B7-33
preclinicalAlso known as: H2-relaxin analog B7-33
**Mechanism of Action** B7-33 is a single-chain analog of human relaxin-2 (H2-relaxin) engineered to selectively activate the relaxin family peptide receptor 1 (RXFP1). Unlike native H2-relaxin, which requires a two-chain structure for full receptor binding and signaling, B7-33 retains RXFP1 agonism while lacking the complex conformational requirements of the parent hormone. Activation of RXFP1 by B7-33 triggers downstream anti-fibrotic pathways, including inhibition of TGF-β1 signaling, suppression of collagen deposition, and promotion of matrix metalloproteinase activity, thereby reducing extracellular matrix accumulation in fibrotic tissues. **Key Research Findings** Preclinical studies (15 PubMed-indexed references) demonstrate that B7-33 attenuates fibrosis in multiple organ systems, including cardiac, renal, and pulmonary models. In rodent models of myocardial infarction and hypertensive heart disease, B7-33 reduced cardiac fibrosis and improved diastolic function without significant hemodynamic effects. Similarly, in models of renal fibrosis (e.g., unilateral ureteral obstruction), B7-33 decreased interstitial collagen and preserved renal architecture. Notably, B7-33 exhibits a shorter half-life and reduced off-target vasodilation compared to native relaxin, suggesting an improved safety profile for chronic fibrotic conditions. **Clinical Relevance** B7-33 remains in preclinical development, with no human trials reported to date. Its potential lies in treating fibrotic diseases such as heart failure with preserved ejection fraction, chronic kidney disease, and idiopathic pulmonary fibrosis, where current therapies are limited. The simplified structure may enable easier synthesis and formulation compared to native relaxin, but further validation of efficacy, dosing, and long-term safety in animal models is required before advancing to clinical testing. For research purposes only — not medical advice.
Key data
Research & studies
B7-33 and relaxin equivalently reduced left ventricular fibrosis, inflammation, and cardiomyocyte hypertrophy.; B7-33 and relaxin restored blood vessel density and aortic contractility.; Perindopril lowered systolic blood pressure and reduced inflammation and vascular rarefaction but not fibrosis or hypertrophy.; B7-33 provided more rapid anti-fibrotic effects compared to perindopril.
B7-33 reduced infarct size from 45.32% to 21.99% at 24 hours post-injury.; B7-33 preserved fractional shortening at 24 hours and 7 days post-myocardial infarction.; In vitro, B7-33 improved cardiomyocyte survival and reduced GRP78 expression after simulated ischemia-reperfusion.; B7-33 attenuated tunicamycin-induced GRP78 upregulation in an ERK1/2-dependent manner.
Frequently asked questions
What is B7-33?
**Mechanism of Action** B7-33 is a single-chain analog of human relaxin-2 (H2-relaxin) engineered to selectively activate the relaxin family peptide receptor 1 (RXFP1). Unlike native H2-relaxin, which requires a two-chain structure for full receptor binding and signaling, B7-33 retains RXFP1 agonism while lacking the c
How does B7-33 work?
Single-chain relaxin-2 analog that activates RXFP1 to reduce organ fibrosis without the full hormone's complexity.
What is the research status of B7-33?
B7-33 is currently classified as preclinical, with 15 research references on record. This is for research purposes only and is not medical advice.
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