BPC-157 vs KPV

Both are sold as components of the same multi-peptide research blends, which is where this pairing usually comes up: someone reading a blend's label wants to know what each part of it is. They are different classes of molecule, described in separate literatures, and treated differently by regulators.

What this comparison cannot establish

No study on either research index places both compounds in the same model. The two columns are separate literatures set side by side, not a head-to-head trial, and nothing here supports a conclusion that one compound does more than the other.
A property appearing in both columns does not mean it was measured the same way. The two bodies of work differ in size, in study type, and in how much of each is independent of the parties selling the material.
Neither compound is an approved drug in the United States. Rows describing regulatory or pharmacopoeial status record how each is treated administratively. They are not findings about what either does.

Published properties

Only properties both compounds publish are listed. Every value carries the primary source it came from.

Property	BPC-157	KPV
Substance class	Synthetic pentadecapeptide. Its sequence is a 15-amino-acid fragment of BPC, a roughly 40 kDa protein isolated from human gastric juice and first described in 1993. BPC-157 as supplied is made by solid-phase synthesis, not isolated from gastric juice; sources that describe the pentadecapeptide itself as "isolated from human gastric juice" are conflating the fragment with the parent protein. source	Synthetic tripeptide of lysine, proline and valine. FDA's evaluation states "KPV is reported to be a tripeptide composed of the amino acids lysine (K), proline (P), and valine (V)" and that "It is naturally produced in the body and is a fragment derived from the neuropeptide produced in the pituitary gland called alpha-melanocyte-stimulating hormone (alpha-MSH)". PROVENANCE: FDA's footnote for that second sentence points at a wellness-clinic blog post, not at a published characterisation. The relationship itself is independently documented in the peer-reviewed literature — see the parent_hormone_relationship entry, which carries a primary source. source
Sequence	H-Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val-OH source	H-Lys-Pro-Val-OH source
Other names	Bepecin; PL-14736; PL-10; PLD-116; Body Protection Compound 157. FDA notes that BPC-157 is a common name and not a United States Adopted Name, and that multiple salts and derivatives, including different active moieties, are sold commercially under that same common name. source	KPV is the common name; FDA's abbreviation list expands it as "lysine-proline-valine". FDA states that "KPV is a common name and not a United States Adopted Name (USAN)" and that it "has encountered multiple salts, and derivatives, including different active moieties, sold commercially under the same common name for similarly situated products". FDA also states that inconsistent naming conventions that do not follow INN, IUPAC or USAN standards "represent a safety risk for patients as they may be dosed with a different BDS than the physician ordered". source
Cas number	137525-51-0 source	67727-97-3 source
Unii	8ED8NXK95P source	READ THE DISCREPANCY BEFORE USING THIS. FDA's Global Substance Registration System holds an approved record for "L-lysyl-L-prolyl-L-valine" with the UNII 7V6LGD8S5R, CAS 67727-97-3, formula C16H30N4O4 and molecular weight 342.4344, cross-referenced to PubChem CID 125672. Two other FDA surfaces disagree with it. FDA's own 503A evaluation lists the UNII code for both KPV (free base) and KPV acetate as "Not available", and the withdrawn nomination answered "Does the substance have a UNII code? NO". FDA's public UNII lookup at precision.fda.gov returns "The UNII (7V6LGD8S5R) does not exist" for that code as of this entry. The registry record is recorded here with that conflict stated rather than resolved. source
Acetate salt identifiers	BPC-157 acetate is a separate substance from BPC-157 (free base), with UNII PAR2FC72XP and CAS 216441-37-1 against the free base's 8ED8NXK95P and 137525-51-0. FDA states the two are different active pharmaceutical ingredients and therefore different bulk drug substances, sharing the same active moiety. Both nomination packages FDA reviewed named one form and attached a certificate of analysis for the other. source	KPV acetate is a separate bulk drug substance from KPV (free base) in FDA's analysis, with molecular formula C16H30N4O4.CH3COOH and molecular weight 402.5 g/mol against the free base's C16H30N4O4 and 342.43 g/mol. Neither has a UNII code in FDA's evaluation, and FDA notes that "The CAS number for KPV acetate is the same as that for KPV (free base) in most public references" — so, unlike BPC-157, the CAS number does not separate the two forms here. FDA states the two are different active pharmaceutical ingredients sharing the same active moiety, and that the single nomination it received named one form in the title of its certificate of analysis and a different one by molecular formula. source
Molecular formula	C62H98N16O22 source	C16H30N4O4 source
Molecular weight	1419.5 g/mol source	342.43 g/mol source
Appearance	White to off-white lyophilised powder, stated under FDA's physicochemical characterisation heading for BPC-157 (free base). FDA describes BPC-157 acetate separately as a white to off-white solid powder. source	KPV (free base) is described by FDA as a white to off-white lyophilized powder. FDA describes KPV acetate separately as a white to off-white solid powder. source
Solubility	Soluble in water at 5 mg/mL. PROVENANCE: FDA states this in its characterisation section for both the free base and the acetate, but footnotes it to supplier product pages rather than to a published measurement. Because the substance is water-soluble and would be solubilised before administration, FDA does not consider particle size a critical quality attribute for the solution dosage forms it reviewed. source	Different for the two forms, and both figures are supplier-sourced. FDA states that KPV (free base) "is soluble in water up to 0.70 mg/mL" and that KPV acetate "is reported to dissolve in water at 5 mg/mL". PROVENANCE: FDA's footnotes attribute the free-base figure to a supplier certificate of analysis and the acetate figure to a supplier product page, not to a published measurement. FDA treats the free base's low solubility as a characterisation gap, writing that because the nominator gave no formulation detail it "cannot evaluate how the physical and chemical characteristics, especially limited water solubility (0.7 mg/mL) and particle size, impact the performance of final products". source
Storage	READ THE PROVENANCE BEFORE USING THIS. FDA's evaluation reports that lyophilised BPC-157 (free base) is stable at room temperature for three weeks, that it is recommended to be held desiccated below -18 degrees C because exposure to moisture greatly decreases the long-term stability of lyophilised peptides, and that once reconstituted it is stable for two to three weeks at 4 degrees C and for three to four months at -20 degrees C. FDA's own footnotes attribute every one of those figures to supplier product pages, not to a published stability study, and FDA states the conclusion as what is "reported in the literature" rather than as an agency determination. No peer-reviewed forced-degradation or shelf-life study for BPC-157 was located. FDA separately warns that peptides such as this one are extremely sensitive to formulation, process and environmental conditions including pH, temperature, concentration and excipients, which may lead to aggregation and degradation and to loss of biological activity, and that significant amounts of aggregates can form during storage. source	READ THE PROVENANCE BEFORE USING THIS. FDA's evaluation reports that lyophilized KPV (free base) "is stable up to 3 years when stored at -20 degrees C in a tightly closed container, up to 2 years at 4 degrees C, and up to 3 months at 15 degrees C", and that on reconstitution "the aqueous solution is recommended to be stored at -80 degrees C for 6 months, at -2 degrees C for 1 month, and 10 degrees C for 1 week". FDA's footnote attributes every one of those figures to a supplier certificate of analysis, not to a published stability study, and FDA states the conclusion as what "is reported" rather than as an agency determination. For KPV acetate, FDA reports a different condition from the nominator's certificate of analysis: "in a sealed container at 2 degrees C to 8 degrees C". There is no United States, European, Japanese or International pharmacopoeial monograph for either form and no approved product label, so no body with standing to determine handling conditions has done so. FDA separately warns that peptides "can be extremely sensitive to product formulation, process, and environmental conditions (e.g., pH, heat (temperature), concentration, in-process related impurities, excipients etc.), which may lead to the aggregation and degradation of peptides", that this "could result in loss of their biological activity", and that significant amounts of aggregates can form during storage. source
Human pharmacokinetics	None established. FDA found no human pharmacokinetic data for BPC-157 by the oral, subcutaneous, nasal or transdermal route. In the two published studies that gave BPC-157 as a rectal enema, the authors report that BPC-157 was not detected in plasma samples; in one abstract the authors state that most plasma concentrations were below the lower limit of quantification of the assay, with no further detail given. source	None. FDA states it "did not identify clinical studies in humans assessing pharmacokinetics or pharmacodynamics of KPV (free base) or KPV acetate via any route of administration". FDA also states that neither the nominator submitted nor did the agency identify any nonclinical pharmacokinetic or toxicokinetic study of either substance, so there is no animal figure to quote either. source
Approval status	Not an approved drug anywhere. FDA states that neither BPC-157 (free base) nor its acetate form is a component of an FDA-approved drug, and that a search identified no approved product containing either substance in any country. source	Not an approved drug anywhere. FDA states there is "no applicable United States Pharmacopeia (USP) or National Formulary (NF) drug substance monograph for KPV (free base) or its acetate form, and neither are a component of an FDA-approved drug". FDA adds that a search of the European Pharmacopoeia (11.8 edition, 2025) and the Japanese Pharmacopoeia (18th Edition) found no monograph for either form, and that the European Medicines Agency "did not list any products containing KPV (free base) or KPV acetate that are authorized for use". source
Fda 503a bulks list status	Not on the 503A Bulks List. In an evaluation dated 5/11/2026, FDA concluded that a balancing of the statutory criteria weighs against adding BPC-157 (free base) and BPC-157 acetate to that list, and wrote "Accordingly, we propose not adding BPC-157 (free base) or BPC-157 acetate to the 503A Bulks List." FDA's stated grounds were that both substances are not well characterised physicochemically, that there is a lack of information on their safety profile and immunogenicity risk, that the evidence is insufficient to reach a conclusion on effectiveness for the nominated use, and that approved drug products already exist for that condition. source	Not on the 503A Bulks List. In an evaluation dated 5/12/2026, FDA concluded that a balancing of the statutory criteria weighs against adding KPV (free base) or KPV acetate to that list, and wrote "Accordingly, we propose not adding KPV (free base) or KPV acetate to the 503A Bulks List." FDA's stated grounds were that both substances are not well-characterised physically and chemically, that the extent of use in compounding is unknown, and that there is "non-existing information on the use of these substances administered in humans to make a conclusion on their clinical safety and effectiveness", alongside the existence of approved therapies for the conditions proposed. source
Fda advisory committee review	FDA put BPC-157 (free base) and BPC-157 acetate to its Pharmacy Compounding Advisory Committee on July 23, 2026, with the published voting questions "Should BPC-157 (free base) be placed on the list?" and "Should BPC-157 acetate be placed on the list?". An advisory committee recommendation does not bind FDA, and as of the date of this entry FDA had not published minutes, a transcript or a vote record for that meeting. source	FDA put KPV-related bulk drug substances to its Pharmacy Compounding Advisory Committee at a meeting held July 23-24, 2026, with the published voting questions "Should KPV (free base) be placed on the list?" and "Should KPV acetate be placed on the list?". The same meeting covered BPC-157, TB-500, MOTS-c, Emideltide, Epitalon and Semax. An advisory committee recommendation does not bind FDA, and as of the date of this entry FDA's meeting page carried briefing documents, the questions, the agenda, the roster and the presentation slides, but no minutes, transcript or vote record. This file therefore does not state how the committee voted. source
Compounding volume reported to fda	Zero. FDA reports that according to its outsourcing facility product reporting data from January 2017 to June 2025, there were no reported compounded drug products containing BPC-157 (free base) or BPC-157 acetate. FDA notes separately that compounders operating under section 503A generally do not report to that database, so this figure covers registered outsourcing facilities rather than all compounding. source	Zero. FDA reports that according to outsourcing facility product reports submitted to the agency, outsourcing facilities "have not reported preparing single or multiple-API compounded drug products containing KPV (free base) or KPV acetate from January 2017 to June 2025". FDA notes separately that compounders operating under section 503A generally do not report to that database, so this figure covers registered outsourcing facilities rather than all compounding. source
Anti doping status	Prohibited. The United States Anti-Doping Agency states "Yes, BPC-157 is prohibited under the S0 Non-Approved Substances category of the List." FDA's evaluation states the same, citing the World Anti-Doping Agency prohibited list. source	Not established by any source this file could verify, and deliberately not inferred. No statement from a national or international anti-doping authority naming KPV was retrievable during data entry; the United States Anti-Doping Agency's published prohibited-list page does not name KPV, lysine-proline-valine or alpha-MSH. What was verified is narrower: a 2026 peer-reviewed critical review in a sports medicine journal names KPV among "synthetic fragments" that are "promoted for muscle growth, fat metabolism, recovery, and anti-inflammatory effects" in recreational and professional sport and bodybuilding, and states that clinical evidence supporting peptide use in sport is limited. That review records promotion, not prohibited status. Athletes should ask their own anti-doping authority rather than rely on this entry. source

What the research does not show

There is no published, adequately reported, randomised controlled trial of BPC-157 in people for any condition. The single randomised comparison that exists was published only as a conference abstract, and FDA states the data presented there are inadequate to support either efficacy or safety.
FDA's regulatory evaluation found only five clinical studies of BPC-157 in the entire published medical literature. Two of them are meeting abstracts rather than full papers. FDA describes the set as short in duration, small in sample size, exploratory in the doses used, and limited in the safety information the authors provided, and notes that safety monitoring is unclear for most of them. source
An independent systematic review of the orthopaedic literature screened 544 articles published between 1993 and 2024 and included 36 studies, of which 35 were preclinical and 1 was clinical. Its authors classify the body of work as level IV and level V evidence and state plainly that no clinical safety data were found. source
Route of administration in the published human studies does not match how the substance is actually supplied and used. FDA states it identified no study that gave BPC-157 to humans by the oral, subcutaneous, nasal or transdermal route. The two human studies FDA identified in which the substance was given repeatedly both used a rectal enema, a route almost nobody buying this compound uses.
The same gap exists in the animal safety work. FDA states that neither the nominators submitted, nor did FDA identify, nonclinical pharmacokinetic, acute toxicity, repeat-dose toxicity or developmental toxicity studies by any of the oral, rectal, transdermal, subcutaneous or nasal routes. The available animal toxicology used the intramuscular route, and because the absolute bioavailability of the other routes in rats and dogs is unknown, FDA states the intramuscular no-observed- adverse-effect levels cannot be used to estimate levels for those routes. source
The animal pharmacology does not establish a dose-response relationship. Across the rodent studies FDA reviewed, doses separated by three orders of magnitude (nanograms per kilogram versus micrograms per kilogram) produced effects of the same magnitude, so no dose-response could be established. FDA states the molecular targets of BPC-157 have not been identified and its mechanism of action remains poorly understood, which makes the biological plausibility of the reported effects difficult to assess. source
The 28-day animal toxicology carries unresolved signals rather than a clean result. FDA summarises the repeat-dose intramuscular studies in rats and dogs as showing clinically relevant safety signals including shortened and prolonged activated partial thromboplastin time, suggestive of altered clotting properties, and liver-associated signals comprising raised serum ALT, glucose and triglyceride levels. FDA states longer repeat-dose studies were unavailable to show whether those findings reproduce or whether further signals emerge, and that no carcinogenicity study exists. source
The published human studies that report favourable outcomes are uncontrolled and rely on self-report. The interstitial cystitis study cited here enrolled 12 women at a single private clinic, had one arm and no control group or blinding, and measured outcome with a self-rated Global Response Assessment questionnaire. The knee-pain report is a retrospective chart review in which some participants received BPC-157 combined with a second peptide, so nothing in it can be attributed to BPC-157 alone. source
A registered phase 1 study in healthy volunteers (NCT02637284) was started in 2015 and its results were never posted; FDA searched and was unable to find an associated published study. An independent review records that the researchers cancelled submission of the results in 2016. The trials that would characterise this substance in people were begun and then not reported. source
The evidence base is concentrated in a very small number of authors. A news investigation quotes a review team's count that the vast majority of the roughly 200 BPC-157 studies listed on PubMed include either Predrag Sikiric or Sven Seiwerth, both of the University of Zagreb, as a main author. That is a reported count from journalism rather than a published bibliometric analysis, and is recorded here as such. What can be checked directly is that the originating 1993 paper came from that same department, and that the reference list of FDA's own evaluation is dominated by papers from it. source
Nobody has measured what BPC-157 does in a person's bloodstream. FDA states there is no information with which to assess its human pharmacokinetics. The half-life, bioavailability and excretion figures on this page are from rats and dogs, and the route that produced them is not a route anyone has studied in people.
FDA considers the substance itself poorly characterised. Its evaluation concludes that both BPC-157 (free base) and BPC-157 acetate are "not well-characterized from the physical and chemical characterization perspective", citing naming conventions that do not follow USAN, INN or IUPAC standards, and missing or inadequate data on peptide-related impurities and aggregates, microbial quality, bacterial endotoxins and particle size. FDA notes that inconsistent naming is itself a safety risk because a patient may receive a different substance from the one intended. source
Commercial certificates of analysis for this substance generally report purity and nothing else. FDA reviewed the certificates supplied with both nominations and searched the literature for others, and found that most contain only purity testing results, with no impurity limits or results that would demonstrate control of the impurity profile, and no bioburden or bacterial endotoxin testing. FDA states that because of this it cannot rule out the potential for immunogenicity from those impurities and from peptide-related aggregates. source
The storage and solubility figures published on this site, and on every other site that carries them, trace back through FDA's evaluation to supplier product pages rather than to a published stability study. They are recorded here because FDA recorded them, with that provenance stated. No peer-reviewed shelf-life determination for this compound was located.
Much of the literature does not say which substance it studied. FDA notes repeatedly that published articles do not clearly identify whether the BPC-157 used was the free base or the acetate salt, and that it is often unclear whether a product described in a source was compounded at all. Findings reported for "BPC-157" therefore cannot always be assigned to a specific substance.
Adverse events reported to FDA exist but cannot be attributed. Every case FDA retrieved was confounded — by a second peptide given at the same time, by missing information about duration and concomitant medicines, or by use within a multi-ingredient product. Absence of a clean signal in a database this sparse is not evidence of safety.
The published research does not establish a dose, a route, a schedule, a duration, or a formulation for any use in a person, and it does not establish what happens with long-term use, because no long-term human study has been published.

What the research does not show about KPV

There is no human data of any kind. Not a weak trial, not an uncontrolled case series, not a pharmacokinetic sample — nothing. FDA searched the published medical literature, ClinicalTrials.gov, its own adverse event system and its foods complaint system, and states that it did not find information on products containing KPV administered to humans by any route. Everything else on this page is chemistry, regulatory record, or animal and cell-culture work.
No clinical trial of KPV has ever been registered. A query of the ClinicalTrials.gov registry on 2026-09-17 returned a total count of 0 for KPV as an intervention and 0 on a free-text search of the whole registry. There is not a completed trial whose results went unpublished, nor a trial under way; there is no trial. source
The evidence base is preclinical and narrow. FDA's reviewers identified pharmacological studies in in vitro and in vivo models and nothing beyond them, and the published work clusters in two areas: rodent gut inflammation (mouse DSS and TNBS colitis, mouse transfer colitis, mouse colitis-associated tumour models) and inflammation in cultured cells. Cell lines and mouse colitis models are not people with a condition, and a result in one is not a prediction about the other. source
A large share of the animal work does not test KPV on its own; it tests a delivery system carrying KPV, and the delivery system is doing much of the work. Laroui 2010 loaded KPV into 400 nm nanoparticles inside an alginate-chitosan hydrogel and reports that "KPV can be delivered at a concentration that is 12,000-fold lower than that of KPV in free solution, but with similar therapeutic efficacy". Xiao 2017 used hyaluronic-acid- functionalised nanoparticles inside a chitosan/alginate hydrogel and reports that the functionalised system performed better than the plain nanoparticle system. Later papers in this line use self-assembled carrier-free nanodrugs, mucoadhesive hydrogels and cross-linked hydrogels. None of that transfers to the raw peptide, and a result obtained with a nanoparticle is a result about the nanoparticle. source
Route of administration in the published work does not match how this compound is supplied or used. The mouse colitis studies delivered KPV in drinking water or by targeted colonic release. The single nomination FDA evaluated proposed a topical cream or gel. FDA's internet survey found the compound promoted instead as "single-API injectable, oral, topical, and nasal spray drug products". No study exists for any of those routes in a person, and the routes studied in rodents are not the routes being sold. source
The one human-tissue permeation experiment found that unaided permeation was undetectable. In dermatomed human cadaver skin, passive diffusion gave KPV permeation below the assay's detection limit; only microneedle abrasion, iontophoresis, or both together produced measurable transport. FDA reads this both ways, noting it "could limit the systemic bioavailability of KPV applied topically" and equally "could also limit the potential usefulness of KPV as a topical therapeutic agent". A topical product that does not cross the stratum corneum is not a mild version of one that does. source
Much of the literature people cite for KPV is not about KPV. FDA records that of the nine references submitted with the nomination, "eight references are studies on various alpha-MSH ... derivatives conducted in animals" and one concerned skin permeation — none was a study of KPV given to humans. FDA separately excluded from its own evaluation the submitted articles describing N-acetylated KPV and the KPV dimer, as "out of the scope of this evaluation". The parent hormone, the acetylated peptide, the dimer and the tripeptide are four different molecules. source
Where a study has compared the parent hormone with the tripeptide directly, they behaved differently. Getting 2003 reports that macrophage activation, measured as release of KC and interleukin-1 beta, "was inhibited by alpha-MSH and MTII but not by KPV", and that KPV "failed to increase cAMP" where the melanocortin agonist did. Anyone extending an alpha-MSH finding to KPV is extending it across a difference that this paper measured. source
Null results exist and are rarely cited. A 2018 study that modified the lysine residue of the tripeptide reports that antimicrobial assays "under a variety of conditions, showed no activity for Ac-KPV-NH2 or the alpha- or epsilon-glycoalkylated analogs". Separately, a published comment on the 2000 antimicrobial paper reports that its authors repeated the growth inhibition assays and could not observe the effect; as abstracted, the experiments they describe used alpha-MSH rather than the tripeptide, so the failed replication bears on the parent hormone directly and on the tripeptide only by association. source
The mechanism is unknown, which makes the animal findings hard to assess. FDA states that "the molecular targets underlying the pharmacological effects of KPV-related BDSs remain unknown", and that several lines of evidence indicate melanocortin receptors are unlikely to be those targets — KPV did not displace radiolabelled alpha-MSH binding in three preparations, and pharmacological and genetic approaches failed to implicate the MC2, MC3 or MC4 receptors. The proposed alternatives, NF-kappa B inhibition and PepT1-mediated uptake, are proposals in the literature, not established targets. source
There is no toxicology. FDA states that it identified no acute toxicity study, no repeat-dose toxicity study, no genotoxicity study, no developmental or reproductive toxicity study and no carcinogenicity study of either form, and no pharmacokinetic or toxicokinetic study in any species. Unlike BPC-157, where a published preclinical safety package at least exists to argue about, here there is nothing to read. source
The absence of adverse event reports is not a safety finding. FDA retrieved no reports from its adverse event system through December 3, 2025 and no cases from its foods complaint system since 2004 — and states in the same document that reporting is voluntary, that compounders operating under section 503A generally do not report adverse events to FDA, and that it "cannot make definitive conclusions regarding the safety of KPV based on FAERS data alone". An empty database for a substance nobody reports on says nothing. source
FDA considers the substance itself poorly characterised, and the certificates of analysis circulating for it report purity and little else. FDA found no certificate of analysis for the free base in the nomination at all, and states that the ones it found in the literature "only contain purity testing result", with no impurity limits, no aggregate data and no microbiological testing. For the acetate the nominator's certificate gave impurity totals but no identification of any individual impurity. A purity percentage without an impurity profile does not address what FDA names as the concern. source
The naming of this compound does not distinguish the substances being sold. FDA treats KPV (free base) and KPV acetate as different active pharmaceutical ingredients, records that "The CAS number for KPV acetate is the same as that for KPV (free base) in most public references", and lists no UNII code for either. Published work exists on the free acid (H-Lys-Pro-Val-OH), on the amide (H-KPV-NH2) and on the acetylated amide (Ac-KPV-NH2). A figure attached to the name "KPV" in a third-party source cannot be assigned to a specific substance without checking, and the usual identifiers do not settle it. source
The storage and solubility figures published on this site, and on every other site that carries them, trace through FDA's evaluation to supplier product pages and supplier certificates of analysis rather than to a published stability study. They are recorded here because FDA recorded them, with that provenance stated. The one exception is the forced-degradation chemistry, which comes from a peer-reviewed stability-indicating assay and is labelled as such.
Immunogenicity and aggregation have not been assessed for this compound at all. FDA states there is insufficient data to conclude that either form does not present those risks, and notes that peptides as short as two residues have been shown to aggregate. Short does not mean inert.
The anti-doping position is unresolved rather than permissive. No statement from an anti-doping authority naming this compound was retrievable during data entry, and this file does not infer one in either direction from statements about other substances.
The published research does not establish a dose, a route, a schedule, a duration, or a formulation for any use in a person, and it does not establish what happens with long-term use, because no human study of any length has been published.

BPC-157 monograph · Research index · Reading a certificate of analysis