B7-33 (Relaxin)

Relaxin-2 Analog · Anti-Fibrotic & Cardiovascular

Overview

B7-33 is a single-chain peptide analog of human relaxin-2 that selectively activates the relaxin family peptide receptor 1 (RXFP1). Unlike native relaxin-2, which requires a complex two-chain A/B structure connected by disulfide bonds, B7-33 achieves RXFP1 activation with a much simpler single-chain design. This makes it significantly easier and more cost-effective to synthesize. Preclinical research demonstrates potent anti-fibrotic, vasodilatory, and cardioprotective properties, positioning B7-33 as a promising therapeutic candidate for fibrotic diseases, heart failure, and vascular dysfunction.

Selectively activates RXFP1, the primary receptor for relaxin-2, triggering downstream signaling cascades that inhibit fibroblast activation and collagen deposition, promote extracellular matrix remodeling via increased matrix metalloproteinase (MMP) activity, enhance nitric oxide-mediated vasodilation, and reduce inflammatory cytokine expression. B7-33 appears to preferentially engage pERK1/2 signaling pathways while showing reduced cAMP activation compared to native relaxin-2, suggesting biased agonism at RXFP1.

Reduces myocardial fibrosis and collagen deposition, attenuating adverse cardiac remodeling in preclinical heart failure models.

Enhances nitric oxide-mediated vasodilation, reducing vascular resistance and improving blood flow in preclinical studies.

Demonstrates cardioprotective effects in animal models of heart failure, improving cardiac function and reducing fibrotic burden.

Inhibits fibroblast differentiation into myofibroblasts and reduces extracellular matrix deposition in multiple organ systems.

Mechanism

Reduces myocardial fibrosis and collagen deposition, attenuating adverse cardiac remodeling in preclinical heart failure models.

Research areas

B7-33 is a single-chain peptide analog of human relaxin-2 that selectively activates the relaxin family peptide receptor 1 (RXFP1). Unlike native relaxin-2, which requires a complex two-chain A/B structure connected by disulfide bonds, B7-33 achieves RXFP1 activation with a much simpler single-chain design. This makes it significantly easier and more cost-effective to synthesize. Preclinical research demonstrates potent anti-fibrotic, vasodilatory, and cardioprotective properties, positioning B7-33 as a promising therapeutic candidate for fibrotic diseases, heart failure, and vascular dysfunction.
Selectively activates RXFP1, the primary receptor for relaxin-2, triggering downstream signaling cascades that inhibit fibroblast activation and collagen deposition, promote extracellular matrix remodeling via increased matrix metalloproteinase (MMP) activity, enhance nitric oxide-mediated vasodilation, and reduce inflammatory cytokine expression. B7-33 appears to preferentially engage pERK1/2 signaling pathways while showing reduced cAMP activation compared to native relaxin-2, suggesting biased agonism at RXFP1.
Reduces myocardial fibrosis and collagen deposition, attenuating adverse cardiac remodeling in preclinical heart failure models.
Enhances nitric oxide-mediated vasodilation, reducing vascular resistance and improving blood flow in preclinical studies.
Demonstrates cardioprotective effects in animal models of heart failure, improving cardiac function and reducing fibrotic burden.
Inhibits fibroblast differentiation into myofibroblasts and reduces extracellular matrix deposition in multiple organ systems.
Shows protective effects against kidney fibrosis progression in preclinical disease models.

Research notes

Injection site reactions (redness, mild irritation)
Potential transient hypotension due to vasodilatory effects
Persistent or symptomatic hypotension (dizziness, lightheadedness, fainting)
Severe injection site reactions or signs of infection
Allergic reactions (rash, swelling, difficulty breathing)
Pre-existing hypotension or conditions exacerbated by vasodilation
Pregnancy or breastfeeding (no safety data available)
Concurrent use of potent antihypertensive agents without medical supervision
No human safety data exists -- all protocols are extrapolated from preclinical research
B7-33 reduces myocardial fibrosis, enhances vasodilation through nitric oxide pathway, and demonstrates cardioprotective effects in heart failure models. These anti-fibrotic and vasoprotective properties position it for potential use in cardiac remodeling, though all current data is preclinical.
No. B7-33 is teratogenic and contraindicated in pregnancy or potential pregnancy. The mechanisms affecting tissue remodeling and fibroblast function create theoretical teratogenic risk. No safety data exists for pregnant or breastfeeding women.

References

FAQs

Why is B7-33 easier to synthesize than native relaxin-2?

B7-33 is a single-chain peptide analog that retains RXFP1 activation while avoiding native relaxin-2's complex two-chain A/B structure connected by disulfide bonds. This simplified single-chain design is significantly easier and more cost-effective to synthesize while achieving equivalent biological activity.

Can B7-33 cause dangerous drops in blood pressure like other vasodilators?

Preclinical research suggests transient hypotension due to vasodilatory effects is possible. Users may experience symptomatic hypotension including dizziness or lightheadedness. Those with pre-existing hypotension or on antihypertensive medications must be cautious. No human data exists on hypotension incidence or management.