Description
B7-33 is a linear, single-chain 24-amino-acid peptide derived from the B-chain of human relaxin-2 (H2 relaxin). It belongs to the class of relaxin analogues and binds the relaxin family peptide receptor 1 (RXFP1), a G-protein-coupled receptor expressed on fibroblasts, endothelial cells and cardiomyocytes, among others. While native H2 relaxin has a complex two-chain structure with three disulfide bridges that complicates synthesis and stability, B7-33 reduces this scaffold to a single linear chain.
What makes the mechanism notable: in research, B7-33 is regarded as a functionally selective (biased) agonist. In cells that natively express RXFP1, it preferentially activates the pERK1/2 pathway, while the strong cAMP activation of native relaxin is largely absent. This cAMP activation is exactly what the literature associates with the tumor-promoting effects reported for the native hormone. The anti-fibrotic pathway of B7-33 is attributed in preclinical work to activation of RXFP1-angiotensin II type 2 receptor heterodimers, with downstream pERK1/2 signaling and upregulation of the collagen-degrading enzyme matrix metalloproteinase-2 (MMP-2).
Only preclinical pharmacokinetic data exist. The unmodified peptide has a very short residence time in serum (in vitro half-life of roughly 6 minutes), which is why research is exploring lipidated and nanoparticle-bound variants to extend stability. In animal models, B7-33 was administered subcutaneously. Notably, the peptide acts only weakly in HEK cells with artificially overexpressed RXFP1, yet shows relaxin-equivalent anti-fibrotic effects in fibroblasts with natural receptor density.
The central research findings come from rodent models of heart and lung. Studies suggest that, in a research context, B7-33 can reduce or reverse organ fibrosis across several preclinical models and that after experimental heart injury it favorably influenced infarct size and markers of cardiac function. In a cardiomyopathy model it reduced fibrosis faster than an established ACE-inhibitor comparator. All of these data come from animal models and cell culture. No robust human studies on B7-33 exist.
B7-33 is a research substance, intended solely for research and educational purposes. In the TPD catalog you can get B7-33 in 10-packs at 10mg per vial. This information is for research and educational purposes only. Not medical advice.
Studies
- A single-chain derivative of the relaxin hormone is a functionally selective agonist of RXFP1 - Chemical Science 2016: First description of B7-33; binds RXFP1, preferentially activates pERK over cAMP, reverses organ fibrosis across three preclinical rodent (heart/lung) models, mechanism via RXFP1-AT2R heterodimers and MMP-2. Preclinical.
- B7-33 attenuates myocardial infarction-related adverse cardiac remodeling in mice - Journal of the American Heart Association 2020: In a mouse ischemia-reperfusion model, B7-33 reduced infarct size and preserved cardiac function (fractional shortening) versus vehicle. Preclinical, animal model.
- Single-chain relaxin mimetic B7-33 reduces left ventricular fibrosis faster than perindopril in cardiomyopathy - Biomedicine & Pharmacotherapy 2023: In an isoprenaline cardiomyopathy model in mice, B7-33 lowered LV fibrosis equivalently to relaxin and faster than the ACE inhibitor perindopril. Preclinical, animal model.
- A lipidated single-B-chain derivative of relaxin improves in vitro serum stability - International Journal of Molecular Sciences 2023: Structure-activity study; fatty-acid conjugation extended the in vitro half-life from roughly 6 to 60 minutes without loss of activity. Preclinical, in vitro.
- Coatings releasing the relaxin peptide analogue B7-33 reduce fibrotic encapsulation - ACS Applied Materials & Interfaces 2019: B7-33-releasing implant coatings reduced capsule thickness by about 49% in a mouse foreign-body-reaction model. Preclinical, animal model.
Stack Notes
- BPC-157 addresses a different repair pathway (angiogenesis, fibroblast migration, tendon/tissue), while B7-33 in research targets RXFP1-mediated fibrosis breakdown. Mechanistically complementary in tissue-remodeling models.
- TB-500 (Thymosin B4) is associated in recovery research with cell migration and actin regulation. Pairing it with the anti-fibrotic RXFP1 pathway of B7-33 covers two separate axes of tissue modulation.
- GHK-CU is linked in the literature to collagen remodeling and matrix metalloproteinase modulation. Since B7-33 acts on collagen breakdown via MMP-2 in a research context, this is a mechanistically coherent remodeling combination.
- MOTS-C is a mitochondria-derived peptide with a research focus on metabolic and cellular stress pathways. As a complement to B7-33 in models that consider cardiovascular and metabolic strain together, it is mechanistically interesting.
- Tesamorelin addresses the GHRH axis and thus an entirely different pathway. In research stacks that look at tissue remodeling alongside the somatotropic axis, it is used as a complementary building block.
