B7-33
A single-chain relaxin-2 analogue that selectively activates RXFP1 receptors to inhibit fibrosis and reduce inflammation without the off-target effects of full relaxin.
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Compound Profile
B7-33
Key Data
Research reference only
Research Focus
Preclinical data
⚠ Research & Educational Use Only. B7-33 is a research chemical documented here for scientific education. All information references peer-reviewed literature and preclinical/clinical study data. Not for human consumption. Not medical advice. Consult a licensed researcher or healthcare professional before any laboratory use.
- Selectively activates RXFP1 (relaxin family peptide receptor 1) - the receptor mediating relaxin's antifibrotic and vasodilatory effects
- Potent antifibrotic properties - inhibits collagen deposition and promotes collagen degradation in fibrotic tissue
- Cardiac fibrosis research - reduces myocardial fibrosis in heart failure models
- B7-33 is not FDA-approved for human use. It is a research chemical for scientific study only.
Research At a Glance
- Selectively activates RXFP1 (relaxin family peptide receptor 1) - the receptor mediating relaxin's antifibrotic and vasodilatory effects
- Potent antifibrotic properties - inhibits collagen deposition and promotes collagen degradation in fibrotic tissue
- Cardiac fibrosis research - reduces myocardial fibrosis in heart failure models
- Renal fibrosis - reduces renal scarring in kidney injury models
In Plain English
Simple summaryB7-33 is a synthetic single-chain analogue of relaxin -- specifically of the B-chain segment (residues 7-33) of the two-chain relaxin-2 protein. Relaxin is a polypeptide hormone that promotes tissue remodeling and reduces fibrosis: it inhibits collagen production, breaks down existing collagen, and reduces organ stiffening in the heart, lungs, kidneys, and liver. The therapeutic appeal is obvious -- fibrosis underlies heart failure, chronic kidney disease, liver cirrhosis, and pulmonary fibrosis. B7-33 was developed because full relaxin-2 requires both A and B chains (complex to manufacture) and has a short half-life. B7-33 retains relaxin receptor (RXFP1) activation with a simpler single-chain structure and showed protection against cardiac fibrosis and diastolic dysfunction in mouse models.
- Selectively activates RXFP1 - the receptor mediating relaxin's antifibrotic and vasodilatory effects
- Potent antifibrotic properties - inhibits collagen deposition and promotes collagen degradation in fibrotic tissue
- Cardiac fibrosis research - reduces myocardial fibrosis in heart failure models
The full scientific detail, mechanisms, citations, and dosing data, follows below.
What is B7-33?
Tap any underlined term for an instant definition.
B7-33 is a synthetic single-chain analogue of human relaxin-2, engineered to selectively activate the RXFP1 receptor while avoiding some of the complex off-target pharmacology of native relaxin. Relaxin is a peptide hormone naturally produced during pregnancy that remodels the cervix and relaxes pelvic ligaments, while also having systemic effects on the cardiovascular and renal systems. These systemic effects - particularly antifibrotic and vasodilatory properties - have attracted significant pharmaceutical interest.
Native relaxin is a two-chain peptide (A and B chains linked by disulfide bonds, similar in structure to insulin), which creates manufacturing complexity and stability challenges. B7-33 was developed as a single-chain simplification, retaining the key B-chain sequence (residues 7-33) that contains the receptor-binding epitope for RXFP1. By presenting this binding epitope in a single chain without the A-chain, B7-33 achieves selective RXFP1 agonism with a simpler, more stable molecule.
The antifibrotic properties of relaxin/RXFP1 signalling are mediated through multiple mechanisms: inhibition of TGF-beta-stimulated fibroblast differentiation (preventing the transformation of normal fibroblasts into myofibroblasts that deposit excess collagen), activation of matrix metalloproteinases (enzymes that degrade existing collagen), and reduced expression of profibrotic cytokines. Together, these actions both prevent new fibrosis and promote resolution of existing fibrous tissue.
In the cardiovascular context, cardiac fibrosis is a major component of heart failure progression - as the heart remodels in response to pressure overload or injury, cardiomyocytes are replaced by scar tissue that reduces contractile function. B7-33 and related relaxin analogues have shown promising results in reducing this fibrosis and improving cardiac function in heart failure models, driving interest from the cardiology research community.
B7-33 represents a newer generation of peptide research tools compared to native relaxin - more manufacturable, more stable, and potentially more receptor-selective. It is one of several anti-fibrotic peptide candidates being investigated as potential therapeutics for cardiac, renal, pulmonary, and hepatic fibrosis.
By the Numbers
Key Research Benefits
Documented effects observed in preclinical and clinical studies on B7-33. See all Healing & Recovery peptides for comparison.
Common Stacks
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Side Effects & Risks
Adverse effects reported in the research literature. All data sourced from preclinical and clinical study reports. View all peptides' side effects →
Dosing Data from the Literature
Doses referenced below are sourced from published preclinical and clinical studies. Use the peptide dose calculator to convert these values to injection volume.
B7-33 research doses are derived from preclinical studies. No established human clinical dose is yet published.
Preclinical reference doses: 0.5-2 mg/kg in rodent models Frequency: daily or twice daily in most preclinical protocols Research focus areas: cardiac, renal, and pulmonary fibrosis; vascular biology
Administration in Research Settings
Standard reconstitution and administration methodology for laboratory research use.
Reconstitute B7-33 with sterile or bacteriostatic water. Administer subcutaneously. Monitor blood pressure during research protocols given the vasodilatory mechanism.
What the research doesn't show
The anti-fibrotic rationale is scientifically compelling, but serelaxin's Phase 3 failure was a significant setback for the entire relaxin receptor field. B7-33 is an improvement in manufacturability but inherits the same fundamental question: does RXFP1 activation in failing human hearts produce meaningful clinical benefit? Mouse model results for anti-fibrotic compounds have a poor track record translating to human outcomes.
Medical Expert Videos
Physicians, researchers, and pharmacologists explain B7-33, covering mechanisms of action, clinical context, and study findings.
Videos sourced from YouTube search. KnowYourPeptide does not endorse any individual creator. For research education only.
The Bottom Line
B7-33 has a growing body of preclinical evidence and a well-characterised safety profile in research settings. The most-studied application is: selectively activates rxfp1 - the receptor mediating relaxin's antifibrotic and vasodilatory effects.
The most commonly reported side effect in research subjects is hypotension - the vasodilatory mechanism can lower blood pressure significantly. It is a research chemical, not approved for human use.
Frequently Asked Questions
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Quick Reference
How It Compares
Full relaxin-2 (serelaxin) was tested in heart failure Phase 3 trials (RELAX-AHF-2) but failed on the primary mortality endpoint, dampening commercial enthusiasm for the mechanism. B7-33's advantage over serelaxin is simpler manufacturing; its challenge is that the clinical failure of serelaxin has made the RXFP1 pathway harder to fund. Pirfenidone and nintedanib are approved anti-fibrotics for pulmonary fibrosis but work through TGF-beta, not the relaxin pathway.
Compare B7-33 side-by-sideResearch Use Only
This information is for educational research purposes only. This is not medical advice. Consult a qualified healthcare professional.