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.
Updated 2026-04-07. Numbers and descriptions here follow the published literature rather than marketing material.
The peptide was first described in the early 1990s by a group studying gastric secretions and tissue repair. Its fifteen-residue chain is usually written as GEPPPGKPADDAGLV in single-letter code. The free peptide has the formula C62H98N16O22 and a theoretical mass near 1419.5 daltons. These identifiers are established chemical facts that can be checked against standard peptide databases. There is no ambiguity about the primary structure.
Most published findings come from rodent experiments using induced injury or surgical models. Human reports remain scarce and are largely observational, which limits how much can be stated with confidence. Questions about absorption, distribution, metabolism, and clearance in people are still open. Dose translation between species is likewise unresolved. Researchers tend to read the animal literature as a starting point rather than a settled account.
BPC-157 is a synthetic peptide composed of fifteen amino acids. Its sequence corresponds to part of a protein found in human gastric juice, which is the origin of the "body protection compound" label. In laboratory work the material is treated as a defined research chemical rather than a finished product. Published research has centered on animal models, and the peptide is not an approved medicine in most countries.
Published studies on BPC-157 are dominated by animal models. Commonly used endpoints include healing of surgically induced lesions in the stomach, tendon-to-bone attachment after transection, and recovery from experimentally induced vascular or intestinal damage. Many of these reports come from a small number of research groups, and the peptide is often described as acting across a wide range of tissue types. That breadth is itself a point of discussion, since one molecule influencing many unrelated systems is unusual.
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.
| Property | Value | Notes |
|---|---|---|
| Amino acid count | 15 residues | Synthetic pentadecapeptide chain |
| Sequence | GEPPPGKPADDAGLV | Single-letter amino acid code |
| Molecular formula | C62H98N16O22 | Free peptide, without counter-ion |
| Theoretical mass | Approximately 1419.5 daltons | Varies slightly with adducts and counter-ions |
| Origin | Fragment of a human gastric juice protein | Source of the BPC designation |
The main chemical liabilities of this sequence are peptide-bond hydrolysis and possible aspartate-related reactions, since the peptide contains aspartic acid residues but no cysteine, methionine, or tryptophan. Absence of those three residues removes the most common oxidation and disulfide pathways from consideration. Studies of related peptides indicate that aspartate isomerisation and aspartimide formation occur most readily at Asp-Gly and Asp-Ala positions, and open questions remain about how quickly those reactions proceed under ordinary laboratory conditions. Storage guidance typically emphasises cool, dry, dark conditions to slow hydrolysis.
Identity and purity are usually assessed with reversed-phase high-performance liquid chromatography, often paired with mass spectrometry using electrospray or MALDI ionisation. Amino acid analysis and peptide mapping by enzymatic digestion provide additional sequence-level confirmation. Purity is commonly reported as an area percentage from a chromatographic trace, and water content can be measured by Karl Fischer titration. Reported masses may differ by tens of daltons between sources because preparations can contain acetate or trifluoroacetate counterions, and such differences are not by themselves evidence of a different peptide.
BPC-157 is normally distributed as a lyophilised powder that ranges from white to off-white in appearance. The peptide dissolves readily in water, normal saline, and common aqueous buffers, and it is poorly soluble in nonpolar solvents such as hexane or vegetable oils. Lyophilised vials take up moisture if left open, which changes the mass of powder in the container and complicates any later weighing. Because the material is handled in small quantities, static and adhesion to glass or plastic can also cause noticeable losses during transfer.
A freeze-dried sample is generally the most stable form and is commonly held at minus twenty degrees Celsius or lower for long-term keeping, with brief transfers at room temperature. The solid is hygroscopic, so vials are warmed to ambient temperature before opening to prevent condensation from degrading the contents. Light exposure and repeated temperature cycling are both avoided in routine handling. Storage over a desiccant is a common laboratory practice that limits moisture uptake during repeated access.
Once dissolved, the material is considerably less stable than the dry solid. Aqueous solutions are usually kept cold and used within a short window, and neutral or mildly acidic buffers are preferred over strongly alkaline conditions. Freeze-thaw cycles promote aggregation and loss of material to container surfaces, so dividing a batch into single-use aliquots is standard. Adsorption to plastic and glass can lower the measured concentration, meaning solution strength may need rechecking before an experiment.
Identity and purity are established with complementary methods rather than one test. Reverse-phase high-performance liquid chromatography separates the main peak from deletion sequences and oxidized variants, and its area percentage is the usual purity figure. Mass spectrometry confirms the expected molecular mass and can flag truncations or modifications that chromatography alone might miss. Amino acid analysis and peptide mapping add sequence-level confirmation, while residual counter-ion and water content are measured separately.
BPC-157 is a synthetic pentadecapeptide whose sequence is commonly given as Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val. It is described in the literature as a fragment of a larger protein found in human gastric juice, referred to as body protection compound. The peptide was first characterized in the early 1990s by a research group in Zagreb, Croatia. Its molecular formula is C62H98N16O22 and its monoisotopic mass is approximately 1419 daltons.
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.
Most published work on BPC-157 consists of preclinical studies, including rodent models of tissue injury, gastrointestinal lesions, and vascular or tendon damage, together with in vitro cell assays. Reviews frequently note that the mechanisms proposed in these papers remain incompletely characterised and that findings have not been confirmed in large randomised human trials. The compound is widely sold as a research chemical rather than a licensed medicine, and labels commonly carry a statement that it is not for human use. Whether any of the reported animal effects translate to humans is an open question rather than an established result.
Terminology in the literature is not fully standardised. Papers and product listings use BPC-157, BPC 157, and the longer phrase stable gastric pentadecapeptide BPC 157 interchangeably, and synonyms such as bepecin or PL 14736 appear in older or company-linked publications. Purity claims and reported masses can also differ between sources because peptide preparations may include counterions, residual solvents, or bound water. This variability complicates direct comparison of results across studies and makes the exact identity and grade of a given sample worth verifying. Discussions of the compound should therefore specify the source, salt form, and stated purity where those are known.
=== Gastrointestinal === CCK is synthesized and released by enteroendocrine cells in the mucosal lining of the small intestine (mostly in the duodenum and jejunum), called I cells, neurons of the enteric nervous system, and neurons in the brain. It is released rapidly into the circulation in response to a meal. The greatest stimulator of CCK release is the presence of fatty acids and/or certain amino acids in the chyme entering the duodenum. In addition, release of CCK is stimulated by monitor peptide (released by pancreatic acinar cells), CCK-releasing protein (via paracrine signalling mediated by enterocytes in the gastric and intestinal mucosa), and acetylcholine (released by the parasympathetic nerve fibers of the vagus nerve). Once in the circulatory system, CCK has a relatively short half-life.
=== Pausinystalia johimbe === Yohimbine should not be confused with yohimbe but often is. Yohimbe is the common English name for the tree species P. johimbe (also called Corynanthe johimbe) and, by extension, the name of a medicinal preparation made from the bark of that tree, sold as an aphrodisiac. In contrast, yohimbine is a pure alkaloid that can be isolated from yohimbe bark. Yohimbine is just one of at least 55 indole alkaloids that have been isolated from the bark; and, while it has been described as the most active of these, it constitutes only 15% of the total alkaloid content. Others include rauwolscine, corynanthine and ajmalicine; the bark also contains non-alkaloids about which virtually nothing is known. Yohimbe, thus a complex mixture, has been studied far less thoroughly than yohimbine, the pure compound. Pharmaceutical grade yohimbine is usually presented as the hydrochloride, which is more soluble. The traditional source of yohimbine is the bark of the African tree P. johimbe. It has other uses, but the tree is sought out primarily for its bark; in practice, harvesting the bark kills the tree. Tree density is relatively low (average ≈ 4 harvestable trees/hectare). The high demand for medicines based on the bark has led to the tree's over-exploitation. The bark is traded in local markets and, because it is scarce, it is often adulterated with that of other species which contain little yohimbine. The species is becoming endangered. Around the year 2000, Cameroon was shipping P. johimbe to Europe at the rate of about 100 tonnes annually.
=== Connective tissue disorders === Marfan's Syndrome is a connective tissue disorder that can lead to chronic aortic or mitral regurgitation. Osteogenesis imperfecta is a disorder in formation of type I collagen and can also lead to chronic aortic regurgitation.
Sources: en.wikipedia.org
The results tend to show that the experimental HLB of sucrose monoesters, composed of 100% of monoesters for purified products and around 70-80% for industrial blends, would be rather around 11-12 for short fatty chains (6 to 12 carbons) and around 10-11 for long fatty chains (14 to 18 carbons). These values would better describe their emulsifying behavior and would better make the correspondence with other families of surfactants. Notably, the experimental range of HLB of sucrose esters would not be so wide as the calculated HLB indicated on suppliers technical sheets, especially not as high as HLB 16. It is also important to point out the fact that in experiments, the residual amount of fatty acid (even less than 2% in weight) and the state of protonation of the latter has a significant effect on the phase properties and the emulsifying properties of sucrose esters, because the deprotonated fatty acid is highly surface active while the protonated fatty acid is not. This state of protonation has also an impact on the experimental determination of the HLB. The "wide range of HLB" currently defined for sucrose esters marketed blends, which is supposed to spread up to 16, should be considered with a critical point of view at the light of these observations. While the use of the different grades of sucrose esters is well documented in some applications, notably for food formulations, clarifying their HLB scale on an experimental basis will help their implementation in new applications not yet documented.
PIK3R2 and PIP5K1A are two kinases that create substrates for PSD4. PSD4 (Pleckstrin and Sec7 Domain containing 4) is a GEF (Guanine nucleotide Exchange Factor) that loads ARL14/ARF7 with GTP. ARL14/ARF7 is a Small GTPase protein that is selectively expressed in immune cells. This protein is localized within MHC-II compartments in immature dendritic cells. ARF7EP is an effector of ARL14/ARF7 that interacts with MYO1E. MYO1E is a protein that controls MHC-II compartments with an actin-based mechanism.
Vitamin C or ascorbate is a water-soluble vitamin found in citrus and other fruits, berries and vegetables. It is found as a form of ascorbic acid. It is an essential nutrient involved in the repair of tissue, the formation of collagen, and the enzymatic production of certain neurotransmitters. It is required for the functioning of several enzymes and is important for immune system function. It is also an antioxidant. Most animals are able to synthesize their own vitamin C. However, higher primates (including humans), most bats, guinea pigs, some fish species, and some bird species must acquire it from dietary sources because a gene for a synthesis enzyme has mutations that render it dysfunctional; humans obtain this vitamin from those fruits and vegetables. It is also a generic prescription medication and in some countries is sold as a non-prescription dietary supplement. As a therapy, it is used to prevent and treat scurvy, a disease caused by vitamin C deficiency. Vitamin C may be taken by mouth or by intramuscular, subcutaneous or intravenous injection. Various health claims exist on the supposition that moderate vitamin C deficiency increases disease risk, such as for the common cold, cancer or COVID-19. There are also claims of benefits from vitamin C supplementation in excess of the recommended dietary intake for people who are not considered vitamin C deficient. Vitamin C is generally well tolerated. Large doses may cause gastrointestinal discomfort, headache, trouble sleeping, and flushing of the skin.
=== Secondary glaucoma === Secondary glaucoma (H40.3-H40.6) encompasses numerous subtypes: inflammatory glaucoma (all types of uveitis, Fuchs heterochromic iridocyclitis); phacogenic glaucoma (angle-closure with mature cataract, phacoanaphylactic glaucoma from lens capsule rupture, phacolytic glaucoma, lens subluxation); glaucoma secondary to intraocular hemorrhage (hyphema, hemolytic/erythroclastic glaucoma); traumatic glaucoma (angle recession glaucoma); postsurgical glaucoma (aphakic pupillary block, ciliary block); neovascular glaucoma; drug-induced glaucoma (corticosteroid-induced, alpha-chymotrypsin); and glaucoma of miscellaneous origin (associated with intraocular tumors, retinal detachments, severe chemical burns, essential iris atrophy, or toxic glaucoma). Neovascular glaucoma, an uncommon type of glaucoma, is difficult or nearly impossible to treat, and is often caused by proliferative diabetic retinopathy (PDR) or central retinal vein occlusion (CRVO). It may also be triggered by other conditions that result in ischemia of the retina or ciliary body. Individuals with poor blood flow to the eye are highly at risk for this condition. Neovascular glaucoma results when new, abnormal vessels begin developing in the angle of the eye that begin blocking the drainage. People with such a condition begin to rapidly lose their eyesight. Sometimes, the disease appears very rapidly, especially after cataract surgery procedures. Toxic glaucoma is open-angle glaucoma with an unexplained significant rise of intraocular pressure following an unknown pathogenesis.
Sources: en.wikipedia.org
The peptide is synthetic, but its sequence matches a segment of a protein present in human gastric juice. It does not occur as a free fifteen-residue peptide in the body.
Rodents account for the large majority of published experiments. Human data are sparse and mostly observational, so cross-species extrapolation remains uncertain.
It is not an approved therapeutic in most jurisdictions. Regulatory status varies by country, and several places restrict it as a research chemical.
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.