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B7-33

Aliases: B7-33 relaxin mimetic

Last verified: 2026-09-24

Research chemicalPreclinical evidencePeptidesLow interest

The short version

B7-33 is a typical nice idea from academic peptide engineering: isolate just the part of relaxin that does the antifibrotic job. The animal data are neat and consistent. But the context of the relaxin field is instructive: serelaxin, the 'proud' recombinant relaxin with strong preclinical and early clinical story, failed in the large randomized trial for acute heart failure — an effect seen in small studies did not reproduce. B7-33 is a step further removed: nothing human. Buying a B7-33 vial today is buying a 2014 hypothesis.

Identity & type

Molecular type
peptide
Molecular weight
~3 kDa
Origin
An engineered single-chain peptide based on relaxin's B-chain; related to serelaxin (recombinant relaxin that failed in phase 3).

Mechanism of action

A single-chain relaxin mimetic — an RXFP1 receptor agonist that in animal models of fibrosis and heart activates the cAMP/CREB pathway and reduces TGF-beta1-mediated fibroproliferation; designed to retain the antifibrotic effect without the hypotensive action of full relaxin.

not confirmed in humans

Dosing & routes

Official / clinical context

No official context exists.

Regulator-approved labeling and published study designs — never a recommendation.

Community-reported practice

Very rare in the community; occasionally in 'cardioprotective' stacks by analogy with BPC-157. No reported measurements.

Unverified self-reports. Not medical advice. Not endorsement.

Protocol — official vs community

Official / label

No approved protocol exists — preclinical agent. B7-33 has only animal-model data (fibrosis and cardiac models, µg/kg ranges); no human dose has ever been defined.

Duration:

It is designed to keep relaxin's antifibrotic effect while dropping its hypotensive action — a design goal demonstrated in animals, not people.

Community (anecdotal)

Structured protocol data for this entry is coming.

Human evidence

None. No registered human trial.

Preclinical evidence

A solid mechanistically coherent series of animal studies — but context matters: the closer relative serelaxin failed in a large phase 3 (RELAX-AHF), showing how far preclinical fibrosis work must travel to become clinical proof.

Known risks

  • Everything unknown — no human datatheoretical
  • Unverified qualitycharacterized

Teal: characterized in clinical/labeling contexts. Amber: theoretical or reported outside controlled settings.

Unknowns & evidence gaps

  • Everything — from pharmacokinetics to effect

Frequently asked questions

References

  1. B7-33 antifibrotic program — preclinical studies (Monash/Baker institutes)
  2. RELAX-AHF phase 3 — serelaxin in acute heart failure (negative), context for the relaxin class