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B7-33

F

lead outcome

Human evidence for any indication

grades vary by outcome ↓

Peptide

also called — B7-33 · single-chain relaxin analog · H2 relaxin B-chain derived peptide · INCI: none

anti-fibrotic (preclinical)RXFP1 / relaxin-receptor agonist

Reference entry — not sold here. A single-chain relaxin analog with an elegant anti-fibrotic design and rodent-only data. No human trials. No dosing published here.

In brief

B7-33 is a designed single-chain peptide derived from the B-chain of H2 relaxin, built to keep relaxin's anti-fibrotic activity while shedding the difficulties of the full two-chain protein. In rodent models it reduces fibrosis in heart, lung and kidney by acting as a biased agonist at the relaxin receptor RXFP1 — switching on the anti-fibrotic pathway while largely sparing the blood-pressure pathway. The design is genuinely elegant, and it sidesteps the disappointing clinical record of full-length relaxin (serelaxin). But there are no human studies of any kind — no trial, no pharmacokinetics, no safety data. A mechanistically interesting anti-fibrotic candidate, entirely untested in people.

Legal standing, by region

European Union

Not approved

No marketing authorisation; research chemical only.

United States

Not FDA-approved

Not FDA-approved; not a supplement; no clinical trials registered.

International

Approved nowhere

Approved in no jurisdiction for any indication.

Evidence, by outcome

How we grade →

An honest grade per outcome — drawn from the evidence, not any catalogue. Hype and undemonstrated marketing claims grade low.

OutcomeEvidence base · effectGrade

Human evidence for any indication

Any "research dose" is extrapolated from rodent studies, not a validated human protocol.

None. No clinical trial of B7-33 has been published or registered; no human pharmacokinetic, efficacy or safety data exist. · Nothing demonstrated in humans.

F

Anti-fibrotic effect in animal models (the lead claim)

Preclinical and concentrated in the originating research groups; anti- fibrotic candidates translate to humans poorly as a class.

A designed single-chain peptide derived from the B-chain of H2 relaxin, reported in rodent models to reduce fibrosis in heart, lung and kidney via the relaxin receptor RXFP1 and downstream ERK1/2-pMAD signalling, while avoiding relaxin's blood-pressure effects. · Consistent anti-fibrotic signal in animals.

C

RXFP1 receptor biased-agonism (mechanism)

Demonstrated within the originating programme; biased agonism in cells is not a human outcome.

Reported to act as a biased agonist at RXFP1 — activating the anti-fibrotic pMAD pathway while largely sparing the cAMP pathway linked to relaxin's hemodynamic effects. A specifically articulated design rationale. · Coherent, elegant mechanism in models.

C

Design advantage over full relaxin

A better-designed molecule is not a proven one, and the parent protein's clinical program was disappointing.

Full-length relaxin (serelaxin) failed to meet endpoints in acute heart failure (RELAX-AHF-2). B7-33 is a stable single-chain fragment designed to keep the anti-fibrotic activity without the full protein's manufacturing and hemodynamic complications. · Engineering rationale addresses relaxin's liabilities.

C

Safety

Rodent tolerability only; gray-market identity/purity risks apply.

No human data · Unknown in humans.

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Disclosure

Vallydia sells its own cosmetic serums, and some ingredients graded here belong to the same categories as those products. Grades are drawn from the published evidence by the method we publish, and applied to our own ingredients on the same terms — our copper-peptide serum is graded no more kindly than the peptides it competes with. We disclose the interest so you can weigh it.

Trade names shown here (for example Matrixyl, Argireline, Syn-Ake) are the property of their respective owners and are used only to identify the ingredient under discussion. Their appearance implies no affiliation with, or endorsement by, the proprietor.

Evidence changes

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The honest part

B7-33 has a sophisticated design — biased agonism at a relaxin receptor to isolate anti-fibrotic signalling — and a real, if single-source, rodent record. The honest limits are stage and translation: no human data at all, and anti- fibrotic candidates (including full relaxin itself) have a poor track record of reaching approval. Credit the design; do not mistake it for a therapy.

Identity

B7-33 is a single-chain peptide derived from the B-chain of H2 relaxin, the human hormone best known for softening connective tissue in pregnancy and for its anti-fibrotic signalling. Native relaxin is a two-chain, insulin-like protein that is awkward to manufacture and carries blood-pressure effects; B7-33 is the stripped-down, single-chain attempt to keep the useful half.

Mechanism (as proposed)

B7-33 is reported to act as a biased agonist at the relaxin receptor RXFP1. The elegance of the design is selectivity: it is said to activate the pERK1/2–pMAD pathway responsible for relaxin's anti-fibrotic effects while largely sparing the cAMP pathway tied to relaxin's hemodynamic (blood-pressure-lowering) actions. In rodent models of cardiac, pulmonary and renal fibrosis, it reduced scarring. The concept — isolate one arm of a receptor's signalling to keep the benefit and drop the liability — is exactly the kind of rational design that looks good on paper.

Reading the evidence honestly

Two facts frame B7-33 honestly. First, the anti-fibrotic record is preclinical and concentrated in the originating groups — consistent direction from a few labs, not broad replication. Second, and decisively, there are no human studies of any kind. It is also worth remembering that full-length relaxin (serelaxin) failed its major acute-heart-failure endpoint (RELAX-AHF-2), and anti-fibrotic drugs as a class translate to humans poorly. B7-33 has cleared a preclinical bar that its own parent protein could not turn into clinical success. Interesting design, unproven molecule.

Sources — 2 cited

01Hossain MA, Bathgate RA, et al. (B7-33, a single-chain functionally selective relaxin analog — design and anti-fibrotic activity in animal models.)

02RELAX-AHF-2 and serelaxin literature (full-length relaxin clinical context).

Updated 2026-08-07 (No clinical trial registered — re-check for any first-in-human study.)

Grades reflect the published evidence, not our interest. No dosing, reconstitution, or administration is published for research compounds — that restraint is deliberate.

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This site provides neutral scientific reference and sells only products lawful in your region. Nothing here is medical advice, a recommendation, or an offer to supply unapproved medicines. No dosing or administration is published for research compounds. Cosmetic peptides per Regulation (EC) 1223/2009. Unapproved injectable peptides are neither sold nor advertised in the EU (Directive 2001/83/EC, Title VIII). © 2026 Vallydia.