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…
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, nitric oxide-mediated vasodilation, and reduce…
Reduces myocardial fibrosis and collagen deposition, attenuating adverse cardiac remodeling in preclinical heart failure models.
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.
Mechanism
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…
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, nitric oxide-mediated vasodilation, and reduce…
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…
- 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, nitric oxide-mediated vasodilation, and reduce…
- Reduces myocardial fibrosis and collagen deposition, attenuating adverse cardiac remodeling in preclinical heart failure models.
- 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.
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)
References
- pubmed.ncbi.nlm.nih.gov/29378218/
- pubmed.ncbi.nlm.nih.gov/28058093/
- pubmed.ncbi.nlm.nih.gov/31789427/
- pubmed.ncbi.nlm.nih.gov/28500779/
- pubmed.ncbi.nlm.nih.gov/27838392/
Questions
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 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.