If you have been reading about pentadecapeptide and want a single page that covers the useful parts, this is it: definitions, context, how it is studied, and the questions that come up repeatedly.
Last reviewed on 2026-02-01. Where a claim depends on a specific study, the study is described rather than over-claimed.
Interest in the peptide has grown through online communities that discuss self-administered use, which sits outside formal research settings. Regulatory status varies by country, and in many jurisdictions the compound is not approved as a therapeutic product. Questions about optimal routes of administration, long-term effects, and dose-response relationships remain open. Published pharmacokinetic data in humans are limited, and much of what circulates in popular discussion is extrapolated from animal work rather than measured directly in people.
BPC-157 is a synthetic peptide built from fifteen amino acids, referred to in the literature as a pentadecapeptide. Its sequence was derived from a larger protein found in human gastric juice, commonly called body protection compound. Researchers first described the fragment in the early 1990s and named it after the parent protein plus a numeric identifier. The peptide does not correspond to a single marketed medicine; it is primarily a laboratory research material. Suppliers distribute it as a lyophilized powder intended for experimental use.
Published work on BPC-157 spans several decades and covers a wide range of experimental models. Much of the early literature reports outcomes in animal studies involving induced injury to the gastrointestinal tract, tendons, and other tissues. The volume of preclinical reports is large, while controlled human trials remain scarce. This imbalance is a recurring point of discussion, because animal findings do not automatically translate into human effects. Reviews often note that study designs differ substantially across laboratories.
Human data are far more limited than animal data. A small number of clinical reports exist, generally with few participants and without the randomization or blinding expected in later-phase trials. No large, independently replicated human trial has appeared in the indexed peer-reviewed literature. Statements about effects in people therefore rest on extrapolation from animal work rather than on direct evidence, and the strength of that extrapolation remains an open question rather than a settled matter.
Proposed mechanisms include interaction with the nitric oxide system, modulation of growth factor signaling, and effects on blood vessel formation. None of these has been established as the primary mode of action, and some proposed pathways rest on indirect measurements. Whether the reported effects depend on a specific receptor has not been determined. Stability in gastric acid, unusual for a peptide of this size, is also reported in animal work, but the reason for it is not firmly established.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic pentadecapeptide | Fifteen amino acids; sequence matches a fragment of a gastric juice protein |
| Molecular formula | C62H98N16O22 | Corresponds to a molecular mass near 1419 Da |
| Primary origin | Fragment of human gastric juice protein BPC | First characterized in the early 1990s |
| Common synonyms | BPC 157; PL 14736; pentadecapeptide BPC 157 | Naming conventions vary across publications |
| Reported stability | Stable in gastric juice during in vitro incubation | Based on laboratory incubation, not clinical data |
Material of this kind is sold for laboratory research, and labels typically state that it is not intended for human or veterinary use. In many countries it is not an approved medicine, and sports antidoping rules place it among prohibited non-approved substances. Buyers commonly review a certificate of analysis, an independent test report, and the declared storage conditions. Batch-to-batch variation in purity and in counterion content is possible, and how much that variation affects experimental outcomes remains an open question.
Lyophilized peptide is normally kept at minus twenty degrees Celsius or colder, away from light and moisture. Powder held under those conditions is widely treated as stable for long periods, although published stability studies for this exact sequence are sparse and often come from suppliers rather than independent laboratories. Once dissolved, solutions are generally handled cold and used within a short window, because peptide bonds can hydrolyze over time. Repeated freeze-thaw cycles are usually avoided to limit losses, and exact shelf-life figures depend on the buffer and the concentration involved.
Supplied material is typically a lyophilized white to off-white powder. The peptide is freely soluble in water and in common aqueous buffers, which allows it to be handled as a stock solution. Because the sequence contains no cysteine, disulfide cross-linking is not a route of degradation. The absence of aromatic residues means ultraviolet absorbance at 280 nm is minimal, so quantification usually relies on peptide bond absorbance near 214 nm or on amino acid analysis.
Common synonyms in catalogs include pentadecapeptide BPC 157, BPC157, and the full sequence name. A CAS registry number in the 137525-51-0 range is frequently listed, though the assignment should be verified against the supplier certificate of analysis. The name itself is not a pharmacopoeial designation, and there is no standardized international nonproprietary name. Distinguishing genuine material from related fragments generally requires mass spectrometry, since several truncated sequences share similar chromatographic behavior.
=== Transitional National Legislative Assembly (2016–2021) === As a result of a peace agreement that came into effect in 2015, a Transitional National Legislative Assembly was formed with 400 members. The membership is as follows:
The lesions occur as multiple cutaneous and subcutaneous nodules up to 4 cm diameter. They may disappear spontaneously, or regress and appear at new sites simultaneously. Topographically lesions may be found on the face, ears, nose, neck, trunk, extremities (including foot pads), perineum and scrotum. Treatment options in SH and CH. SH has proven to be a difficult and frustrating condition to treat. Consequently, many of the early cases were euthanized. Originally we treated dogs with Thymosin (derived from bovine thymus) because of reports of its effectiveness in human LCH cases. Some dogs appeared to respond to this, but not consistently. The original rationale for using thymosin was that SH was likely an immunoregulatory disorder and not cancer. In the majority of instances corticosteroid treatment is ineffective, although in some instances of CH (about 10% of cases), steroid administration is very effective in controlling lesions so steroids are worth trying in this disease given the expense of the alternatives. More recently we have had success with immuno-suppressive doses of Cyclosporin A or Leflunomide. These drugs are potent inhibitors of T cell activation and their ability to abrogate clinical disease gives further support for SH and CH being disorders of immune regulation. Treatment with these drugs is exorbitantly expensive and may be needed for life in dogs with continuously active disease, which usually is the case in advanced SH.
== Adverse effects == Adverse effects of yohimbine in humans at high doses include hypertension (high blood pressure), tachycardia (rapid heartbeat), agitation, hypervigilance, anxiety, tremors, nausea, and urinary frequency. The drug is described as producing a psychoactive state of considerable anxiety along with tenseness, restlessness, and irritability and as being "extremely unpleasant", at least at the assessed doses. In animals, yohimbine likewise produces effects suggestive of severe anxiety. Yohimbine has been used in animals as a model of anxiety in the evaluation of novel anxiolytics.
Like CD38, CD157 is a member of the ADP-ribosyl cyclase family of enzymes that catalyze the formation of cADPR from NAD+, although CD157 is a much weaker catalyst than CD38. The SARM1 enzyme also catalyzes the formation of cADPR from NAD+, but SARM1 elevates cADPR much more efficiently than CD38.
Sources: en.wikipedia.org
Psilocin (4-HO-DMT) is a close positional isomer of bufotenin (5-HO-DMT), which shows peripheral selectivity, and might be expected to have similarly restricted lipophilicity and blood–brain barrier permeability. But psilocin appears to form a tricyclic pseudo-ring system wherein its hydroxyl group and amine interact through hydrogen bonding. This in turn makes psilocin much less polar, more lipophilic, and more able to cross the blood–brain barrier and exert central actions than it would be otherwise. It may also protect psilocin from metabolism by monoamine oxidase (MAO). In contrast, bufotenin is not able to achieve this pseudo-ring system. Accordingly, bufotenin is less lipophilic than psilocin in terms of partition coefficient. But bufotenin does still show significant central permeability and, like psilocybin, can produce robust hallucinogenic effects in humans.
=== Emulsification === Due to the hydrophilic property of sucrose and the lipophilic property of fatty acids, the overall hydrophilicity of sucrose esters can be tuned by the number of hydroxyl groups that are reacted with fatty acids and the identity of the fatty acids. The fewer free hydroxyl groups and the more lipophilic fatty acids, the less hydrophilic the resulting sucrose ester becomes. Sucrose esters' HLB values can range from 1-16. Low HLB (3.5-6.0) sucrose esters act as a water-in-oil emulsifier while high HLB (8-18) sucrose esters act as an oil-in-water emulsifier.
== Bare lymphocyte syndrome == One type of MHC class II deficiency, also called bare lymphocyte syndrome, is due to mutations in the genes that code for transcription factors that regulate the expression of the MHC class II genes. It results in the depletion of CD4 T cells and some immunoglobulin isotypes even though there are normal levels of both CD8 T cells and B cells present. Deficient MHC class II molecules are unable to present antigens to T cells and properly activate T cells. T cells are then unable to proliferate and secrete cytokines which normally participate in the immune response. Not only do the deficient MHC class II molecules affect the activation and proliferation of T cells but also the rest of the immune response cascade which includes B cells. Therefore, with this decrease in the number of T cells, the T cells cannot interact and activate the B cells. Normally when B cells are activated they divide, proliferate and differentiate, which includes the differentiation of these cells into plasma cells which are responsible for producing antibodies. However, when there is a deficiency in MHC class II molecules B cells are not activated and cannot differentiate into plasma cells which causes them to be deficient in antibodies which are unable to perform as they are expected. The only current form of treatment is a bone-marrow transplant; however, even this does not cure the disease and most patients do not live past age ten.
==== Tolerable upper intake level ==== In 2000, the Institute of Medicine of the US National Academy of Sciences set a tolerable upper intake level (UL) for adults of 2,000 mg/day. The amount was chosen because human trials had reported diarrhea and other gastrointestinal disturbances at intakes of greater than 3,000 mg/day. This was the Lowest-Observed-Adverse-Effect Level (LOAEL), meaning that other adverse effects were observed at even higher intakes. ULs are progressively lower for younger and younger children. In 2006, the European Food Safety Authority (EFSA) also pointed out the disturbances at that dose level, but reached the conclusion that there was not sufficient evidence to set a UL for vitamin C, as did the Japan National Institute of Health and Nutrition in 2010.
Central nervous system: fatigue, dizziness, drowsiness, lightheadedness, confusion, nightmares, agitation, increased anxiety, difficulty sleeping, seizures (infrequently), temporary confusion (delirium), rarely induction of hypomania and psychosis, extrapyramidal side effects (rarely), abuse in patients with polytoxicomania (rarely), ringing in the ears (tinnitus) Anticholinergic: dry mouth, constipation, even ileus (rarely), difficulties in urinating, sweating, precipitation of glaucoma Antiadrenergic: Low blood pressure, (if patient arises too fast from the lying/sitting position to standing—known as orthostatic hypotension), abnormal heart rhythms (e.g., sinus tachycardia, bradycardia, and atrioventricular block) Allergic/toxic: skin rash, photosensitivity, liver damage of the cholestatic type (rarely), hepatitis (extremely rare), leuko- or thrombocytopenia (rarely), agranulocytosis (very rarely), hypoplastic anemia (rarely) Others: frequently increased appetite and weight gain, rarely nausea, rarely high blood pressure. May increase or decrease liver enzyme levels in the blood of some people. The side effects of low-dose doxepin for insomnia in long-term clinical trials (28 to 85 days) in adults and elderly people were as follows:
Sources: en.wikipedia.org
=== Legal status === In April 2025, the Committee for Medicinal Products for Human Use (CHMP) of the European Medicines Agency adopted a positive opinion, recommending the granting of a marketing authorization for the medicinal product Tepezza, intended for the treatment of adults with moderate to severe thyroid eye disease. The applicant for this medicinal product is Amgen Europe B.V. Teprotumumab was authorized for medical use in the European Union in June 2025. The CHMP's opinion is based on data from three randomized, placebo-controlled trials in a total of 225 participants with active thyroid eye disease, and one trial in 62 participants with chronic thyroid eye disease. After 24 weeks, participants treated with teprotumumab experienced a significant reduction (-2 to -2.3 mm) in protrusion of the eyeball from the eye socket (proptosis) and in the clinical activity score, a standard tool to evaluate inflammatory signs and symptoms of thyroid eye disease, compared to participants treated with placebo. The reduction in proptosis was smaller (-1.5mm) in participants with chronic thyroid eye disease.
Even after being expelled from the government of Peru and the Gran Colombo-Peruvian war ended, he would continue to rant against Peru and its people in multiple letters, considering them the greatest disgrace on the American continent and with a people complicit in tyranny, seeing the country as epitome of all the anarchic defects that plagued Latin America after the independences:"What men, or what demons, are these! From one end to the other, the New World seems an abyss of abomination; and if anything were lacking to complete this frightful chaos, Peru, with too much, would be enough to fill it. Accomplice of their tyrants during the War of Independence, without yet achieving its freedom, Peru anticipates tearing up its own bosom in the first days of its existence.The gallant General San Martín, at the head of the Chileans and the Argentineans, expels to the Spaniards from Trujillo to Ica. For Lima, there was no Peru but freedom, and at once some were bent on getting rid of San Martín, whose services they most urgently needed.
== C == Calymmatobacterium granulomatis Campylobacter Campylobacter coli Campylobacter fetus Campylobacter jejuni Capnocytophaga canimorsus Cardiobacterium hominis Chlamydia Chlamydia trachomatis Chlamydophila Chlamydophila pneumoniae (formerly Chlamydia pneumoniae) Chlamydophila psittaci (formerly Chlamydia psittaci) Citrobacter Citrobacter freundii Citrobacter koseri Clostridioides difficile (also known as C. diff) Clostridium Clostridium botulinum Clostridium novyi Clostridium perfringens (formerly Clostridium welchii) Clostridium septicum Clostridium tetani Corynebacterium Corynebacterium diphtheriae (formerly Mycobacterium diphtheriae) Corynebacterium urealyticum Coxiella burnetii Cutibacterium acnes (formerly Propionibacterium acnes)
== History == Tiagabine was discovered at Novo Nordisk in Denmark in 1988 by a team of medicinal chemists and pharmacologists under the general direction of Claus Bræstrup. The drug was co-developed with Abbott Laboratories, in a 40/60 cost sharing deal, with Abbott paying a premium for licensing the IP from the Danish company. It was approved for treatment of epilepsy in the United States in September 1997. In 2005, a bolded warning was added to the labeling of tiagabine by the United States Food and Drug Administration cautioning about association of new-onset seizures in people without epilepsy and discouraging off-label use. Tiagabine was previously subject to Risk Evaluation and Mitigation Strategies (REMS) in the United States, which was instituted in 2010. However, this requirement was eliminated in 2012. United States patents on tiagabine listed in the Orange Book expired in April 2016.
Sources: en.wikipedia.org
It is a synthetic peptide of fifteen amino acids whose sequence matches a fragment of a protein found in human gastric juice. It is studied mainly in laboratory and animal research rather than as an approved medicine.
The letters abbreviate body protection compound, the name given to the parent protein isolated from gastric juice. The number is an identifier attached to the specific fragment, not a dose or a description of a chemical property.
The sequence corresponds to a segment of an endogenous gastric protein, but the isolated fifteen-amino-acid peptide is a synthetic construct. Whether the free fragment circulates in humans at measurable levels is not clearly established in the published literature.
It is not authorized as a medicine in the United States or the European Union. Regulatory treatment varies by jurisdiction, and in several places it is handled as a research chemical. Therapeutic claims are not supported by large human trials.