B7-33

guinea pig

Also seen as: H2 relaxin B(7-33), relaxin B-chain 7-33, B7 33, B733

The Dose Guy’s verdict

Sep 1, 2026
5 sources

B7-33 is the most interesting anti-fibrotic peptide nobody has tested in a human. The animal work on tissue remodeling is genuinely good, across multiple models and labs, and the mechanism is clean. But zero human trials, zero human safety data, and a short-lived molecule with no human pharmacokinetics make this a research compound, not something I can tell you to run. If fibrosis is your actual concern, that is a conversation with a cardiologist or rheumatologist, not a vial.

Would I take it?Not yet. The science needs a person, not another mouse.

What it is

A single-chain peptide built from the B-chain of human relaxin-2, designed to hit the relaxin receptor RXFP1 in a biased way. Full-length relaxin activates multiple downstream signals. B7-33 preferentially drives the ERK pathway, the one tied to breaking down collagen and remodeling fibrotic tissue, while largely skipping the cAMP arm. That selectivity is the entire pitch: the anti-fibrotic upside of relaxin without the rest of the hormone’s profile.

It sits apart from the Khavinson bioregulator family that fills most of this shelf, led by epitalon. B7-33 came out of modern Australian peptide chemistry, and its evidence base is animal pharmacology, not Soviet-era gerontology. The closest clinical comparison is relaxin-2 itself, which failed its heart-failure program. B7-33 is a stripped-down second attempt at the same idea.

What the research shows

No human trials. Zero. Everything below is animal or in-vitro work. Read it as “interesting,” not “evidence it works in you.”

All animal and in-vitro work. No human study of any kind:

In mice after cardiac ischemia and reperfusion, B7-33 reduced infarct size to 21.99% versus 45.32% with vehicle at 24 hours, p=0.02.JAHA 2020 · mouse ischemia-reperfusion

In male mice with isoprenaline-induced cardiomyopathy, B7-33 at 0.25 mg/kg/day reduced left ventricular fibrosis after treatment from days 7 through 14, while perindopril at 1 mg/kg/day did not.Biomed Pharmacother 2023 · mouse cardiomyopathy

In mice, subcutaneous implants releasing B7-33 had 49.2% less capsule thickness over 6 weeks than coated implants without the peptide.ACS Appl Mater Interfaces 2019 · mouse implant

Unmodified B7-33 had an in vitro serum half-life of approximately 6 minutes. Fatty-acid conjugation with an appropriate spacer increased it to 60 minutes.IJMS 2023 · in vitro serum stability

Unlike human relaxin-2, B7-33 did not promote prostate tumor growth in the in vivo model reported in its discovery study.Sci Adv 2016 · discovery · prostate tumor model

No human trial, case series, or safety study exists for B7-33.as of Aug 2026

Realistic protocols

I am not writing a dosing protocol for a peptide with no human pharmacokinetics. In vitro, unmodified B7-33 degrades in minutes, and the lipidated version that lasts longer has not left the bench. Nobody has worked out a route, a dose, or a formulation that survives long enough to matter in a person. If you source B7-33 and run it anyway, treat yourself as the experiment: go low, go short, log everything, and understand that you are genuinely in unmapped territory.

Side effects

No human has been dosed in a published study and no meaningful community run reports exist, so this is mechanism-informed guesswork:

unknownZero human safety data. In the animal data, B7-33 did not promote tumor growth in a prostate cancer model, unlike full-length relaxin-2, but that is one check in one species. The long-term consequences of modulating tissue remodeling in a person are genuinely unknown.

Where to buy

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