B7-33 vs BPC-157.

B7-33 is an experimental single-chain peptide derived from the B-chain of the human hormone relaxin-2 (H2 relaxin). Native relaxin is a complex two-chain molecule linked by disulfide bonds and is difficult and costly to manufacture; B7-33 is a simplified 24-amino-acid single-chain mimetic intended to keep the useful anti-fibrotic activity while being easier to make. It is a laboratory research compound only, studied in cells and animals for fibrosis of the heart, kidney, lung, and blood vessels. It has never been tested in humans and has no approved use. It is categorized under healing because its studied effects are anti-fibrotic and tissue-remodeling.

BPC-157 (sometimes written PL 14736 or "Body Protection Compound 157") is a synthetic pentadecapeptide, a chain of 15 amino acids (Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val, MW ~1419 Da). It was designed as a stable partial sequence derived from a larger protein reported in human gastric juice, and is studied chiefly as a cytoprotective and tissue-healing agent. It is not a naturally occurring hormone or an approved drug; nearly all of its reputation rests on animal experiments.

B7-33 is a functionally selective (biased) agonist of the relaxin family peptide receptor 1 (RXFP1). Rather than strongly activating the cAMP pathway like native relaxin, it preferentially signals through the pERK pathway at RXFP1. This biased signaling is proposed to drive anti-fibrotic effects, notably increased activity of matrix-degrading enzymes such as MMP-2, which break down excess collagen, while potentially avoiding some effects tied to broader relaxin signaling. In preclinical models it has shown vasoprotective and cardioprotective actions consistent with relaxin biology. The single-chain design is meant to preserve receptor engagement without the manufacturing burden of the two-chain hormone.

BPC-157's most consistently reported mechanism is modulation of the nitric oxide (NO) system: it promotes endothelial NO production and its protective and vasoactive effects are blunted by NO-synthase blockade (e.g., L-NAME) in animal and tissue models. In endothelial cells it has been reported to activate a Src–caveolin-1–eNOS pathway and to enhance VEGFR2-driven signaling, which is the proposed basis for its pro-angiogenic ("new blood vessel") effects on healing tissue. In cultured tendon fibroblasts it upregulates the growth hormone receptor and supports cell survival and migration. It is also described as interacting with multiple cytoprotective and neurotransmitter (e.g., dopaminergic, serotonergic) systems, though these are largely inferred from preclinical pharmacology rather than direct human data.

All evidence is preclinical: cell-culture and animal studies, with no clinical trials. B7-33 has never been administered to a human being in a registered study, so no efficacy or safety claim about people can be drawn from the literature that exists. The founding paper (Hossain et al., Chemical Science, 2016) described the design of B7-33 and showed it binds RXFP1 and preferentially activates pERK over cAMP, with anti-fibrotic activity in cell and animal models of heart, lung, and kidney fibrosis. That work combined receptor pharmacology in transfected cell lines with short rodent experiments, using tissue collagen content and enzyme activity as endpoints, in small groups, without the randomization and blinding conventions that govern clinical research. Subsequent work reported vascular and cardiac benefits, including a study finding that B7-33 maintained relaxin's cardioprotective effects and reduced left-ventricular fibrosis more rapidly than the ACE inhibitor perindopril in an experimental model of cardiomyopathy (Alam et al., Biomedicine and Pharmacotherapy, 2023). Additional reports describe effects in myocardial-infarction remodeling and in hypertrophic-scar fibroblasts in vitro. These are early-stage animal and laboratory findings; no human efficacy or safety has been demonstrated, and translation to people is unproven. The cautionary comparison is the parent molecule. Serelaxin, recombinant human relaxin-2, travelled the whole distance: it produced encouraging earlier-phase signals in acute heart failure, then failed to improve clinical outcomes in the large RELAX-AHF-2 trial, and analyses of that dataset have continued to examine why its biomarker and end-organ signals did not convert into patient benefit. A biased RXFP1 agonist that performs well in rodent fibrosis models is therefore starting from a class whose flagship compound already failed a definitive human outcome trial. For B7-33 itself there is no human pharmacokinetic data, no dose-finding work, no formal toxicology package, no immunogenicity assessment, and no registered clinical trial.

The evidence base is overwhelmingly preclinical: hundreds of rodent and in vitro studies (a large fraction from a single Croatian research group led by Predrag Sikiric) report accelerated healing of tendon, muscle, ligament, bone, gut, and nervous tissue, plus gastrointestinal cytoprotection. Human evidence is extremely thin: there is no completed, published, adequately powered randomized controlled trial demonstrating a clinical benefit, and reports of human use (e.g., small uncontrolled case series for joint pain, and an early-phase inflammatory bowel disease program under the code PL 14736) are limited, often unpublished, lack placebo controls, and represent the lowest tiers of clinical evidence. Mechanistic and animal plausibility for tissue repair is genuinely interesting, but it has NOT been confirmed to translate into proven efficacy or safety in people. Any claim that BPC-157 reliably heals injuries in humans goes beyond what the published data support.

There are no human safety data for B7-33 because it has not entered clinical trials; all information comes from cell and animal experiments. Preclinical reports have not flagged prominent toxicities in the models studied, but absence of reported harm in a handful of animal studies is not evidence of human safety. Those studies were small, short, and designed to detect efficacy signals rather than toxicity, and none included the systematic histopathology, reproductive testing, or repeat-administration escalation that regulators require before a first human exposure. Relaxin biology indicates where problems would be looked for. Relaxin is a vasodilator and a systemic tissue-remodeling hormone, so blood pressure effects, renal hemodynamic changes, and unwanted matrix degradation in tissues that were not the target are the plausible concerns for any RXFP1 agonist. The anti-fibrotic mechanism that is desirable in a scarred heart is not obviously desirable everywhere else in the body. Clinical experience with serelaxin showed that an RXFP1 agonist can be given to acutely ill patients without an alarming adverse-event profile, but serelaxin is a different molecule with different signaling bias and different pharmacokinetics, and that experience does not transfer to a single-chain mimetic. Purity, dosing, and long-term effects in humans are entirely unknown, and immunogenicity against a synthetic single-chain sequence has never been assessed. Products marketed online as B7-33 are research chemicals, not medicines, and are not intended for human use, with no verified identity, sterility, or endotoxin testing behind them. This entry is educational only and does not provide any usage guidance.

There is no robust human safety dataset: long-term controlled toxicology and pharmacokinetic data in people are essentially absent, so its safety profile in humans is genuinely unknown. Animal studies have generally reported low acute toxicity, but rodent safety does not establish human safety, and theoretical concerns exist given its angiogenic (blood-vessel-promoting) activity, including unstudied implications for tumor biology. Most material sold online is research-use-only product of unverified identity, purity, and sterility, which adds contamination and mislabeling risks independent of the peptide itself. This entry intentionally gives no dosing, route, or protocol information.

B7-33 is a preclinical research compound with no FDA or other regulatory approval and no approved indication. It has not been evaluated in human clinical trials. It is sold, where sold, only as a research reagent labeled not for human consumption.

BPC-157 is not approved by the FDA (or other major regulators) for any indication and remains an investigational/research-use-only compound. The FDA placed it in Category 2 of the 503A bulk-substances review in 2023 (citing significant safety questions and restricting compounding); reporting in 2026 indicates it was later removed from that Category 2 list amid a renewed review; removal is not approval and does not establish safety or efficacy.