Overview
B7-33 is a synthetic single-chain peptide derived from the B-chain region of human relaxin-2, with molecular mass about 2,986.54 g/mol and formula C131H229N41O36S. It was designed to capture useful anti-fibrotic and tissue-remodeling effects of relaxin while avoiding the complexity of full two-chain relaxin peptides. Researchers have studied it mainly in cardiac, renal, and pulmonary fibrosis models.
The peptide acts through relaxin family peptide receptor 1, or RXFP1, but with functionally selective signaling. Instead of simply copying relaxin, B7-33 appears to favor pathways such as ERK1/2 and matrix metalloproteinase activation that reduce collagen accumulation and myofibroblast activity. This selectivity is the reason it is discussed as a potentially cleaner anti-fibrotic research tool.
B7-33 is not FDA-approved for heart failure, fibrosis, pulmonary disease, or tissue remodeling. Human clinical dosing, long-term safety, immunogenicity, and drug interactions are not established. The evidence is promising but early, and most practical claims come from preclinical models rather than patient trials.
This guide covers B7-33's relaxin biology, anti-fibrotic mechanisms, safety unknowns, and practical interpretation for peptide users who may see it marketed as a cardiac or lung remodeling compound.
Quick facts
- Mechanism
- Functionally selective RXFP1 agonist with anti-fibrotic signaling
- Primary use
- Anti-Fibrotic Research
- Evidence
- limited
- FDA
- Not approved
- Route
- Subcutaneous or infusion-based animal research
- Typical results
- Reduced fibrosis markers in animal cardiac and pulmonary models
Chemical information
B7-33 is a single-chain relaxin-2 B-chain analog with molecular mass about 2,986.54 g/mol. Its simplified structure was designed to preserve RXFP1 anti-fibrotic signaling without the full two-chain relaxin hormone architecture.
How B7-33 works
B7-33 activates RXFP1-related signaling in a way that emphasizes anti-fibrotic downstream effects. In fibroblast and animal models, it reduces collagen deposition, myofibroblast activation, and fibrotic remodeling signals. The mechanistic focus is not broad stimulation of tissue growth but rebalancing extracellular matrix turnover through relaxin-linked pathways.
Relaxin has long been studied for vasodilatory, renal, and anti-fibrotic effects, but full relaxin is structurally complex. B7-33 was engineered as a single-chain analog that can engage RXFP1 and promote selective signaling, especially ERK1/2 activation and matrix metalloproteinase-2 activity. These pathways can support collagen breakdown and oppose transforming growth factor beta-driven fibrotic programs.
In myocardial infarction and cardiomyopathy models, B7-33 reduced fibrosis-related gene expression and improved remodeling markers. Pulmonary and renal fibrosis models also support an anti-fibrotic direction. Still, these outcomes depend on disease model, timing, route, and endpoint. Reducing scar formation in a rodent model is not the same as treating established human fibrosis.
The most important user-facing point is that anti-fibrotic does not mean universally regenerative. Fibrosis is part of wound repair, immune response, and structural stabilization. Blocking or altering matrix deposition at the wrong time may be harmful, so this peptide belongs in controlled research settings.
- RXFP1 agonism: Engages the relaxin receptor involved in matrix remodeling
- Functional selectivity: Favors anti-fibrotic signaling rather than broad relaxin mimicry
- ERK1/2 activation: Linked to downstream matrix-regulating effects
- MMP-2 support: May increase collagen-degrading enzyme activity
- TGF-beta opposition: Reduces pro-fibrotic fibroblast signaling in models
- Single-chain design: Easier peptide architecture than full two-chain relaxin
Pharmacokinetics
Published human PK for B7-33 is not established. Animal studies use experimental dosing and delivery routes, so half-life, bioavailability, and dose-response claims for humans should be treated as unknown.
| Parameter | Value | Significance |
|---|---|---|
| Human PK | Not established | No approved dose interval or half-life exists |
| Route studied | Parenteral in animal models | Most fibrosis data come from controlled injections or infusion |
| Target receptor | RXFP1 | Receptor engagement drives anti-fibrotic signaling |
| Metabolism | Peptidase degradation expected | Standard peptide clearance is likely |
| Distribution | Unknown in humans | Tissue exposure cannot be assumed from rodent efficacy |
| Duration | Model-dependent | Anti-fibrotic outcomes may persist beyond peptide exposure |
Dosing & administration
No FDA-approved B7-33 dosing exists. Published work uses animal-model protocols selected for specific fibrosis endpoints, not wellness or body-recomposition goals. Human dose conversion would be speculative without clinical pharmacokinetic and safety data.
Research protocols should define the fibrosis model, route, treatment timing, tissue histology, collagen measures, blood pressure monitoring, and inflammatory markers. Anti-fibrotic effects are meaningful only when measured against the right disease stage and comparator.
For peptide users, B7-33 should not be treated as a general recovery peptide. The biologic target is extracellular matrix remodeling, and unsupervised use could theoretically affect normal scar formation, vascular tone, or reproductive relaxin pathways.
Important: These dosing ranges are not FDA-approved. Any use should be under qualified medical supervision.
Side effects & safety
B7-33's preclinical safety profile is encouraging but incomplete. Human safety, reproductive effects, blood-pressure effects, immunogenicity, and long-term fibrosis remodeling consequences remain unresolved.
Common
- • Injection site reactions
- • Transient blood pressure changes by relaxin-class analogy
- • Headache or flushing by vasodilatory analogy
- • Fatigue
- • Fluid-balance uncertainty
- • No perceived effect in non-fibrotic contexts
Serious / potential risks
- • Unknown human immunogenicity
- • Potential hypotension in vulnerable users
- • Unintended interference with wound healing
- • Unknown effects in pregnancy or reproductive signaling
- • Contamination or mislabeling from research sources
Drug interactions
Interaction data are not established; cautions are based on relaxin biology, vascular effects, and fibrosis-modifying pathways.
| Medication | Interaction | Recommendation |
|---|---|---|
| Antihypertensives | Relaxin-pathway agents may affect vascular tone | Monitor blood pressure in formal research settings |
| Anti-fibrotic drugs | Potential overlapping matrix-remodeling effects | Avoid uncontrolled stacking |
| Anticoagulants | Tissue remodeling and vascular effects may complicate bleeding risk interpretation | Use caution in studies |
| Immunosuppressants | Fibrosis and inflammation pathways overlap | Require supervised protocols |
| Pregnancy-related medications | Relaxin biology is reproductive and vascular | Avoid in pregnancy unless formal research approval exists |
Storage & handling
Lyophilized (powder)
- • Store at -20°C to 4°C (freezer or refrigerator)
- • Protect from light and moisture
- • Stable for 12–24 months when stored properly
- • Keep in original sealed container until reconstitution
Reconstituted solution
- • Refrigerate at 2–8°C after reconstitution
- • Use bacteriostatic water for multi-dose reconstitution
- • Typical stability: 14–28 days refrigerated
- • Do not freeze reconstituted solution
Cost & availability
| Source | Cost | Notes |
|---|---|---|
| Research peptide vendors | $150-$600+ per vial | Cost varies by synthesis quality and quantity |
| Custom synthesis | $1,000-$5,000+ | Sequence, purity, and folding verification matter |
| Preclinical study costs | Thousands to tens of thousands | Histology and fibrosis assays dominate real research cost |
The bottom line
B7-33 is one of the more scientifically interesting fibrosis peptides because it narrows relaxin signaling toward RXFP1 anti-fibrotic pathways. The evidence is promising but preclinical. It is not an approved therapy and should not be treated as a casual recovery or anti-aging injection.
Best for
- • Fibrosis researchers studying RXFP1 signaling
- • Preclinical cardiac remodeling models
- • Pulmonary or renal fibrosis mechanism studies
Not for
- • Self-treatment of heart or lung disease
- • Use during active wound healing without research oversight
- • Pregnancy or fertility contexts
- • Replacing approved cardiovascular or pulmonary care
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Frequently asked questions
References
- [1] Hossain MA, Kocan M, Yao ST, et al.. A single-chain derivative of the relaxin hormone is a functionally selective agonist of the G protein-coupled receptor, RXFP1. Chemical Science (2018). PMID: 30155023
- [2] Chow BSM, Kocan M, Shen M, et al.. B7-33, a functionally selective relaxin receptor 1 agonist, attenuates myocardial infarction-related adverse cardiac remodeling in mice. Journal of the American Heart Association (2020). PMID: 32295457
- [3] Samuel CS, Lekgabe ED, Mookerjee I. The effects of relaxin on extracellular matrix remodeling in health and fibrotic disease. Advances in Experimental Medicine and Biology (2007). PMID: 17656774
- [4] Samuel CS, Royce SG, Hewitson TD, et al.. Anti-fibrotic actions of relaxin. British Journal of Pharmacology (2017). PMID: 28185322
- [5] Martin B, Gabris-Weber BA, Reddy R, et al.. The single-chain relaxin mimetic B7-33 maintains cardioprotective effects and reduces left ventricular fibrosis. Frontiers in Pharmacology (2023). PMID: 36753958
- [6] Bathgate RAD, Halls ML, van der Westhuizen ET, et al.. Relaxin family peptides and their receptors. Physiological Reviews (2013). PMID: 23303914