At a glance

Anti-fibrotic potential (preclinical)
Cardioprotection / reduced cardiac remodeling (preclinical)
Receptor-selective, tumor-sparing signaling (preclinical)
Unknown human safety / no clinical data
Research-chemical purity / sourcing risk
Very short half-life limits practical activity
BenefitSide effectHealth risk· more & brighter bars = stronger

Effects

  • Anti-fibrotic (preclinical): In rodent and in-vitro models, reduced scarring/fibrosis in heart, lung and kidney tissue with potency similar to H2 relaxin.[4][7][1]
  • Cardioprotective (preclinical): In mouse models of myocardial infarction and cardiomyopathy, B7-33 attenuated adverse cardiac remodeling and reduced left-ventricular fibrosis.[3][8]
  • MMP-2 upregulation: Increased activity of the collagen-degrading enzyme MMP-2 in cardiac fibroblasts and renal myofibroblasts, an effect blocked by an RXFP1-specific antagonist.[6][9]
  • Receptor-selective signaling: Activates pERK1/2 without the cAMP-linked vascular/proliferative effects of relaxin, and unlike relaxin did not promote prostate tumor growth in vivo (mice).[4][2]
Classification

Synthetic relaxin-2 B-chain peptide; RXFP1 biased agonist[2][3]

Development stage

Preclinical / research-only (no human trials)[5]

Active half-life

~6 min in vitro (serum)[10]

Route

Parenteral in studies — subcutaneous; intranasal in lung models[8][4]

Structure

26 amino acids, single chain[2]