B7-33

B7-33 is a synthetic, single-chain peptide of 24 amino acids derived from the B-chain of human relaxin-2 (also called H2 relaxin or serelaxin). Natural relaxin-2 is a hormone with two chains and three disulfide bridges - hard and expensive to make. B7-33 is the attempt to strip that complex structure down to the minimum that still works at the relaxin receptor RXFP1.

The research focus is squarely on anti-fibrosis: the question of whether excessive scar and connective tissue in organs (heart, lung, kidney) can be pushed back in models. That is exactly what B7-33 was studied for in animal models.

One thing up front that runs through this whole entry: all of the data on B7-33 is preclinical. That means mice, rats and cell culture. There is not a single human study. B7-33 is a genuine experimental peptide, not a proven agent. This information is for research and educational purposes only. No medical recommendations.

B7-33 binds to RXFP1, the body's own receptor for relaxin-2. The interesting part: it is what's called a functionally selective agonist. Once activated, RXFP1 can trigger several signaling pathways - simplified, the cAMP pathway and the pERK pathway (ERK1/2). B7-33 shifts the balance preferentially toward pERK and barely triggers cAMP.

Why that matters in a research context: in the first description, the strong cAMP rise from relaxin-2 was linked to unwanted, tumor-promoting behavior. B7-33 largely bypasses that pathway - in the same paper it did not promote prostate tumor growth in a model, unlike full relaxin. The anti-fibrotic effect runs, preclinically, through RXFP1-AT2R receptor heterodimers and ultimately the collagen-degrading enzyme MMP-2.

And again, the reality anchor: all of this is described in cells, mice and rats. Whether and how this selective signaling profile transfers to humans is simply not studied.

Before you start, have everything ready:

B7-33 is a small, relatively short-lived peptide (in serum tests its half-life was very short, on the order of a few minutes). That is another reason nothing here is clearly established - working cleanly and keeping it cold is still mandatory.

The powder is dissolved with bacteriostatic water. How much water you use determines the concentration and therefore how many units you later draw on the insulin syringe for your dose.

Use the peptide calculator for exactly that: pick vial size and water volume to immediately see the concentration and units per dose. Because the relevant amounts are very small, a larger water volume tends to help - then each dose lands on a readable unit count instead of a tiny line.

Injection is subcutaneous, into the fat layer under the skin. Typical sites are the belly (avoid right around the navel), the front and the inner side of the thigh or the back of the upper arm.

Rotate the injection site every time.

The body of evidence is small but consistent - and entirely in animal or cell models:

• First description (Chemical Science 2016): B7-33 binds RXFP1, preferentially activates pERK over cAMP and prevented or reduced organ fibrosis in three rodent models (heart and lung). Unlike full relaxin, it did not promote prostate tumor growth.
• Heart attack model (JAHA 2020): In mice after ischemia-reperfusion, B7-33 reduced infarct size and preserved cardiac pump function better than vehicle - via an ERK1/2-dependent mechanism.
• Cardiomyopathy model (Biomedicine & Pharmacotherapy 2023): B7-33 reduced left ventricular fibrosis faster than the established ACE inhibitor perindopril and retained further cardioprotective effects of relaxin.
• Vascular model (Eur J Pharmacol 2017): In rat and mouse vessels, B7-33 replicated the vasoprotective effects of serelaxin.

It sounds promising - but every single result comes from rodents or cell culture. What happens in humans, nobody knows. Set expectations honestly.

There is no reliable human side-effect profile, because there are no human studies. Everything that can be said here is speculation based on the mechanism and on experience with the related relaxin.

• Relaxin and its analogs are vasodilatory - theoretically conceivable would be effects on blood pressure, dizziness or skin flushing.
• As with any subcutaneous injection: local reactions at the site (redness, tenderness).
• Peptides can generally trigger immune or allergic reactions.

Because hard safety knowledge is missing, this counts double: conservative and cautious. When in doubt, restraint is the more honest choice.

B7-33 is one of those compounds where the mechanism story is clean and elegant - a single-chain mini-relaxin that selectively switches on only the favorable pathway - while transferability to humans stays completely open. It is a tool from the lab, not from the clinic.

Anyone looking into it should do so with the attitude that fits a pure research peptide: curiosity yes, cure promises no. There is nothing to suggest B7-33 does in humans what it did in the mouse.

The undissolved powder is robust, normal room temperature (around 20 to 25 degrees) is fine, ideally kept in the dark. Once mixed, it keeps for at least 4 to 6 months in the fridge (2 to 8 °C). The bacteriostatic water brings a preservative that keeps the dissolved form stable longer. As a small peptide, B7-33 is sensitive - avoid heat, direct light and repeated freeze/thaw cycles.