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BPC-157
BPC-157 is a synthetic peptide that is being investigated for its regenerative e ects. It shows high e cacy for rats
su ering toxic or surgical trauma, but there is currently no evidence that it provides bene ts for people.
This page features 36 unique references to scienti c papers.

History (/history/BPC-157/)

Summary
All Essential Bene ts/E ects/Facts & Information

In Progress

This page on BPC-157 is currently marked as in-progress. We are still compiling research.

SUPPLEMENTS
BPC-157 is a peptide chain consisting NUTRITION
of 15 amino acids. STORE
It is considered synthetic because this particular sequence does not exist in
nature. It is derived from a protective protein found in the stomach.

Researchers have conducted numerous rodent studies on BPC-157 that show it has protective e ects extending beyond the stomach
and intestinal tract. BPC-157 has been shown to bene t ulcers in the stomach, intestinal damage such as stulas and in ammatory
disorders, bone and joint healing and growth rates, and organ damage. It also has some in uences on the brain. Researchers have
observed marked protective e ects when BPC-157 is administired to rats alongside a research toxin or damaging surgical procedure.

More research is needed to clarify whether BPC-157 has multiple mechanisms of action, but current research suggests BPC-157
in uences several growth factors usually involved in angiogenesis (the production of blood vessels) and other factors involved in
regeneration following damage.

BPC-157 shows promise, but human studies are needed to demonstrate that these bene ts extend beyond research animals.

The majority of studies on BPC-157 are done on rats given injections of the supplement. While BPC-157 is a stable peptide, peptides
are a group of compounds that are normally poorly absorbed after oral supplementation, so researchers use injections in rodent
studies instead. Furthermore, there is no human evidence for BPC-157 and the majority of the research has been conducted by a
single research group. Due to its synthetic nature, there may be legal issues associated with the sale of this supplement in certain
regions and it may be banned by some sport organizations.

Follow this Page for updates

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Things to Know

Also Known As
PL 14736, PL-10, Bepecin

Do Not Confuse With

TB-500

Things to Note
BPC-157 is a patented supplement and there may be crossover between those mentioned in the patent and the researchers of
many of the relevant studies.[1]

BPC-157 is a synthetic subtance (not occurring in nature) and may not be WADA approved

Is a Form Of
Nootropic

Caution Notice
Due to the current status as a synthetic substance (not occurring in nature) BPC-157 may not be WADA approved; use with
caution

Examine.com Medical Disclaimer (/disclaimer)

How to Take
Recommended dosage, active amounts, other details

The closest possible recommended dose is based on rat studies where oral administration showed bene t, as most studies
administer the supplement via injection. The oral dose that was e ective in rats, 10 g/kg, is estimated to be equivalent to 1.6 g/kg,
or:

110 g for a 150lb person

145 g for a 200lb person

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180 g for a 250lb person

()
There are currently no human pharmacokinetic studies to assess species di erences.

Scienti c Research

Table of Contents:
1 Sources and Composition

1.1 Structure

1.2 Physicochemical Properties

2 Molecular Targets

2.1 Angiogenesis

3 Pharmacology

3.1 Metabolism

4 Neurology

4.1 Dopaminergic Neurotransmission

4.2 Serotonergic Neurotransmission

4.3 Neuroprotection

4.4 Depression

5 Bone and Joint Health

5.1 Collagen and Joints

6 Peripheral Organ Systems

6.1 Stomach

6.2 Intestines

7 Other Medical Conditions

7.1 Parkinson's

7.2 Multiple Sclerosis

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1 Sources and Composition

()
1.1. Structure
BPC-157 is the term used to refer to a pentadecapeptide, a protein with 15 amino acids. BPC is an acronym for 'Body Protection
Compounds' and refers to "peptides comprising 8-15 amino acids residues with a molecular weight of 900-1,600 daltons" according to
the patent for BPC-157,[1] although another study claims that BPC refers to a gastroprotective protein used to isolate BPC-157.[2] This
particular sequence does not share homology with other known gastric peptides,[2] with at least one study noting that this sequence
did not register in the Protein BLAST database (as of 2016[3]). There are a few studies in which this peptide is also referred to as PL
14736, PL-10,[4] and Bepecin[3]. This entry will use the acronym BPC-157 exclusively.

BPC-157 is a peptide consisting of 15 amino acids. While they are 'natural' compounds, this particular sequence is not
known to occur in nature and is derived from another protein.

1.2. Physicochemical Properties

BPC-157 is freely soluble in water of normal pH value.[5] The pentadecapeptide sequence is Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-
Asp-Ala-Gly-Leu-Val[5] and is stated to be quite stable relative to other peptides by not degrading in stomach acid (ex vivo) for at least
24 hours.[2][6] It has been shown to be moderately stable in plasma ex vivo, with 36% of the intact peptide remaining after 60 minutes.
[3]

2 Molecular Targets

2.1. Angiogenesis
When researchers tested BPC-157 in a CAM assay (chick embryo), it seemed to be capable of increasing the process of angiogenesis
(blood vessel production) by 129+/-7% and 152+/-14% when administered in doses of 0.01 g and 0.1 g, respectively. This e ect was
later con rmed in HUVECs, where concentrations of 0.1 g/mL and 1 g/mL increased the formation of perfect tubes by 119+/-9%
and 147+/-7% over 24 hours of incubation (with 1 g/mL being determined to be the optimal concentration in HUVECs).[7] This
observation was con rmed in rats given limb damage as well. After a week of treatment with BPC-157, there appeared to be more
blood vessels in the damaged limb than control.[7]

An increase in VEGFR2 expression was noted in the rats with an injured limb given BPC-157 compared to control, which was thought
to underlie the increase in blood vessel production. When tested further, researchers discovered that VEGF-A is wholly una ected at
the concentration of 1 g/mL, while VEGFR2 increased in a time-dependent manner within the cell and then proceeded to activate the
VEGFR2-Akt-eNOS pathway (a pathway important to angiogenesis).[7] When dynasore, a VEGFR2 inhibitor,[8] was introduced, the entire
pathway was no longer activated and tube formation no longer occurred in vitro.[7]

BPC-157 appears to activate a protein known as VEGFR2 and internalizes it within a cell, which then activates a particular
pathway (VEGFR2-Akt-eNOS) that is important in blood vessel production and repair.

BPC-157 has also been found to stimulate the mRNA of the growth factor EGR-1 in intestinal cells (Caco-2) at 10-100 M, with most
e cacy at 50 M. A related protein, mRNA NAB2, was also increased shortly after. Both of these e ects parallel the e ects of PDGF-
BB (an endogenous growth factor) although they require much higher concentrations. EGF-1 protein content also appeared to be
increased.[4]

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The growth factor EGF-1 may also be related to the observed bene ts of BCP-157.

3 Pharmacology

3.1. Metabolism
When incubated in plasma ex vivo, it appears that a large amount of the peptide detected is registered as 'metabolites' (79+/-2%) of
the parent compound within 60 minutes, although it then seems to stabilize, with the remaining intact peptide remaining for up to
240 minutes.[3]

There does appear to be some degradation of BPC-157 in plasma, although what remains after this degradation is
currently not known. The e ects of orally ingested BPC-157 are also currently unknown.

4 Neurology

4.1. Dopaminergic Neurotransmission

It has been mentioned indirectly by the author of many BPC-157 studies that no known binding to dopamine receptors has been
found, though there is no citation provided for this particular claim.[9]

When administered at 10 ng/kg or 10 g/kg, BPC-157 administered at the same time as amphetamine found that only the higher dose
was able to attenuate some observable e ects of the amphetamine (rat behaviours such as compulsive sni ng, licking, and gnawing).
Administering the BPC-157 an hour after amphetamine also showed some bene ts.[2] When rats were previously given haloperidol
(which makes rats subsequently more sensitive to the e ects of amphetamine[10]) coadministration of BPC-157 appeared to mitigate
the expected haloperidol-induced sensitivity.[2] This apparently antagonistic e ect may also apply chronically, meaning a single dose
of BPC-157 (10 g/kg I.P; 10 ng/kg ine ective) given before chronic amphetamine administration seemed to attenuate the behavioral
e ects of amphetamine in rats throughout the observation period.[11]

There appear to be some in uence of BPC-157 on dopaminergic systems, where it limits the e cacy of dopamine
agonists. It is not currently known how this occurs.

4.2. Serotonergic Neurotransmission

BPC-157 has been investigated for its involvement in the serotonergic system due to its involvement in gut health, with researchers
suggesting a possible brain-gut axis due to the e ects of BPC-157 in both of these areas.[12] In regard to a connection between the
brain and intestines, serotonin is a likely player due to its high prevalence in the intestines.[13]

Researchers found that rats given 10 g/kg (subcutaneous injection) of BPC-157 acutely experience increased serotonin synthesis
after 40 minutes in several brain regions, including the substantia nigra reticulata and medial anterior olfactory nucleus while
simultaneously experiencing a decrease in the hypothalamus, hippocampus (ventral and dorsal), amd the thalamus (dorsal but not
ventral).[14] When this dose was given for one week, the increase in serotonin synthesis in the substantia nigra persisted (occurring in
both the reticulata and compacta) while the decreases in serotonin synthesis seen with a single dose no longer persisted.[14]

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There appears to be some interactions between BPC-157 and serotonin in the brain, but the underlying mechanisms are
unknown.

4.3. Neuroprotection
BPC-157 appears to have protective e ects on brain tissue when administered to rats (either in drinking water or injections) alongside
the toxin cuprizone by reducing the amount of damaged cells in numerous brain regions, including the hippocampus.[15] Cuprizone[15]
is a toxin used to mimic the damages seen in multiple sclerosis[16] and potentially schizophrenia.[17]

Oral ingestion of BPC-157 at an estimated 10 g/kg (0.16 g/mL in water) was similarly e ective as injections of 10 ng/kg and 10
g/kg[15] although cuprizone is known to be a toxin that can induce neuronal damage (speci cally demyelination) without necessarily
reaching the brain.[18]

Orally ingested BPC-157 has shown neuroprotective e ects in rats given neurotoxins. The precise mechanism of how it
exerts these e ects is unknown but may be intestinal.

4.4. Depression
In female rats subject to a forced swim test (Porsolt's swim test), BPC-157 (intraperitoneal administration) at the doses of both 10
ng/kg and 10 g/kg seem to perform to a statistically equal degree to the active controls of both imipramine (15 mg and 30 mg) and
nialamide (30 mg and 40 mg), all of which outperformed the control group.[5] BPC-157 also appeared e ective in assisting these rats
in a model of chronic unpredictable stress similar to 30 mg of imipramine.[5]

5 Bone and Joint Health

5.1. Collagen and Joints

At concentrations of 2 g/mL in tendon broblasts which were then explanted, BPC-157 cells appeared to grow faster than broblasts
not treated with BPC-157 within two days, reaching a signi cantly larger amount after one week. This e ect was associated with both
increased oxidative resistance to hydrogen peroxide and a concentration-dependent increase in the proteins FAK and paxillin not
seen in control.[19] F-actin formation, important for the spreading process of tendon broblasts,[20] also appeared to be greatly
increased with BPC-157 relative to control[19] and are related to the actions of the aforementioned proteins (FAK and paxillin).[21]

This study also found that ex vivo tendon broblasts in isolation were una ected by BPC-157, only those explanted into rats,[19] an
e ect also noted elsewhere when cultured tendocytes were una ected by BPC-157 alone.[22] However, the growth inhibitory e ect of
4-hydroxynonenal (HNE) was negated by BPC-157 in these cells.[22]

BPC-157 appears to allow tendon broblasts to grow and spread faster, although this e ect may not persist in the
broblasts alone, suggesting other cells may be required for this e ect or BPC-157 may work by negating suppressing
factors.

Researchers have observed bene ts when putting BPC-157 on a sponge during surgery, where it appeared to improve the rate of
collagen reformation, initially outperforming platelet-growth factor after four days but eventually being equipotent after eight days[4].
Bene ts have been seen in rats given intraperitoneal injections after an Achilles heel injury, where the rate of injury healing was
visually con rmed with smaller cut size and depth.[22]

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Some evidence suggests that BPC-157 can assist tendon regenesis after surgical damage.

6 Peripheral Organ Systems

6.1. Stomach
The protective e ects of BPC-157 on ulcers has been found to be prevented in rats by coadministration of haloperidol (Alpha-1A and
Dopamine receptor antagonist), phentolamine (Alpha adrenergic antagonist, nonselective), and clonidine (Alpha-2A adrenergic
antagonist, similar to agmatine (/supplements/agmatine/)) but was not a ected by prazosin, domperidone, or yohimbine
(/supplements/yohimbine/).[23]

The anti-ulcer actions of BPC-157 in the stomach may be related to the dopamine and adrenaline systems.

BPC-157 has shown protective e ects against various agents that induce stomach ulcerations, such as cyclophosphamide[24] and
haloperidol.[25]

6.2. Intestines
When it comes to in ammation, BPC-157 has shown bene t in rats against the toxins trinitrobenzene sulfonic acid (TNBS)[6] and
cysteamine,[26][27][15] where both biomarkers of in ammation and visual markers of damage were reduced when BPC-157 was
administered alongside the toxins. BPC-157 is not unique in this regard, as other active controls like ranitidine and omeprazole have
shown e cacy in the same model of intestinal in ammation,[27] though it was mentioned in a review by the authors[28] that BPC-157
may be more practical due to proven bene ts in other complications of intestinal disease: anastomosis healing, short bowel
syndrome, and stulas.

An anastomosis is a connection between two things that are not normally connected, with a stula being an abnormal type commonly
seen during intestinal diseases. Numerous studies have shown BPC-157 injections in rats having a mending property on anastomosis
in numerous body regions, including aortic[29] and esophagogastic.[30] In studies assessing the intestines, bene ts have been shown
to colovesical,[31] rectovaginal,[32] colon-colon,[15] and ileoileal[33] stulas. This particular bene t may be related to nitric oxide
signaling (potentially the VEGFR2-Akt-eNOS pathway BPC-157 in uences[7]) since L-NAME, a nitric oxide synthase inhibitor, worsens
anastomosis healing in a manner ameliorated by BPC-157.[30]

Studies assessing BPC-157 in experimental models of short bowel syndrome also nd bene t, with injections of BPC-157 ameliorating
this state[34][35] even when the state is worsened with the addition of L-NAME and diclofenac.[35]

Most BPC-157 studies on intestinal damage use rats that undergo surgical-induced damage for experimental purposes.
BPC-157 appears to have very potent protective e ects in rats by mitigating damage to the tissue and structural
abnormalities caused by the damage.

Most notably, a bene t for anastomosis healing (esophagogastric) has been found in rats given BPC-157 in drinking water
(approximately 10 ng/kg or 10 g/kg daily) without an injection, with no signi cant di erence in e cacy between the two doses and
statistically similar e cacy to injections of 10 ng/kg and 10 g/kg.[30]

It is possible, based on limited evidence, that BPC-157 may be orally active in the alimentary canal (the pathway between
the mouth and anus).

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7 Other Medical Conditions

()
7.1. Parkinson's
One study in rats using the toxin MPTP (which induces damage similar to what is seen in Parkinson's Disease in rodents),
administration of BPC-157 intraperitoneally appeared to mitigate some of the damage caused by MPTP.[36]

7.2. Multiple Sclerosis

In rodents given cuprizone (to induce damage similar to what is seen in multiple sclerosis[16]) those given BPC-157 alongside the
cuprizone (0.16 ng/mL or 0.16 g/mL in drinking water over four days or 10 ng/kg or 10 g/kg intragastrically on the nal day) seemed
to exhibit signi cantly less brain damage and clinical abnormalities from the cuprizone than did control rats not given BPC-157.[15]

Scienti c Support & Reference Citations

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23.SikiriP,etal.PentadecapeptideBPC157interactionswithadrenergicanddopaminergicsystemsinmucosalprotectioninstress(https://www.ncbi.nlm.nih.gov/pubmed/9073154).DigDisSci.(1997)

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25.BilicI,etal.HaloperidolstomachlesionsattenuationbypentadecapeptideBPC157,omeprazole,bromocriptine,butnotatropine,lansoprazole,pantoprazole,ranitidine,cimetidineandmisoprostolinmice

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26.SikiricP,etal.Therapyeffectofantiulceragentsonnewchroniccysteaminecolonlesioninrat(https://www.ncbi.nlm.nih.gov/pubmed/11595451).JPhysiolParis.(2001)

27.SikiricP,etal.Cysteaminecolonandcysteamineduodenumlesionsinrats.AttenuationbygastricpentadecapeptideBPC157,cimetidine,ranitidine,atropine,omeprazole,sulphasalazineandmethylprednisolone

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28.SikiricP,etal.Focusonulcerativecolitis:stablegastricpentadecapeptideBPC157(https://www.ncbi.nlm.nih.gov/pubmed/22300085).CurrMedChem.(2012)

29.HrelecM,etal.AbdominalaortaanastomosisinratsandstablegastricpentadecapeptideBPC157,prophylaxisandtherapy(https://www.ncbi.nlm.nih.gov/pubmed/20388960).JPhysiolPharmacol.(2009)

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32.BaricM,etal.StablegastricpentadecapeptideBPC157healsrectovaginalfistulainrats(https://www.ncbi.nlm.nih.gov/pubmed/26872976).LifeSci.(2016)

33.VuksicT,etal.StablegastricpentadecapeptideBPC157intrialsforinflammatoryboweldisease(PL10,PLD116,PL14736,Pliva,Croatia)healsileoilealanastomosisintherat

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36.SikiricP,etal.AbehaviouralstudyoftheeffectofpentadecapeptideBPC157inParkinson'sdiseasemodelsinmiceandgastriclesionsinducedby1methyl4phenyl1,2,3,6tetrahydrophyridine

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(Common misspellings for BPC-157 include BCP-157, BPC157, BCP157)

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