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Research profile

BPC-157

Pentadecapeptide BPC 157

  • In vitro: 3
  • Animal: 6
  • Human, observational: 3
  • Human, controlled: 0
  • Review: 3

Registered trials2, listed apart from the publications

Content reviewed October 6, 2026

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How to read this profile
In vitro
In vitro. Cell cultures, isolated tissue or cell-free systems.
Animal
Animal. Animal models; a result in an animal is not a result in humans.
Human, observational
Human, observational. Observations in people without a controlled comparison group.
Human, controlled
Human, controlled. Studies in people with an assigned control group.
Review
Review. A synthesis of published literature, not new data.

Overview

In plain English

BPC-157 is a short synthetic peptide: a chain of 15 amino acids, the building blocks of proteins. A research group in Zagreb, Croatia, described it in the early 1990s as a fragment of a larger protein that the group had isolated from gastric juice.

Researchers have mainly studied it in rats and in cells grown in the laboratory (cell culture). In rats, it was tested in experimental models in which a tissue is damaged on purpose (the stomach lining, the Achilles at the back of the ankle, a thigh muscle, the skin) or blood flow to a limb or to the brain is interrupted, and the tissue's structure, strength or function is then measured. In cell culture, researchers looked at how fibroblasts (the cells that build connective tissue) and the cells lining blood vessels move, survive and switch particular genes and signaling proteins on or off.

The evidence is at an early stage. Most of it comes from animal and cell studies, much of it from the group that first described the peptide. The human reports listed here are three small studies with no comparison group: a review of 16 patients' records, a pilot study in 12 women and a pilot study in 2 adults. No completed randomized controlled trial with published results was found. Two randomized, placebo-controlled trials are registered: one was recruiting at the last registry check, and the other has an unknown status and no posted results.

The most important limitation is that a result in rats or in cultured cells does not show what happens in people. No receptor for the peptide (a molecule on or in cells that would recognize it) has been identified, and published human data on how the body handles it and on its long-term safety are very limited.

Key findings from published research

Selected observations from the publications listed in this profile, which are a curated subset of the literature, not all of it. Each one names the system it was observed in and links its source; a finding in cells or animals is not a result in people.

  1. In vitro

    In fibroblasts isolated from rat Achilles tissue, cell migration and spreading increased with the peptide's concentration, together with greater phosphorylation (activation) of the signaling proteins FAK and paxillin; cell proliferation did not change.

    (Chang et al. · 2011 · PMID 21030672 (opens PubMed in a new tab))

    Limits: Rat cells in culture; the study identified no receptor for the peptide.

  2. In vitro

    In cultured human umbilical vein endothelial cells (cells that line blood vessels), VEGFR2 expression increased and the receptor was internalized, and the VEGFR2–Akt–eNOS pathway was activated over time; the endocytosis inhibitor dynasore blocked the internalization and suppressed the pathway activation.

    (Hsieh et al. · 2017 · PMID 27847966 (opens PubMed in a new tab))

    Limits: Cell culture. The same paper measured blood flow and vessel counts in a rat model; those results are not summarized here.

  3. In vitro

    In isolated rat aorta, the peptide relaxed the vessel in a concentration-dependent way; the effect was weaker without the vessel's inner lining (endothelium) and was inhibited by L-NAME or hemoglobin, which block nitric oxide. In cultured endothelial cells, phosphorylation of Src, caveolin-1 and eNOS increased.

    (Hsieh et al. · 2020 · PMID 33051481 (opens PubMed in a new tab))

    Limits: Isolated tissue and cultured cells; no measurement in a living animal or in people.

  4. Animal

    In a rat model in which blood flow to the brain was stopped for 20 minutes and then restored, hippocampal expression of genes including Egr1, Akt1, Vegfr2 and Nos3 was higher, and expression of Nos2 and Nfkb lower, than in saline controls.

    (Vukojević et al. · 2020 · PMID 32558293 (opens PubMed in a new tab))

    Limits: A single study by the group that first described the peptide; not repeated by an independent group.

  5. Review

    A 2025 systematic review found 36 eligible studies, 35 of them preclinical; the one human study was a retrospective review of patient records, and no controlled human trial was identified.

    (Vasireddi et al. · 2025 · PMID 40756949 (opens PubMed in a new tab))

Identifiers

Name
BPC-157
Scientific name
Pentadecapeptide BPC 157
Synonyms
BPC 157; BPC157
Sequence
Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val (GEPPPGKPADDAGLV)
Molecular formula
C62H98N16O22
Molar mass
1419.5 g/mol
CAS number
137525-51-0
UNII
8ED8NXK95P

Evidence

Human, controlledHuman, observationalAnimalIn vitro12 listed publications· 2 registered trials

Human, animal and in vitro evidence are kept apart: where a result was observed decides what it can say. In vitro covers cultured cells and tissue studied outside the body. Reviews are listed under Publications; registered trials are listed below, apart from the publications.

Human evidence

Human, controlledHuman, observational3 listed publications

The human reports summarized in this profile are three small uncontrolled studies. The first is a retrospective chart review with a telephone survey of 16 people with knee pain of various causes; it had no control group, outcomes were self-reported, and the abstract does not report imaging or validated function instruments. The second is a single-arm, open-label pilot study in 12 women with interstitial cystitis, assessed with a Global Response Assessment questionnaire. The third is an uncontrolled pilot study in 2 adults who had been exposed to the peptide before, with blood markers and vital signs measured at baseline and after exposure; its result is not summarized in this profile. The three reports share a first author, come from private-clinic settings and were published in an alternative-medicine journal. Other human reports exist but are not summarized here: reviews by the originating group mention early trials from the compound's development period whose detailed results were not located in the indexed literature. A 2025 systematic review (36 studies: 35 preclinical and 1 in humans; search through June 2024) found no human safety data, and the single human study it included was retrospective. No completed randomized controlled trial with published results was identified. Two registered trials are listed separately, by their registry entries: a randomized, placebo-controlled trial that was recruiting at its last registry update, with no results, and an earlier registered study whose registry status is unknown and which has no posted results.

Listed publications at this level

Animal evidence

Animal6 listed publications

Most of the evidence comes from rat models. The models studied include gastric and duodenal lesion models (restraint stress, cysteamine, ethanol), Achilles tenotomy, surgical detachment of the quadriceps muscle, a cutaneous alkali-burn model, hindlimb ischemia and hippocampal ischemia/reperfusion. The endpoints measured include mucosal lesion counts, biomechanical measures (load to failure, Young's modulus), functional indices, histology, extracellular matrix deposition, blood flow and vessel counts, and performance on memory and coordination tests. The authors report differences from control groups on these endpoints; their direction and size are not summarized in this profile. Most of these abstracts do not state sample sizes, blinding is rarely described, and much of the work comes from the originating group. None of the studies listed here used large animals.

Listed publications at this level

In vitro and isolated-tissue evidence

In vitro3 listed publications

The cell and tissue systems studied include primary rat Achilles-derived fibroblasts, Achilles explants, cultured tenocytes, human umbilical vein endothelial cells (HUVEC), NIH 3T3 fibroblasts and isolated rat aorta. In Achilles-derived fibroblasts, faster outgrowth from explants, greater migration and greater survival under oxidative stress were observed, without a direct increase in proliferation, together with FAK–paxillin activation and increased GHR expression. In cultured tenocytes, the peptide alone did not change growth but counteracted growth inhibition by 4-hydroxynonenal. In HUVEC, greater proliferation, migration and tube formation were described, as well as increased VEGFR2 with Akt–eNOS activation. In isolated rat aorta, nitric oxide-dependent vasodilation was observed. None of the studies listed here identified a specific receptor for the peptide, and none used human tenocytes, human gastric mucosa or primary human neurons.

Listed publications at this level

Registered trials

2 registered trials

Registry entries, listed apart from the publications and not counted with them. Each links to its ClinicalTrials.gov record and shows only the registered phase, design, enrollment and status, and where its results stand. Results announced by a sponsor are marked as not peer-reviewed and are not summarized here.

Scientific detail

The technical layer: molecular identity, the mechanisms investigated with the evidence level at which each was observed, and the limits of the evidence. The plain-English summary is under Overview.

Molecular summary

BPC-157 is a synthetic pentadecapeptide with the sequence GEPPPGKPADDAGLV, the molecular formula C62H98N16O22 and an approximate molecular mass of 1419 Da. It was described in the early 1990s by Sikirić's group (University of Zagreb) as the 15-amino-acid fragment of a larger peptide (BPC) found in gastric juice, and later papers from the same group call it a "stable gastric pentadecapeptide".

It has been studied mainly in rat models of experimental gastric, musculoskeletal, vascular and nervous-system lesions. Proposed mechanistic hypotheses include modulation of the nitric oxide system (Src–caveolin-1–eNOS), VEGFR2–Akt–eNOS signaling in endothelial cells, the FAK–paxillin pathway and GHR expression in Achilles-derived fibroblasts, and changes in early-response genes (Egr-1, c-Fos, c-Jun).

Most of the evidence comes from rat models and cell cultures, much of it from the originating group and a small number of other laboratories; the human reports summarized in this profile are one retrospective chart review and two uncontrolled pilot studies, and no completed randomized controlled trial with published results was identified. It has not received regulatory approval.

Mechanisms investigated

Mechanistic hypotheses and observations as they were studied. The evidence level shows where each one was observed; none has been shown in people.

  1. 01Modulation of the nitric oxide system (Src–caveolin-1–eNOS)

    In vitro

    In isolated rat aorta, concentration-dependent vasodilation was observed that was attenuated without endothelium and inhibited by L-NAME or hemoglobin. In cultured endothelial cells, nitric oxide generation and phosphorylation of Src, caveolin-1 and eNOS increased, the phosphorylation changes were abolished by a Src inhibitor, and caveolin-1/eNOS association was reduced. This is a mechanistic hypothesis from one ex vivo and in vitro study; it has not been evaluated in humans.

  2. 02VEGFR2–Akt–eNOS signaling in endothelial cells

    In vitro

    In human umbilical vein endothelial cells (HUVEC), increased VEGFR2 expression and internalization and time-dependent activation of the VEGFR2–Akt–eNOS pathway were described, with greater tube formation; the endocytosis inhibitor dynasore blocked the internalization and suppressed the pathway activation. The pathway itself was measured only in these cultured cells: in the rat hindlimb ischemia model of the same study, blood flow, vessel counts and vascular VEGFR2 were measured, not Akt or eNOS activation. Another study, in HUVEC and a rat alkali-burn model, reported changes in ERK1/2 phosphorylation and in c-Fos, c-Jun and Egr-1 expression in the endothelial cells, alongside greater endothelial migration. The relevance of this endothelial signaling in humans has not been studied.

  3. 03FAK–paxillin pathway and migration of Achilles-derived fibroblasts

    In vitro

    In fibroblasts isolated from the rat Achilles, greater migration, cell spreading and F-actin formation were observed, together with a concentration-dependent increase in FAK and paxillin phosphorylation without changes in total protein. No direct effect on proliferation was observed, although survival under oxidative stress (H2O2) was greater. These findings are limited to primary cultures of rat cells.

  4. 04GHR expression and JAK2 signaling

    In vitro

    A microarray analysis in rat Achilles-derived fibroblasts identified GHR, a class I cytokine-family receptor gene, among the most strongly induced genes after exposure to the peptide, with confirmation at the mRNA and protein levels. Subsequent addition of the GHR ligand was associated with greater proliferation and JAK2 activation. This is an in vitro observation whose physiological relevance has not been established.

  5. 05Hippocampal gene-expression changes after experimental ischemia/reperfusion

    Animal

    In a rat model of hippocampal ischemia/reperfusion (bilateral common carotid clamping), hippocampal expression of Egr1, Akt1, Kras, Src, Foxo, Srf, Vegfr2, Nos3 and Nos1 was higher, and that of Nos2 and Nfkb lower, in the BPC-157 group than in saline controls; the study also assessed neuronal damage and performance on memory and coordination tests. These are exploratory findings from a single study by the originating group; they have not been examined by an independent group or in humans.

Limitations

  • Rat models predominate; no completed controlled trial in humans with published results was identified, and neither of the two registered randomized trials has posted results.
  • Much of the primary literature and several reviews come from the originating group (University of Zagreb); an independent review notes that only a handful of research groups have studied the peptide in depth.
  • The human studies summarized here are a retrospective chart review and two uncontrolled pilot studies with small samples (n = 2–16), no control group and no blinding, published in an alternative-medicine journal; the other human reports located have no detailed published results.
  • None of the studies listed identified a receptor or direct molecular target; the proposed mechanisms derive from gene-expression and phosphorylation changes observed in cell cultures and rat tissues.
  • Human pharmacokinetic and safety data are scarce; a 2025 systematic review located no human safety data, and the one pilot listed here that measured blood markers had two participants.
  • Designs, models and endpoints are heterogeneous; randomization and blinded outcome assessment are rarely described in the animal studies.
  • The interstitial cystitis pilot used a compounded preparation; independent characterization of the purity and composition of the material used in the human reports is not described.

What is not known

  • Whether any of the observations in rat models are reproduced in humans.
  • The identity of the receptor or the direct molecular targets of the peptide.
  • The pharmacokinetic profile in humans (absorption, half-life, metabolites).
  • Medium- and long-term safety, including whether the endothelial signaling observed in cell and animal models (VEGFR2–Akt–eNOS) is relevant in tumor settings.
  • The results of the early trials from the compound's development period mentioned in reviews, for which no detailed publication was located.
  • The results of the two registered trials listed in this profile: one had not reported results at the review date, and the other has no posted results and an unknown registry status.
  • Whether the findings are reproducible by independent groups and in species other than rats.

Publications

15 listed publications

Each publication is identified by its PubMed ID or DOI and grouped by evidence level. Each heading is our own description of what was studied. Titles, authors and journals are reproduced exactly as published; when the published wording of one of them falls outside our content rules, it is not shown here, and the record links to PubMed, where it can be read in full.

Human, observational 3

  • Human, observationalObservational study in humans· Homo sapiens

    Uncontrolled pilot study in 2 adults: blood markers and vital signs at baseline and after exposure

    Lee E, Burgess K2025PMID 40131143 (opens PubMed in a new tab)Full record on PubMed

    Model
    Uncontrolled pilot study at a private clinic in 2 adults (aged 58 and 68), both exposed to the peptide before the study; blood markers and vital signs recorded at baseline and after each exposure
    Sample size
    2
    Exposure
    BPC-157; single arm
    Comparator
    No control group

    Blood markers of heart, liver, kidney and thyroid function and vital signs were recorded at baseline and after each exposure, and the participants were asked about adverse events at each visit. With two participants, both previously exposed to the peptide, and no control group or blinding, the study cannot characterize safety; its result is not summarized in this profile.

    Measured endpoints

    Blood markers (heart, liver, kidney, thyroid) and vital signs at baseline and after exposure
    Recorded in both participants; the result is not summarized in this profile.
    Not stated
    Reported adverse events
    Asked about at each visit; a study of two participants cannot characterize safety.
    Not stated

    Limitations: Uncontrolled; two participants, both previously exposed to the peptide; no blinding; a single private clinic; published in an alternative-medicine journal; a study of this size cannot characterize safety.

  • Human, observationalObservational study in humans· Homo sapiens

    Single-arm open-label pilot study: symptom questionnaire in 12 women with interstitial cystitis

    “Effect of BPC-157 on Symptoms in Patients with Interstitial Cystitis: A Pilot Study.”

    Lee E, Walker C, Ayadi B2024PMID 39325560 (opens PubMed in a new tab)Full record on PubMed

    Model
    Single-arm, open-label pilot study at a private clinic in 12 women aged 39–76 with moderate to severe interstitial cystitis
    Sample size
    12
    Exposure
    BPC-157 (compounded preparation); single arm
    Comparator
    No control group

    Symptoms were assessed with the Global Response Assessment questionnaire; the authors report responses from all 12 participants and no dropouts. Because this was an open-label pilot study without a control group or blinding and with a subjective outcome, its design does not allow any change to be attributed to the peptide. The self-rated result is not summarized in this profile.

    Measured endpoints

    Interstitial cystitis symptoms (Global Response Assessment)
    Self-rated by all 12 participants, with no comparison with placebo or a sham procedure; the result is not summarized in this profile.
    Not stated
    Reported adverse events and dropouts
    Recorded during the described follow-up; a single-arm study of 12 participants cannot characterize safety.
    Not stated

    Limitations: Small sample (n = 12); no control group or blinding; subjective self-reported outcome; the study procedure itself may have had an effect; a single private clinic; published in an alternative-medicine journal.

  • Human, observationalObservational study in humans· Homo sapiens

    Retrospective chart review with a telephone survey: self-reported knee pain in 16 people, no control group

    Lee E, Padgett B2021PMID 34324435 (opens PubMed in a new tab)Full record on PubMed

    Model
    Retrospective chart review (2019–2020) with a telephone survey at a private clinic; people with knee pain of various causes
    Sample size
    16
    Exposure
    BPC-157 as recorded in the charts; 4 of the 16 charts also record a second peptide
    Comparator
    No control group

    Of 17 people on record, 16 were reached by telephone 6 months to 1 year later and asked about their knee pain. There was no control group or blinding, the outcome was self-reported, and the abstract does not report imaging or validated function or quality-of-life instruments; the design carries a high risk of selection and recall bias and does not allow any change to be attributed to the peptide. The self-reported result is not summarized in this profile.

    Measured endpoints

    Self-reported knee pain at telephone follow-up
    Self-reported, with no objective measurement and no comparison with a control group; the result is not summarized in this profile.
    Not stated

    Limitations: Retrospective study without a control group or blinding; small sample (n = 16); outcome self-reported by telephone, with no validated scales reported in the abstract; a single private clinic; published in an alternative-medicine journal.

Animal 6

  • AnimalAnimal study· Rattus norvegicus

    Rat quadriceps detachment model: defect size, function, muscle histology and nitric oxide markers

    Japjec M, Horvat Pavlov K, Petrovic A et al.Biomedicines2021PMID 34829776 (opens PubMed in a new tab)Title on PubMedDOI 10.3390/biomedicines9111547 (opens the publisher record in a new tab)

    Model
    Surgical detachment of the quadriceps muscle in the rat; assessment at days 7, 14, 28 and 42
    Exposure
    BPC-157 vs no-peptide controls
    Comparator
    Controls without peptide

    In a rat model of surgical detachment of the quadriceps muscle, the BPC-157 and control groups were compared on defect size, function, muscle atrophy, inflammatory infiltrate and the orientation of the junction tissue from day 7 to day 42, together with eNOS and COX-2 mRNA, oxidative stress and nitric oxide levels; the direction and size of these differences are not summarized in this profile.

    Measured endpoints

    Defect size and function
    Assessed in the BPC-157 and control groups from day 7 to day 42; the direction is not summarized in this profile.
    Not stated
    Muscle atrophy and inflammatory infiltrate
    Assessed histologically at days 28 and 42 in both groups; the direction is not summarized in this profile.
    Not stated

    Limitations: Animal model; no human data; sample size not stated in the abstract; study from the originating group; blinding not described.

  • AnimalAnimal study· Rattus norvegicus (Wistar)

    Rat hippocampal ischemia/reperfusion model: neuronal damage, behavioral tests and hippocampal gene expression

    Vukojević J, Vrdoljak B, Malekinušić D et al.Brain and Behavior2020PMID 32558293 (opens PubMed in a new tab)Title on PubMedDOI 10.1002/brb3.1726 (opens the publisher record in a new tab)

    Model
    Ischemia/reperfusion by bilateral clamping of the common carotid arteries (20 min) in male rats; assessment at 24 and 72 h
    Exposure
    BPC-157 vs saline
    Comparator
    Saline

    In rats subjected to cerebral ischemia/reperfusion, hippocampal expression of Egr1, Akt1, Kras, Src, Foxo, Srf, Vegfr2, Nos3 and Nos1 was higher, and that of Nos2 and Nfkb lower, in the BPC-157 group than in saline controls; Mapk1 was not activated. Early and late hippocampal neuronal damage and performance on memory (Morris water maze), locomotion and coordination tests were also assessed; their direction is not summarized in this profile. Exploratory findings in an animal model.

    Measured endpoints

    Hippocampal neuronal damage after ischemia/reperfusion
    Assessed early and late in the BPC-157 and saline groups; the direction is not summarized in this profile.
    Not stated
    Behavioral tests (Morris water maze, inclined beam, lateral push)
    Performed in both groups; the direction is not summarized in this profile.
    Not stated
    Hippocampal gene expression (Egr1, Akt1, Vegfr2, Nos3, Nos1, Nos2, Nfkb)
    Increased Egr1, Akt1, Vegfr2, Nos3 and Nos1 and decreased Nos2 and Nfkb; Mapk1 was not activated.
    Mixed

    Limitations: Animal model; no human data; sample size not stated in the abstract; study from the originating group; blinding not described.

  • AnimalAnimal study· Rattus norvegicus; HUVEC; chick chorioallantoic membrane

    Rat hindlimb ischemia model, chick chorioallantoic membrane and HUVEC: VEGFR2 expression and Akt–eNOS signaling

    Hsieh MJ, Liu HT, Wang CN et al.Journal of Molecular Medicine (Berlin)2017PMID 27847966 (opens PubMed in a new tab)Title on PubMedDOI 10.1007/s00109-016-1488-y (opens the publisher record in a new tab)

    Model
    Rat hindlimb ischemia (laser Doppler, histology); chorioallantoic membrane (CAM) assay; tube formation in HUVEC
    Exposure
    BPC-157 vs no-peptide controls (ischemia model and in vitro systems)
    Comparator
    Controls without peptide; blockade with dynasore (endocytosis inhibitor)

    In HUVEC, VEGFR2 mRNA and protein increased (VEGF-A did not), with internalization of the receptor, time-dependent activation of the VEGFR2–Akt–eNOS pathway and greater tube formation; these effects were suppressed by the endocytosis inhibitor dynasore. Vascular density in the chorioallantoic membrane assay, and blood flow (laser Doppler), vessel counts and vascular VEGFR2 in rats with hindlimb ischemia, were also measured; the direction and size of these in vivo endpoints are not summarized in this profile.

    Measured endpoints

    Blood flow (laser Doppler) and vessel counts in the ischemic hindlimb
    Measured in the BPC-157 and control groups; the direction is not summarized in this profile.
    Not stated
    VEGFR2 expression and internalization in endothelial cells
    Increased VEGFR2 mRNA and protein and internalization of the receptor, with no change in VEGF-A, in HUVEC.
    Increase
    Activation of the VEGFR2–Akt–eNOS pathway
    Time-dependent activation, blocked by the endocytosis inhibitor dynasore.
    Increase

    Limitations: Animal model and cell cultures; no human data; sample size not stated in the abstract.

  • AnimalAnimal study· Rattus norvegicus; HUVEC; NIH 3T3 cells

    Rat cutaneous alkali-burn model and HUVEC: burned-skin histology, tissue VEGF and endothelial ERK1/2 signaling

    Huang T, Zhang K, Sun L et al.2015PMID 25995620 (opens PubMed in a new tab)Full record on PubMedDOI 10.2147/DDDT.S82030 (opens the publisher record in a new tab)

    Model
    Cutaneous alkali burn in the rat, with histological assessment at day 18; cultured human endothelial cells (HUVEC) and NIH 3T3 fibroblasts
    Exposure
    BPC-157 vs no-peptide control (rat model and cell cultures)
    Comparator
    Model control group without peptide

    In a rat cutaneous alkali-burn model, the BPC-157 and control groups were compared on the size of the burned area, granulation tissue, re-epithelialization, extracellular matrix deposition and tissue VEGF; the direction and size of these endpoints are not summarized in this profile. In HUVEC, greater proliferation, migration and tube formation were described, with regulation of ERK1/2 phosphorylation and of c-Fos, c-Jun and Egr-1 expression; these cell findings refer to HUVEC, not to the NIH 3T3 cells also used. Study by a group independent of the originating group.

    Measured endpoints

    Burned-area size and burned-skin histology (granulation tissue, re-epithelialization, extracellular matrix)
    Assessed in the BPC-157 and control groups up to day 18; the direction is not summarized in this profile.
    Not stated
    Proliferation, migration and tube formation in HUVEC
    Increased proliferation, migration and tube formation in cultured human endothelial cells.
    Increase
    ERK1/2 phosphorylation and c-Fos, c-Jun and Egr-1 expression
    The authors report regulation of ERK1/2 phosphorylation and of c-Fos, c-Jun and Egr-1 expression in the exposed endothelial cells.
    Not stated

    Limitations: Animal model and cell cultures; no human data; sample size not stated in the abstract.

  • AnimalAnimal study· Rattus norvegicus; cultured tenocytes

    Rat Achilles transection model and cultured tenocytes: biomechanical, functional and histological endpoints

    Staresinic M, Sebecic B, Patrlj L et al.Journal of Orthopaedic Research2003PMID 14554208 (opens PubMed in a new tab)Title on PubMedDOI 10.1016/S0736-0266(03)00110-4 (opens the publisher record in a new tab)

    Model
    Complete Achilles tenotomy in the rat; cultured tenocytes exposed to 4-hydroxynonenal
    Exposure
    BPC-157 vs saline vehicle
    Comparator
    Saline

    After complete Achilles tenotomy in rats, the BPC-157 and saline groups were compared on biomechanical measures (load to failure, Young's modulus), the Achilles functional index, the size of the macroscopic defect and histology (inflammatory cells, fibroblasts, reticulin and fibrillar extracellular matrix); the direction and size of the differences are not summarized in this profile. In cultured tenocytes, the peptide alone did not change growth but counteracted the growth inhibition caused by the aldehyde 4-hydroxynonenal.

    Measured endpoints

    Biomechanical properties after Achilles transection (load to failure, Young's modulus)
    Measured in the BPC-157 and saline groups during follow-up; the direction is not summarized in this profile.
    Not stated
    Achilles functional index (AFI)
    Measured in both groups; the direction is not summarized in this profile.
    Not stated
    Growth of cultured tenocytes exposed to 4-hydroxynonenal
    No direct effect on cell growth; the aldehyde-induced inhibition was counteracted both in the presence and in the absence of serum.
    Mixed

    Limitations: Animal model; no human data; sample size not stated in the abstract; blinding not described; study from the originating group.

  • AnimalAnimal study· Rattus norvegicus

    Rat gastric and duodenal lesion models (restraint stress, cysteamine, ethanol): lesion counts and mucosal endothelium

    Sikiric P, Seiwerth S, Grabarevic Z et al.Life Sciences1994PMID 7904712 (opens PubMed in a new tab)Title on PubMedDOI 10.1016/0024-3205(94)00796-9 (opens the publisher record in a new tab)

    Model
    Rat models of gastric and duodenal lesions (restraint stress, cysteamine, 96% ethanol)
    Exposure
    BPC-157 vs reference agents
    Comparator
    H2 receptor antagonists (famotidine, cimetidine), dopaminergic agents and gut peptides (including somatostatin, neuropeptide Y, secretin and cholecystokinin)

    In three rat models of gastric and duodenal lesions, mucosal lesions were counted after BPC-157 and after each of the reference agents, and Monastral blue labeling was used to examine the mucosal endothelium. The authors report differences between BPC-157 and the reference agents; their direction and size are not summarized in this profile. Early primary study in an animal model.

    Measured endpoints

    Gastric and duodenal lesions (restraint stress, cysteamine, ethanol)
    Counted in all three models after BPC-157 and after each reference agent; the direction of the differences is not summarized in this profile.
    Not stated
    Mucosal endothelium (Monastral blue labeling)
    The authors related the lesion counts to the state of the mucosal endothelium.
    Not stated

    Limitations: Animal model; no human data; sample size not stated in the abstract; blinding not described.

In vitro 3

  • In vitroIn vitro study· Rattus norvegicus isolated aorta; cultured vascular endothelial cells

    Isolated rat aorta and cultured endothelial cells: vasomotor tone and Src–caveolin-1–eNOS signaling

    “Modulatory effects of BPC 157 on vasomotor tone and the activation of Src-Caveolin-1-endothelial nitric oxide synthase pathway.”

    Hsieh MJ, Lee CH, Chueh HY et al.Scientific Reports2020PMID 33051481 (opens PubMed in a new tab)DOI 10.1038/s41598-020-74022-y (opens the publisher record in a new tab)

    Model
    Ex vivo rat aortic rings with and without endothelium; 3D vascular smooth muscle cell model; cultured endothelial cells
    Exposure
    BPC-157 vs no-peptide preparations (ex vivo and in vitro)
    Comparator
    Preparations without peptide; L-NAME, hemoglobin, Src inhibitor

    In isolated rat aorta, concentration-dependent vasodilation was observed that was attenuated in the absence of endothelium and inhibited by L-NAME or hemoglobin, indicating a nitric oxide-dependent mechanism. In endothelial cells, nitric oxide generation and phosphorylation of Src, caveolin-1 and eNOS increased and were abolished by a Src inhibitor, with less caveolin-1/eNOS association in co-immunoprecipitation assays. No direct relaxant effect on smooth muscle cells was seen in the 3D model.

    Measured endpoints

    Vasomotor tone in isolated aorta
    Concentration- and endothelium-dependent vasodilation, blocked by nitric oxide synthase inhibitors.
    Increase
    Phosphorylation of Src, caveolin-1 and eNOS
    Increased phosphorylation of all three components, abolished by Src inhibition.
    Increase

    Limitations: Ex vivo and in vitro systems; no in vivo animal or human data.

  • In vitroIn vitro study· Rattus norvegicus (Sprague-Dawley) Achilles-derived fibroblasts

    Rat Achilles-derived fibroblasts: GHR gene and protein expression, proliferation and JAK2 signaling

    Chang CH, Tsai WC, Hsu YH et al.Molecules2014PMID 25415472 (opens PubMed in a new tab)Title on PubMedDOI 10.3390/molecules191119066 (opens the publisher record in a new tab)

    Model
    Primary fibroblasts isolated from rat Achilles; cDNA microarray, quantitative PCR, Western blot
    Exposure
    BPC-157, with and without subsequent GHR-ligand stimulation, vs no-peptide culture
    Comparator
    Culture without peptide

    Microarray analysis identified GHR among the most strongly induced genes in Achilles-derived fibroblasts exposed to the peptide; the concentration- and time-dependent increase was confirmed at the mRNA and protein levels. Subsequent stimulation of pre-exposed cells with the GHR ligand was associated with greater proliferation (MTT, PCNA) and JAK2 activation. In vitro observation whose in vivo relevance was not assessed.

    Measured endpoints

    GHR expression (mRNA and protein)
    Concentration- and time-dependent increase in rat Achilles-derived fibroblasts.
    Increase
    Proliferation after GHR-ligand addition (MTT, PCNA) and JAK2 activation
    Greater proliferation and JAK2 phosphorylation in cells pre-exposed to the peptide and then stimulated with the GHR ligand.
    Increase

    Limitations: In vitro study in rat cells; no animal or human data; the proliferation finding depended on exogenous addition of the GHR ligand.

  • In vitroIn vitro study· Rattus norvegicus Achilles-derived fibroblasts; Achilles explants

    Rat Achilles explants and Achilles-derived fibroblasts: outgrowth, survival, migration and FAK–paxillin signaling

    Chang CH, Tsai WC, Lin MS et al.Journal of Applied Physiology2011PMID 21030672 (opens PubMed in a new tab)Title on PubMedDOI 10.1152/japplphysiol.00945.2010 (opens the publisher record in a new tab)

    Model
    Explant cultures of rat Achilles and primary rat Achilles-derived fibroblasts
    Exposure
    BPC-157 vs no-peptide culture
    Comparator
    Culture without peptide

    In rat Achilles explants, cell outgrowth was faster; fibroblast proliferation (MTT) did not change, but survival under H2O2 stress, transwell migration and cell spreading increased in a concentration-dependent manner, with F-actin formation and higher FAK and paxillin phosphorylation and no change in total protein. The authors propose the FAK–paxillin pathway as a mechanistic hypothesis.

    Measured endpoints

    Migration of Achilles-derived fibroblasts (transwell assay)
    Concentration-dependent increase in migration in cultures of rat Achilles-derived fibroblasts.
    Increase
    Cell proliferation (MTT)
    No direct effect on fibroblast proliferation in culture was observed.
    No change
    FAK and paxillin phosphorylation
    Concentration-dependent increase in FAK and paxillin phosphorylation, with no change in total protein.
    Increase

    Limitations: In vitro study in rat cells; no in vivo animal or human data; no receptor was identified.

Reviews 3

  • ReviewSystematic review

    Systematic review of 36 studies (35 preclinical, 1 in humans): mechanism, musculoskeletal endpoints, biotransformation and safety

    “Emerging Use of BPC-157 in Orthopaedic Sports Medicine: A Systematic Review.”

    Vasireddi N, Hahamyan H, Salata MJ et al.HSS Journal2025PMID 40756949 (opens PubMed in a new tab)DOI 10.1177/15563316251355551 (opens the publisher record in a new tab)

    Model
    Systematic review (PubMed, Cochrane, Embase; through June 2024) of studies on mechanism, musculoskeletal outcomes, biotransformation and safety

    Of 544 records identified, 36 studies were included (35 preclinical and 1 in humans). The authors synthesize functional, structural and biomechanical measures from preclinical musculoskeletal models, together with GHR expression and inflammatory cytokine levels; the only study in humans was retrospective. No human safety data were found, and the evidence was graded as level IV and V.

    Measured endpoints

    Volume and quality of the evidence (36 included studies)
    35 preclinical studies and 1 study in humans were included; there were no controlled trials and no human safety data.
    Not stated

    Limitations: Included evidence graded level IV and V; a single study in humans (retrospective); heterogeneous models; no human safety data were located.

  • ReviewNarrative review

    Critical narrative review of preclinical studies in rodent muscle and connective-tissue models

    Gwyer D, Wragg NM, Wilson SLCell and Tissue Research2019PMID 30915550 (opens PubMed in a new tab)Title on PubMedDOI 10.1007/s00441-019-03016-8 (opens the publisher record in a new tab)

    Model
    Critical narrative review of preclinical studies in rodent muscle and connective-tissue models

    Critical review by an independent group (Loughborough University) of the preclinical literature in small rodent models of muscle and connective-tissue lesions. It notes that only a handful of research groups had studied the peptide in depth, that the effects reported in rodents had yet to be confirmed in humans and that the precise mechanisms still needed to be understood.

    Measured endpoints

    Synthesis of the preclinical evidence in rodent muscle and connective-tissue models
    Preclinical results in small rodent models from a handful of research groups; not confirmed in humans.
    Not stated

    Limitations: Narrative review without a systematic methodology; the evidence reviewed comes almost exclusively from animal studies.

  • ReviewNarrative review

    Narrative review by the originating group: the BPC 157 fragment and its early rat lesion models

    Sikirić P, Petek M, Rucman R et al.Journal of Physiology, Paris1993PMID 8298609 (opens PubMed in a new tab)Title on PubMedDOI 10.1016/0928-4257(93)90038-u (opens the publisher record in a new tab)

    Model
    Narrative review by the originating group of its own preclinical work

    Early overview by the originating group of its own work. It refers back to the group's isolation of a gastric juice peptide (BPC, Mr about 40,000), presents the fully characterized 15-amino-acid fragment BPC 157, which the authors consider essential for the activity they studied, and sets out their hypothesis that the stomach mediates responses to stress in other organs. It summarizes the group's lesion models in several organs and proposes the peptide as a possible endogenous mediator.

    Measured endpoints

    Characterization of the BPC 157 fragment and the group's hypothesis
    The 15-amino-acid fragment is presented as the part of the gastric juice peptide that the authors consider essential for the activity studied in their animal models.
    Not stated

    Limitations: Narrative review of the authors' own work; no human data; the text itself acknowledges that the ultimate mechanism is poorly understood.

For laboratory research use only. Not for human or veterinary use or consumption. Not for diagnostic use. Not evaluated by the U.S. FDA.