B7-33.
B7-33 is an experimental single-chain peptide derived from the B-chain of the human hormone relaxin-2 (H2 relaxin).
B7-33 is an experimental single-chain peptide derived from the B-chain of the human hormone relaxin-2 (H2 relaxin). B7-33 is research / preclinical, and PepCue grades its published evidence F tier (24/100). Also known as single-chain relaxin analog. This is a research reference, not medical or dosing advice.
What it is
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.
How it works
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.
Mechanism pathways
Biased activation of RXFP1 to promote matrix breakdown and vascular protection.
Relaxin is a hormone best known from pregnancy, where it contributes to remodelling of connective tissue and to systemic vasodilation and increased renal blood flow. Its principal receptor, relaxin family peptide receptor 1, is a G-protein-coupled receptor found in heart, kidney, lung, liver, and vasculature. Classical activation raises intracellular cyclic AMP, but the receptor also couples to other cascades including extracellular signal-regulated kinase signalling and nitric oxide production. The reason this receptor attracts interest is fibrosis. Fibrosis is the pathological accumulation of extracellular matrix, principally collagen, that stiffens organs and degrades their function, and it is a common endpoint in chronic heart, kidney, liver, and lung disease with very few effective treatments. Relaxin signalling opposes it from both directions: it suppresses the activation of fibroblasts into collagen-producing myofibroblasts, and it increases the activity of matrix metalloproteinases that degrade collagen already deposited. Combined with vasodilation and improved tissue perfusion, this makes RXFP1 an attractive anti-fibrotic and cardioprotective target. Native relaxin is a two-chain molecule held together by disulfide bonds, structurally similar to insulin. That architecture makes it expensive and difficult to manufacture at scale, which has been a real obstacle to developing it as a medicine. The compound in this group is a single-chain peptide designed to engage RXFP1 without that manufacturing burden. It is also described as functionally selective, or biased. Rather than strongly activating the cyclic AMP pathway as native relaxin does, it preferentially signals through the ERK pathway at the same receptor. Signalling bias means a ligand can trigger some of a receptor's downstream cascades while leaving others comparatively quiet. Here the proposal is that the ERK-biased profile retains the anti-fibrotic actions, including increased matrix metalloproteinase activity, while avoiding effects tied to the broader relaxin signalling profile. Preclinical work has reported vasoprotective and cardioprotective actions consistent with relaxin biology. On clinical relevance, caution is warranted. The receptor and the anti-fibrotic biology are legitimate and well studied, but full-length relaxin itself has been through large human trials in acute heart failure without confirming clinical benefit, which is a sobering precedent for the whole target. This single-chain compound has not been through human trials, is not approved anywhere, and its evidence base is entirely preclinical.
The evidence
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, in brief
A simplified single-chain mimetic of relaxin-2 that acts as a biased RXFP1 agonist, favouring pERK over cAMP signalling and raising collagen-degrading MMP-2. Anti-fibrotic effects have been reported in cell and animal models of cardiac, renal and pulmonary fibrosis, including one cardiomyopathy model where it reduced left-ventricular fibrosis faster than perindopril. All of this is preclinical: B7-33 has never been tested in humans, and no human efficacy or safety has been established.
- Hossain MA et al.: A single-chain derivative of the relaxin hormone is a functionally selective agonist of RXFP1Chem Sci, 2016 (PMID 30155023)
- Alam F et al.: The single-chain relaxin mimetic B7-33 reduces left ventricular fibrosis faster than perindoprilBiomed Pharmacother, 2023 (PMID 36753958)
Evidence maturity
An evidence-only reading: approval status, human vs preclinical data, mechanism and safety. Popularity never raises it. Research file #007
Mostly preclinical or mechanistic; little human data.
Findings come mainly from animal models, not people.
Claim receipts
Popular claims about B7-33, checked against the state of the evidence. The verdict describes evidence maturity, never an invented study result.
All anti-fibrotic findings come from cell culture and short rodent experiments in small groups.
The comparison with an ACE inhibitor was made in an experimental cardiomyopathy model in animals, not in patients.
The single-chain design was made for manufacturability, and the parent class flagship failed a definitive human outcome trial while this peptide has no human data at all.
It has never been given to a human in a registered study, and there is no toxicology package, pharmacokinetic data or immunogenicity assessment.
Safety profile
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.
Compound notes
- B7-33 is an experimental 24-amino-acid single-chain peptide derived from the B-chain of the human hormone relaxin-2.
- Native relaxin is a two-chain disulfide-linked molecule that is difficult and costly to manufacture; B7-33 is a simplified mimetic meant to keep the anti-fibrotic activity while being easier to make.
- It is a functionally selective (biased) agonist at the relaxin family peptide receptor 1 (RXFP1), preferentially signaling through pERK rather than cAMP.
- That biased signaling is proposed to drive anti-fibrotic effects, notably raising matrix-degrading enzymes such as MMP-2 that break down excess collagen.
Same receptor, different signaling bias and a far simpler single-chain structure. B7-33 favors pERK over the cAMP pathway that native relaxin strongly activates.
- Entirely preclinical: cell-culture and animal studies in heart, kidney, lung and vascular fibrosis, with no clinical trials and no demonstrated human efficacy or safety.
- No FDA or other regulatory approval and no approved indication; sold, where sold, only as a research reagent labeled not for human consumption.
- Absence of reported harm in a handful of animal studies is not evidence of human safety; purity and long-term effects in people are unknown.
Regulatory status
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.
Sold research-use-only; human evidence is limited or preclinical.
By the numbers
- 01Simplified 24-amino-acid single-chain mimetic of the two-chain hormone relaxin-2.
- 02Functionally selective (biased) RXFP1 agonist favoring pERK over cAMP signaling.
- 03Studied for anti-fibrotic effects (e.g., raising collagen-degrading MMP-2) in heart, kidney, and lung.
- 04First described by Hossain et al. in Chemical Science (2016).
- 05In a cardiomyopathy model it reduced left-ventricular fibrosis faster than perindopril (Alam et al., 2023).
- 06Entirely preclinical: no human trials, no approval, and no established human safety.
B7-33: research formats
Choose the format you are researching to see route-specific notes.
Entirely preclinical. No human trials, so no route, schedule, or human safety data exist.
B7-33 is a simplified single-chain mimetic of the two-chain hormone relaxin-2, created to keep the anti-fibrotic activity while being easier to manufacture. All published work is in cells and animals, covering fibrosis of the heart, kidney, lung, and blood vessels. It has never been tested in humans, so this page presents no administration format and no example concentration math.
Animal-model administration in the published studies does not translate into a human format. Species, delivery, and exposure all differ, and none of it has been tested for human tolerability.
B7-33 has no regulatory approval anywhere and is sold, where sold, only as a research reagent labeled not for human consumption.
Sources
Every factual claim above resolves to a real, published source.
- A single-chain derivative of the relaxin hormone is a functionally selective agonist of the G protein-coupled receptor, RXFP1Hossain MA, et al. Chem Sci, 2016 (PMID 30155023)
- The single-chain relaxin mimetic B7-33 reduces left ventricular fibrosis faster than perindopril in experimental cardiomyopathyAlam F, et al. Biomed Pharmacother, 2023 (PMID 36753958)
- Relaxin agonists under preclinical and early clinical investigation for the treatment of heart failureExpert Opin Investig Drugs, 2024 (PMID 39641766)
- End-organ protective effect of serelaxin in patients hospitalized for heart failure: Results of the biomarker substudy of Relaxin in Acute Heart Failure-2 (RELAX-AHF-2)Eur J Heart Fail, 2025 (PMID 39663924)
- PubMed search: RXFP1 biased agonist relaxin fibrosisPubMed / NCBI
Cite this page
PepCue. “B7-33: the evidence.” PepCue, reviewed June 1, 2026. https://www.pepcue.app/p/b7-33.
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