B7-33

Anti-VEGFR2 therapy activates CAFs, inducing excessive ECM deposition that limits antiangiogenic efficacy in CCA.; B7-33-SNPs competitively bind pro-angiogenic ligands via angiogenic factor receptors and carry B7-33 peptide to induce fibroblast quiescence.; The nanovesicles synergistically disrupt CAF-angiogenesis crosstalk, reducing microvessel density and fibrotic deposition.; Tumor growth inhibition rate reached 67.7% with simultaneous targeting of stromal desmoplasia and vascular niches.

SPION-RLX was likely phagocytosed by RXFP1-expressing dendritic cells, enabling systemic transport and oral efficacy.; Oral SPION-RLX or SPION-B7-33 every 72 hours for 4 weeks outperformed perindopril in anti-fibrotic effects.; Single-cell transcriptomics suggested phagosomal uptake via scavenger receptors on dendritic cells.; Conjugation to glycinated SPIONs allowed peptide circumnavigation of the gut and prolonged activity.

B7-33, a single-chain peptide derived from H2 relaxin B-chain, showed poor affinity in HEK cells but equivalent potency to H2 relaxin in fibroblasts.; B7-33 demonstrated anti-fibrotic effects in preclinical animal studies.; Aib substitution and hydrocarbon stapling were used to recreate native peptide helicity in the minimal scaffold.

B7-33, a single-chain relaxin agonist, has a short in vitro serum half-life of ~6 minutes.; Fatty-acid conjugation with appropriate spacer length extended the half-life to 60 minutes.; The lipidated B7-33 retained its activity while improving stability.

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 did not reduce fibrosis or hypertrophy.; B7-33 provided more rapid anti-fibrotic effects compared to perindopril.

H2-relaxin and B7-33 reduced mechanical and thermal sensitivity in CFA-inflamed paws at 30 minutes postinjection.; The RXFP1 antagonist B-R13/17K-H2 blocked mechanical but not thermal analgesia.; RXFP1 mRNA was expressed in excitatory neurons of the claustrum, cingulate cortex, and subiculum.; Relaxin-immunoreactive neurons in forebrain and midbrain projected to RXFP1-rich regions like claustrum and cingulate cortex.

All three methods (SHG, MTS, IHC) confirmed significantly increased renal fibrosis after 7 days in UUO-injured mice.; Only the HistoIndex platform detected a significantly increased collagen-to-tissue cross reticulation ratio in UUO-injured mice (P < .001 vs sham).; In treated UUO mice, the HistoIndex platform showed that drug-induced prevention of fibrosis correlated with reduced collagen fiber thickness and cross-reticulation ratio, but increased fiber counts.; Relaxin or B7-33 treatment increased renal MMP-2 and reduced TIMP-1 levels (P < .01 vs UUO alone).

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 decreased GRP78 expression under simulated ischemia-reperfusion.; B7-33 attenuated tunicamycin-induced GRP78 upregulation in an ERK1/2-dependent manner.

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 engagement, B7-33 retains RXFP1 agonism while exhibiting reduced off-t

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.