasma did not find it. [Animal] [24] [32] [33] [31]
What is documented about dosing
No study has established an amount of BPC-157 for a person, so there is no dosing section on this site in the sense other properties use the phrase. What can be reported is what published studies gave to their animals or their patients, in the model or the clinical setting they used, and what kind of figures circulate elsewhere.
Commonly cited protocols (extrapolated, not validated)
Nothing here is a dosing recommendation. Statements about dosing reflect community and research reports only.
| Study | What was given | Frequency | Duration | Notes |
|---|---|---|---|---|
| Rat tendon, muscle and ligament models. Staresinic 2003, Krivic 2006, Staresinic 2006, Novinscak 2008, Cerovecki 2010, Japjec 2021 [4] [5] [7] [8] [11] [9] | A body-weight-scaled regimen reported per study, given into the abdominal cavity in most arms | Per each study protocol | 14 to 90 days depending on the model | Young healthy rats with an injury created by a surgeon. A rodent amount scaled to body weight does not convert to a person, and this site does not print the ladder those studies used |
| Rat models using oral, drinking-water or topical arms. Novinscak 2008, Cerovecki 2010, Japjec 2021, Matek 2025 [8] [11] [9] [10] | The same body-weight-scaled regimens delivered by mouth, in drinking water or as a cream | Per each study protocol | 14 to 90 days | The underreported half of the animal file. Several of these studies reported the same direction from a non-injected arm as from the injected one |
| Rat and dog pharmacokinetics and toxicology. He 2022, Xu 2020 [24] [25] | Ascending intramuscular levels and a single intravenous level, plus a 28-day repeat-dose regimen | Single and repeated, per protocol | Single dose to 28 days | The only formal exposure work that exists. It is where the half-life figure and the coagulation and liver signals both come from |
| Human rectal course, unpublished. Veljaca 2002 and 2003 [32] | Four ascending levels of a rectal preparation in healthy volunteers | Per the study protocol, in two stages with a washout between them | About two weeks | The only human dose-ranging work ever done, and it exists as two conference abstracts read through FDA's review. The compound was not detected in plasma at any level |
| Human rectal course, ulcerative colitis. Ruenzi 2005 [32] | A fixed rectal preparation against placebo | Per the study protocol | Two weeks | The only randomized efficacy study. The amount and schedule are in FDA's reprinting of the abstract and are not published here, because a two-week course in a colitis trial is not a starting point for anything and printing it would supply one |
| Human clinic preparations. Lee 2021, Lee 2024, Lee 2025 [26] [27] [28] | Compounded preparations obtained from 503A pharmacies, given by injection into a knee, into the bladder wall at cystoscopy, or by intravenous infusion | Per each published series: a short course in the joint series, a single procedure in the bladder series, and two consecutive days in the infusion report | One visit to two days | Three different clinical routes and three different preparations, none of them the presentation sold to consumers. The amounts are in the papers and are not reproduced here |
| Community write-ups and vendor pages | Figures circulate. This site does not republish them | Figures circulate | Figures circulate | No trial established an amount for a person by the route those figures describe, because no study of any design has used that route in a person. Republishing a figure would supply an instruction with a hedge around it, which is the thing this site exists not to do |
Two things in that table deserve pulling out. The first is that the marketed presentation, a lyophilised powder in a vial reconstituted and injected under the skin, appears nowhere in it. Not in an animal study, not in a clinic report, not in a registration that has read out.
The second is that a body-weight-scaled rodent regimen is not convertible into a human amount even in principle. Interspecies scaling is unreliable between two mammals given the same route, and none of the animal work here used the route in question. Arithmetic performed on those numbers produces a figure with the appearance of a derivation and none of the content of one.
Main routes people compare, and what each source class actually reported, are set out on the documented protocols page.
Reported effects and what has been measured
What the toxicology record contains
One formal preclinical safety package exists, published in 2020 by a Chinese group, and FDA read it for the July 2026 advisory committee [25] [33]. It is the substance of everything below.
Twenty-eight days of intramuscular treatment in rats and dogs produced what FDA describes as statistically significant safety signals that are potentially clinically relevant. Activated partial thromboplastin time, a standard clotting measure, fell in rats and rose in dogs. Serum triglycerides rose in female rats and in female dogs during treatment, and two weeks after treatment ended female rats showed raised triglycerides, raised alanine aminotransferase, raised glucose and a raised relative liver weight. Serum creatinine fell in female dogs at the highest level tested.
The same package reported no genotoxicity in laboratory or animal assays, and no fetal malformation or effect on fetal viability in rats dosed through the middle of gestation. FDA records that no study covering a complete reproductive cycle or peri- and postnatal development was submitted or found.
FDA's own conclusion is the line that belongs with all of it: longer repeat-dose toxicity studies were unavailable to demonstrate whether these safety signals persist, or whether additional signals emerge with chronic exposure. Twenty-eight days is the longest anyone has looked. [Animal] [25] [33]
What has been reported to regulators
FDA retrieved three adverse event reports from FAERS for its 2026 review, all involving compounded product [33]. A 55-year-old woman reported nine days of redness and swelling around an injection site, while also using an injectable compounded thymosin product. A 28-year-old man using the acetate salt by subcutaneous injection for injury and inflammation developed shortness of breath resulting in an emergency room visit. A 40-year-old woman using BPC-157 together with TB-500 reported diffuse hyperpigmentation and gingival darkening that were reproducible on rechallenge.
FDA's caveat travels with those reports and is not separable from them: it is unclear whether the events were attributable to BPC-157, the agency's ability to interpret FAERS reports is limited by missing information and concomitant medications, and reporting is voluntary, so FDA does not receive all events that may occur, especially for compounded products.
The rechallenge detail on the third report is the only causality-suggestive element in the set, and it is one report. Three reports is also a number that says as much about the reporting channel as about the compound: the compounding and grey markets this substance moves through do not report to FDA at all.
Immunogenicity and characterization, unassessed
FDA's position is that a peptide of this length given by a parenteral or nasal route may pose a significant risk for immunogenicity, potentially amplified by aggregation and by peptide-related impurities, and that peptides given rectally or through the skin may also carry that potential depending on the environment [32]. The nomination did not include, and the agency did not find, information suggesting the substance does not present those risks.
That is a statement about what has not been ruled out rather than a statement that a problem exists, and both halves of it belong on this page.
It sits alongside the characterization finding, which is the other half of the same gap. FDA concluded that both the free base and the acetate salt are not well-characterized from the physical and chemical perspective, on grounds that include naming conventions that do not follow chemical nomenclature standards, missing impurity, aggregate, bioburden and endotoxin data, and no information on the critical attributes of the transdermal cream, oral capsule and rectal suppository forms proposed to it [32]. A substance whose impurity profile has never been described cannot have its risks described either.
The haemostasis signal, and why it sits in two places
The rat work reporting reduced bleeding time under heparin, warfarin and aspirin is in the benefits section above, because that is where the claim is made [21]. Its counterpart belongs here: the formal 28-day toxicology found clotting-time changes in both species it tested, in opposite directions between them [25].
Those are two independent lines arriving at the same organ system from different directions, one as an effect and one as a signal. Nobody has followed up on what the combination means, in any species, and no human coagulation measurement of any kind exists for this compound. [Animal] [21] [25]
Two corrections in the published record
A search of the full PubMed corpus for this compound by publication type returns one withdrawn paper and one corrigendum, both from the same research group [30]. The withdrawn article covered severe electrolyte disturbances in rats and carries a publisher's notice stating that it has been withdrawn at the author's request; PubMed indexes it as a retracted publication, and this page's reference list records both wordings. The corrigendum applies to a 2021 paper on abdominal compartment syndrome in rats, and this site names both the correction and the original wherever either is cited.
No expressions of concern and no retraction-of-publication notices were found anywhere in the corpus.
Also in the record and not a correction: a 2025 comment-and-reply exchange in a journal between two research groups about angiogenesis and the nitric oxide system. It is a scientific disagreement published in the ordinary way, and it corrects nothing.
Two withdrawn or corrected papers in a corpus of 225 records is not a remarkable rate. It is on the page because a site that reports authorship concentration and then omits the corrections would be selecting, and because neither paper is cited for a claim here.
What has not been characterized
No human safety measurement of any kind exists for the route the compound is sold by, because no human study has used it. Nothing in the file establishes what happens after 28 days in any species, what the substance's impurity profile is, or whether it produces an immune response.
FDA's summary sentence covers all of it and is quotable in full: there is insufficient clinical safety information to characterize the safety profile of BPC-157 free base and BPC-157 acetate [33]. This site makes no statement about tolerability, in either direction, because no data exists that could establish one.
Talk to a licensed clinician about anything concerning your health.
Sourcing and quality
What a credible product should show
A certificate of analysis is the document that matters, and most of the work is in reading it rather than in having one. Three things make a certificate checkable: a lot number that matches the vial in front of you, a test date, and the name of the laboratory that ran the test rather than the name of the company selling the material.
What the common tests establish is narrower than it looks. High performance liquid chromatography separates what is in a sample and reports relative peak area, which is a statement about chromatographic purity rather than about identity. Mass spectrometry addresses identity by measuring molecular weight, and for BPC-157 free base that figure is 1419.5 [32]. Neither test says how much peptide is in the vial: that is net peptide content, and it is reported separately, if at all.
This compound has two specific analytical questions attached to it, both of which come out of the agency record. FDA recorded that a common name rather than a standardized chemical name contributes to the substance being poorly characterized, so a certificate should say which form it covers, free base or acetate, since those carry different CAS numbers and different UNII codes [32]. And FDA's characterization finding lists the data classes that were missing from the whole record: impurities, aggregates, bioburden and endotoxin. Those are the four to look for, and their absence is a fact about the document rather than about any particular seller.
Red flags
A certificate with no lot number cannot be tied to the vial in your hand, whatever else it says. A certificate reproduced from a supplier without an independent test is a supplier's claim rather than a verification. A certificate dated well before the material was made covers a different batch.
A purity figure with no method named is not a purity figure. Ninety-nine percent by which measurement, against which reference standard, and with how much peptide in the vial are four separate questions, and one percentage answers none of them.
A certificate that does not say which form it covers is ambiguous by construction for this compound, because the free base and the acetate salt are separate substances with separate identifiers and FDA evaluated them separately.
Widely circulated statistics about what fraction of products in this market are underdosed, or what fraction of certificates are fabricated, trace back to affiliate content sites rather than to a published testing programme. This site does not publish them, because nobody has traced them to primary data. If a figure like that ever appears with a real methodology behind it, it will be cited here by number.
This site names no company adversely and names none favourably either. There is no best-vendor list here, no rating and no top pick, and there will not be one.
Will it show on a drug test?
For a tested athlete the answer is direct, and BPC-157 is one of the few compounds in this catalog where it does not need a derivation. It is named on the face of the S0 class of the WADA 2026 Prohibited List, in the sentence that reads: this class covers many different substances including but not limited to BPC-157, followed by three other examples, two of which are classes of substances rather than single ones [42]. The list's own index carries the entry BPC-157 with its page number.
S0 is Non-Approved Substances, and it is prohibited at all times, in competition and out of it. Its definition covers any pharmacological substance not addressed by another section of the list and with no current approval by any governmental regulatory health authority for human therapeutic use. The list states that all prohibited substances in this class are Specified Substances, which changes how a sanction is calculated rather than whether the substance is banned.
Being named on the face of a class rather than caught by its definition is the practical difference between this compound and most of the catalog. There is no argument to have about whether the definition reaches it.
Whether a test can detect it is a separate question with a thinner answer. Two in-vitro plasma-metabolism studies exist for anti-doping screening purposes, and neither administered BPC-157 to a person [32]. The only human plasma measurements that exist anywhere are the two rectal studies, in which the compound was not detected. Nothing published establishes what a current screening panel would find after real-world use, in either direction.
The US Department of Defense position is separate and it is explicit. The Operation Supplement Safety ingredient and substance index carries a BPC-157 entry reading that BPC-157 is on the DoD Prohibited Dietary Supplement Ingredients list, with a status label of Prohibited [43]. Its linked article, posted 29 April 2025, states that the compound is an unapproved drug that cannot be legally prescribed or sold over the counter, records the S0 listing, and states that the lack of well-designed comprehensive human clinical studies means there is little to no reliable scientific evidence to support the safety or effectiveness of BPC-157 in humans.
Anti-doping status is decided by an athlete's own anti-doping organization against the current list, and that is the only body whose answer counts. Workplace testing is a different system with a different panel and no published position that reaches this compound.
Storage
FDA records that BPC-157 is expected to be stable under storage conditions below minus 18 degrees Celsius, as reported in the literature, and that is the only storage statement in the agency record [32].
No shelf life has been published for any presentation, and the characterization gap covers this too: without impurity and aggregate data there is no baseline against which a degradation product could be identified.
This site publishes no handling or preparation procedure. That is a standing rule and the reasoning is on the editorial policy page.
Regulatory status, as of 8 August 2026
| Body | Position | Date | Document |
|---|---|---|---|
| FDA, 503A Bulks List | Not on the list. BPC-157 appears in FDA's table of bulk drug substances nominated but withdrawn, alongside sixteen other peptides, with the agency's safety text retained beside it. It is not in the active category 2 table on the same page | Page content current 2026-04-22 | FDA, Certain Bulk Drug Substances for Use in Compounding that May Present Significant Safety Risks |
| FDA, retained safety text | Compounded drugs containing BPC-157 may pose risk for immunogenicity for certain routes of administration and may have complexities with regard to peptide-related impurities and active pharmaceutical ingredient characterization. FDA has identified no, or only limited, safety-related information for the proposed routes of administration. Therefore the agency lacks sufficient information to know whether the drug would cause harm when administered to humans | Page content current 2026-04-22 | FDA, Certain Bulk Drug Substances for Use in Compounding that May Present Significant Safety Risks |
| FDA reviewers | Proposed not adding BPC-157 free base or BPC-157 acetate to the 503A Bulks List. Their stated grounds: both forms are not well characterized physicochemically, there is insufficient information on the safety profile and immunogenicity risks, there is insufficient evidence to conclude on effectiveness for ulcerative colitis, and approved products exist for that condition | Briefing document for the 23 and 24 July 2026 meeting | FDA briefing document for BPC-157-related bulk drug substances, fda.gov/media/193343/download |
| Pharmacy Compounding Advisory Committee | Two separate voting questions were put, one on BPC-157 free base and one on BPC-157 acetate, first on the agenda for the morning session. FDA has published no minutes, no transcript and no vote record for the meeting | 2026-07-23 | FDA, Questions for PCAC, fda.gov/media/193711/download; meeting page checked 8 August 2026 |
| Federal Register | Meeting notice, establishment of a public docket and request for comments. The chart of uses in the notice records the use FDA evaluated for this substance as ulcerative colitis | 2026-04-16, 91 FR 20465 | FR document 2026-07361, Docket No. FDA-2025-N-6895 |
| Category 2, the earlier placement | BPC-157 was described as an FDA 503A category 2 substance from 2023. Category 2 is an administrative designation FDA publishes on its own website under its 2016 interim policy guidance, and no Federal Register document exists for the placement. A search of the Federal Register corpus for BPC-157 returns exactly one document, the 2026 meeting notice above | Superseded by the current page | FDA interim policy on compounding using bulk drug substances under section 503A; Federal Register full-text search |
| Approval status | No approved drug product containing this compound anywhere. It is not the subject of a USP or NF monograph and it is not a component of an approved drug, which is what puts it outside all three routes onto the 503A list under section 503A(b)(1)(A)(i) | Checked 2026-08-08 | FDA briefing document for BPC-157-related bulk drug substances |
| WADA | Named on the face of the S0 Non-Approved Substances class, prohibited at all times, in and out of competition. All S0 substances are Specified Substances | Effective 2026-01-01 | WADA 2026 Prohibited List, final English version, 26 pages, S0 at page 4 |
| US Department of Defense, OPSS | On the DoD Prohibited Dietary Supplement Ingredients list, with a status label of Prohibited on the ingredient and substance index. The linked article states it is an unapproved drug that cannot be legally prescribed or sold over the counter | Article posted 2025-04-29, index checked 2026-08-08 | OPSS ingredient and substance index, opss.org/ingredient-and-substance-index |
The regulatory position on BPC-157 moved in 2026, most writing about it predates the move, and the order the events happened in is what makes it readable.
Start with where it actually sits. On FDA's page of bulk drug substances that may present significant safety risks, content current as of 22 April 2026, there are two tables. The first is the active category 2 list, and BPC-157 is not in it. BPC-157 is in the second table, headed bulk drug substances nominated but withdrawn, alongside AOD-9604, cathelicidin LL-37, CJC-1295, epitalon, ipamorelin, KPV, melanotan II, MOTS-c, semax, thymosin alpha-1 and the thymosin beta-4 fragment, among others [36]. The safety text FDA wrote for it is retained beside it and is quoted in full in the table above. Withdrawn refers to the nomination, not to the agency's concerns.
The commonly repeated description of BPC-157 as an FDA 503A Category 2 substance placed on 29 September 2023 needs two corrections rather than one. It is no longer on that table, and there was never a Federal Register document behind the placement. Category 2 is an administrative designation FDA publishes on its own website under the 2016 interim policy guidance on compounding with bulk drug substances, and a search of the entire Federal Register corpus for BPC-157 returns one document: the 2026 meeting notice [35]. Anyone citing a Federal Register number for the 2023 placement is citing something that does not exist.
The 2026 events are the ones that matter now. On 16 April 2026 FDA published a Federal Register notice announcing a Pharmacy Compounding Advisory Committee meeting for 23 and 24 July, establishing a public docket and requesting comments, under Docket No. FDA-2025-N-6895. The chart of uses in that notice records the use FDA evaluated for this substance in three words: ulcerative colitis [35]. Not tendon repair, not muscle recovery, not the joint indications the market sells. The published questions document put BPC-157 first on the morning of 23 July, on two votes, one for the free base and one for the acetate salt [34].
FDA's own reviewers had already published their position in a 68-page briefing document. They concluded that both forms are not well-characterized physicochemically, that there is a lack of evidence to support effectiveness for ulcerative colitis, that there is insufficient clinical safety information to characterize the safety profile, and that available data are too limited to understand historical use in compounding, with no outsourcing facility having reported compounding it. Their overall sentence is that a balancing of the criteria weighs against BPC-157 free base and BPC-157 acetate being placed on that list, and their recommendation is that neither be included [32].
What the committee then did is not on the public record. Checked on 8 August 2026, the meeting page and the 2026 meeting-materials index carry the briefing documents, the introduction, the agenda, the roster, the questions, webcast information and the two presentation decks, and nothing else [37]. No minutes, no transcript, no vote results. A tally has circulated in trade coverage; this site does not publish it, because no primary document supports it and two separate questions were put, so a single number could not be assigned to either even if it were sourced. This page will carry it when FDA publishes minutes. The 503A record on this site sets out the whole meeting, across all seven substances the committee considered, and it is the page to read for how the compounding process itself works.
What a listing would mean, if the agency accepted a recommendation and finished the process, is that a licensed pharmacy could compound the substance for an identified patient against a valid prescription under section 503A. It would not be an approval, it would not create an over-the-counter product, and it would not make a direct unlicensed sale lawful. The process runs through a proposed rule, a comment period and a final rule, and that cannot be bypassed. This page publishes no estimate of how long it takes, because no agency document states one.
The anti-doping and military positions are separate systems and both are unambiguous. BPC-157 is one of only four examples named on the face of the WADA S0 class rather than reached by its definition [42], and it is the only one of the four that is a single named peptide, and the Department of Defense lists it as a prohibited dietary supplement ingredient for Service Members [43]. Neither of those is a safety finding. They are rules positions, and they apply to a defined group of people regardless of what the evidence eventually shows.
BPC-157 compared with other peptides sold for repair and recovery
| Compound | Evidence grade | What the human record covers | Read more |
|---|---|---|---|
| KPV | D | No human study of any design, on any route, confirmed four separate ways including by FDA's own literature search | Its full evidence review, and the two compounds compared head to head |
| GHK-Cu | B | Two completed randomized trials of topical products, 86 evaluable patients in 1992 and 13 in 2006, neither separating from its control on an objective measure | Its full evidence review |
| TB-500 | D | No human study of the fragment on any route. Of the eighteen registrations usually counted for it, seventeen tested thymosin beta-4, a different and much larger molecule, and the eighteenth names TB-500 and states in its own registered text that it is a fictional example record | Its full evidence review |
| Larazotide | Not graded here yet | 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 use it is now sold for | Covered on the healing and recovery page |
Three of these four carry a grade and one does not, and that is deliberate: a grade here is derived from tiered claim rows, and the source review behind those rows has not been run on larazotide.
The comparison that shows what the grade scale measures is BPC-157 against KPV. KPV sits at D because nobody has ever given it to a person. BPC-157 sits higher because it has been randomized against placebo, and the randomized trial did not separate from placebo. The letter records how much research exists and how good it is, not which way the research came out, which is why the sentence beside the badge on this page carries the direction in words. A reader comparing two cards and reading the higher letter as the better answer would have it backwards here.
The GHK-Cu row is the closest structural parallel on this site. Two compounds, both tested against a control, both failing to separate, both grading B for the same reason: being tested and beaten is a stronger evidence position than never having been tested at all, and it is a worse result. TB-500 sits a letter below both, and the two compounds sold beside each other for the same injuries now carry different letters for exactly that reason.
The comparison people actually search for is KPV against BPC-157, and it is set out in full on its own page.
What BPC-157 typically costs
BPC-157 is sold as a lyophilised powder in vials across a wide range of vial sizes, and also in capsule and oral spray presentations. What any of it costs is not published here, and the price comparison page sets out why, along with the four things that actually move a listing.
The one thing worth carrying away is that nothing in a price says anything about identity, content or testing, and for this compound that includes which form the vial holds, since the free base and the acetate salt are separate substances with separate identifiers. Those are certificate questions, and they are covered in the sourcing section above.
Frequently asked questions
Has BPC-157 been tested in people?
Yes, in five studies, and the shape of that record matters more than the count. Two were randomized against placebo, both from the original commercial programme, and neither was ever published beyond a conference abstract: a 53-patient ulcerative colitis study whose between-group difference crossed zero, and a 32-volunteer tolerability and pharmacokinetic study [32]. Three are published in journals and all three are uncontrolled: a 17-patient knee-pain chart review, a 12-patient bladder study, and an infusion report in two people [26] [27] [28].
Is there a completed trial of BPC-157 for an injury?
No study of any design has tested it for an injury in a person. The only randomized human efficacy study tested ulcerative colitis, it reported no separation from placebo, and it has never been published in full [32]. Everything behind the injury claims is rodent work in animals whose tendons, muscles or ligaments were cut, crushed or detached by a surgeon [4] [7] [8] [11].
What about the phase 2 hamstring trial?
That registration is real and its sponsor account is worth reading before anything is built on it. Querying the registry for that sponsor on 8 August 2026 returns eight records: three declare in their own registered text that they are examples rather than studies, and two carry a large manufacturer's own internal protocol identifiers for that manufacturer's own molecules [41]. All eight share a single site, one contact address on a domain that does not match the sponsor name, and a five-week posting window, and six of the eight share an identical start date. The BPC-157 record itself carries no disclaimer and has posted no results [39]. This site therefore states no expectation from it and counts no controlled trial as currently underway.
Is BPC-157 approved by the FDA?
No. It is not an approved drug anywhere and it is not on the FDA 503A Bulks List. It sits in FDA's table of bulk drug substances nominated but withdrawn, with the agency's safety text retained beside it [36]. FDA's own reviewers proposed against adding either the free base or the acetate salt, and an advisory committee took the question up on 23 July 2026 on two separate votes [32] [34].
Was BPC-157 in FDA 503A Category 2?
It was described that way from 2023, and two things about that description need correcting. It is no longer on the active category 2 table: as of the page current 22 April 2026 it is in the nominated-but-withdrawn table instead [36]. And there is no Federal Register document behind the original placement, because category 2 is an administrative designation FDA publishes on its own website under a 2016 guidance. A search of the whole Federal Register corpus for BPC-157 returns one document, the 2026 meeting notice [35].
Will BPC-157 show up on a drug test?
For a tested athlete it is prohibited, and unusually for this catalog it is named rather than derived. BPC-157 appears on the face of the S0 Non-Approved Substances class of the WADA 2026 list, which is prohibited at all times, in and out of competition, and all S0 substances are Specified Substances [42]. Whether a given panel detects it is a different question with no published answer: the two metabolism studies run for screening purposes never gave the compound to a person, and the only human plasma measurements that exist did not detect it.
Has the Department of Defense banned BPC-157?
Yes, by name. The Operation Supplement Safety ingredient index carries a BPC-157 entry stating that it is on the DoD Prohibited Dietary Supplement Ingredients list, with a status label of Prohibited [43]. Its linked article, posted 29 April 2025, records that it is an unapproved drug that cannot be legally prescribed or sold over the counter.
Is subcutaneous BPC-157 studied at all?
No, in either people or animals. FDA searched the literature and reported finding no study administering BPC-157 to humans by the oral, subcutaneous, nasal or transdermal route [33]. The published animal efficacy work used the abdominal cavity, the mouth, the stomach, a topical cream or a local bath, and a 2025 systematic review of the whole orthopaedic literature identifies no subcutaneous study either [29]. It is the route the entire retail market uses.
Why is so much of the research from one group?
Because that group described the parent compound and has worked on it since 1992. Of the 25 preclinical and identity papers cited here, 17 carry the same senior author and a second author appears on all 17. The remaining eight come from five other laboratories. This site prints full author lists in its reference list so a reader can check the overlap rather than take a count at face value. It is a fact about how a literature was produced, not a judgement about any paper in it.
What did the July 2026 advisory committee decide?
Nothing has been published. Checked on 8 August 2026, FDA has posted the briefing documents, the agenda, the roster, the questions, webcast information and the presentation decks for that meeting, and no minutes, no transcript and no vote record [37]. A tally circulates in trade coverage and this site does not carry it, because no primary document supports it and two separate questions were put on this substance, so one number could not be assigned to either. A committee recommendation is advisory in any case: the agency still has to decide, publish a proposed rule, take comment and issue a final rule.
How does BPC-157 compare with TB-500?
They are sold together, they now carry different letters, and only one experiment has ever compared them. A 2026 four-arm rat study of a transected and repaired Achilles tendon tested both and their combination: BPC-157 was numerically better than control and did not reach significance on the total histopathology scores, TB-500 did reach significance, and the combination added nothing over either alone [6]. TB-500 sits at D on its own review, because no human study of the fragment exists on any route. BPC-157 sits at B because it has been randomized against placebo, and that trial did not separate from placebo. The rat study and the letters point in opposite directions, and both are on the record.
How does BPC-157 compare with KPV?
BPC-157 has a human record and KPV has none at all, which is the whole difference. About 80 people have received BPC-157 under a written protocol across five studies, including two randomized against placebo, and no human being has ever been given KPV in a study of any design. The full comparison is on its own page.
What would move BPC-157 to a higher grade?
A completed, published, randomized trial of this compound, in people, for the use it is sold for, reporting whether it met its primary endpoint. Nothing verifiably matching that description is underway. The one randomized efficacy study that has ever read out tested a different condition by a different route, and it did not separate from placebo.
Does BPC-157 have side effects?
No data exists that could characterize them. The only formal toxicology ran 28 days in rats and dogs and found changes in clotting time in both species and in triglycerides, liver enzymes and glucose in female rats, with FDA recording that nothing longer exists [25] [33]. Three adverse event reports have reached FAERS, all involving compounded product, and FDA's caveat that attribution is unclear and reporting is voluntary travels with them. FDA's own summary is that there is insufficient clinical safety information to characterize the safety profile.
What is BPC-157 acetate, and is it the same thing?
It is a salt form, and FDA treated it as a separate substance throughout its 2026 review, with its own voting question, its own CAS number and its own UNII code. The agency reached the same conclusions about both forms: not well-characterized, no adequate effectiveness evidence, and insufficient safety information [32]. A certificate of analysis that does not say which form it covers is ambiguous by construction for this compound.
References
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- 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 and Veljaca 2002 and 2003 meeting abstracts, the characterization findings, and the recommendation against listing. FDA advisory committee materials. 2026. Source document
- US Food and Drug Administration. July 23, 2026 Meeting of the Pharmacy Compounding Advisory Committee: FDA presentations. 149 pages. Carries the pharmacology limitations, the animal pharmacokinetics, the 28-day toxicology signals, the three FAERS reports and the clinical safety conclusion. FDA advisory committee materials. 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, 23 and 24 July 2026. BPC-157 free base and BPC-157 acetate are the first two votes of the 23 July morning session. FDA advisory committee materials. 2026. Source document
- 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 chart of uses records the use evaluated for BPC-157 free base and BPC-157 acetate as ulcerative colitis. Federal Register, document 2026-07361, 91 FR 20465. 2026. Source document
- US Food and Drug Administration. Certain Bulk Drug Substances for Use in Compounding that May Present Significant Safety Risks. Page content current as of 22 April 2026. BPC-157 appears in the second table, bulk drug substances nominated but withdrawn, and not in the active category 2 table. FDA human drug compounding. 2026. Source document
- US Food and Drug Administration. July 23-24, 2026 Meeting of the Pharmacy Compounding Advisory Committee, meeting page and materials index. Page content current as of 6 August 2026 and read on 8 August 2026: briefing documents, agenda, roster, questions, webcast information and two presentation decks are posted, and no minutes, transcript or vote record is. FDA advisory committee calendar. 2026. Source document
- PharmaCotherapia d.o.o. Phase I, pilot study in healthy volunteers to assess the safety and pharmacokinetics of PCO-02, whose active ingredient is BPC-157, a pentadecapeptide from a gastric source (NCT02637284). Randomized, quadruple-masked, placebo-controlled, 42 estimated, single site in Tijuana. Status unknown; first posted and last updated 22 December 2015; no results posted. ClinicalTrials.gov. 2015. Source document
- Hudson Biotech. A randomized, double-blind, placebo-controlled phase 2 trial of pentadecapeptide BPC 157 for accelerated repair of acute grade II hamstring strain confirmed by MRI (NCT07437547). Registered as recruiting, 120 estimated, single site at Peking University Shenzhen Hospital, actual start 2 February 2026, primary completion estimated 14 February 2027; no results posted. Read in full 8 August 2026, together with the sponsor account below. ClinicalTrials.gov. 2026. Source document
- Parlay Wellness, with Citruslabs. A clinical trial to evaluate the effects of peptide gummies on markers of inflammation, physical performance, and recovery (NCT07752381). Single-arm, open-label, no randomization or masking, 40 actual participants, site in Las Vegas. Completed 1 November 2025 and first posted 7 August 2026; no results posted. ClinicalTrials.gov. 2026. Source document
- US National Library of Medicine. ClinicalTrials.gov registry, API v2, read in full on 8 August 2026. An intervention and free-text search for BPC-157 and its variants returns three records: NCT02637284, NCT07437547 and NCT07752381. A sponsor search for Hudson Biotech returns eight records: NCT07437547, NCT07437560, NCT07437586, NCT07467447, NCT07481734, NCT07481747, NCT07487363 and NCT07505745. Three of the eight describe themselves in their own registered text as an example, a mock study or a fictional study, and two carry Eli Lilly protocol identifiers for Lilly molecules. ClinicalTrials.gov. 2026. Source document
- World Anti-Doping Agency. The 2026 Prohibited List, international standard, effective 1 January 2026. 26 pages. BPC-157 is named on the face of class S0 at page 4 and carries its own index entry. WADA. 2026. Source document
- US Department of Defense, Operation Supplement Safety. Ingredient and substance index, and the article BPC-157: a prohibited peptide and an unapproved drug found in health and wellness products, posted 29 April 2025. Index checked 8 August 2026: the BPC-157 entry reads that BPC-157 is on the DoD Prohibited Dietary Supplement Ingredients list, with a status label of Prohibited. OPSS, Uniformed Services University. 2026. Source document