B7-33
A compound aimed at reducing scar-tissue buildup (fibrosis). A single-chain peptide derivative of relaxin, designed to retain anti-fibrotic activity without the cardiovascular side profile of full relaxin. Pre-clinical / early human research.
B7-33: A compound aimed at reducing scar-tissue buildup (fibrosis). A single-chain peptide derivative of relaxin, designed to retain anti-fibrotic activity without the cardiovascular side profile of full relaxin. Pre-clinical / early human research. B7-33 is a single-chain fragment of relaxin designed to keep the anti-fibrotic effect (good for hearts, kidneys, lungs) without dropping blood pressure (the side effect of full relaxin).
B7-33 is a single-chain fragment of relaxin designed to keep the anti-fibrotic effect (good for hearts, kidneys, lungs) without dropping blood pressure (the side effect of full relaxin). Pre-clinical only. Don't use this without medical oversight.
Who it's for
- →Researchers studying fibrotic disease pathways
- →Cardiovascular-research context only
- →Educational reference, not for community use
What to expect
- Week 1
No documented human user reports of acute effects.
- Week 4
Pre-clinical models show anti-fibrotic markers shifting around here.
- Week 8
No long term human data exists.
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How it works (mechanism)
Single-chain peptide derivative of relaxin that retains binding to relaxin receptor RXFP1 with anti-fibrotic signaling, but lacks the cardiovascular receptor crosstalk responsible for relaxin's hypotensive effect.
Dosing protocol
Stacks well with
Side effects
When NOT to use
- ⚠Hypotension or unstable cardiovascular status
- ⚠Pregnancy / nursing
- ⚠Anyone risk-averse to pre-clinical-only data
Common mistakes
- • Treating community-vendor B7-33 as research grade clinical material
- • Running it without published human safety data
- • Stacking it with anything else
What it actually is
B7-33 is a single-chain peptide built from relaxin, the hormone that softens connective tissue in pregnancy. Relaxin has strong anti-fibrotic effects — it reduces scar tissue formation — but it also drops blood pressure and is hard to manufacture. B7-33 was designed to keep the anti-fibrotic action in a simpler molecule. It is preclinical: zero human trials, and no human dosing protocol exists.
Fibrosis is scar tissue replacing functional tissue, and it is what makes chronic damage to heart, lung, liver or kidney permanent. Relaxin acts on the RXFP1 receptor and biases signalling away from the pathways that lay down collagen. B7-33 is a fragment engineered to keep that biased signalling. In animal models it reduces fibrosis in heart and lung. Nothing about that has been tested in a person, and the peptide's measured stability is poor enough that how it would be delivered is itself unresolved.
Forms, and which is which
Everything published is preclinical. There is no human protocol, and per-kilogram animal doses are not directly translatable to people.
Verdict: The honest description of where this compound is.
The native peptide has a measured in-vitro half-life of about six minutes; a lipidated version extends that. No in-vivo pharmacokinetics in humans exist for either.
Verdict: A chemistry fix to an unsolved delivery problem.
Buyer reconstitutes a compound with no human dosing basis and no identity assurance.
Verdict: Unverified material, no protocol to follow even if it were genuine.
Full relaxin went through large heart failure trials and did not meet its endpoints.
Verdict: The parent molecule's clinical programme did not succeed.
What it is claimed to do, graded
Demonstrated in animal models of cardiac and renal fibrosis. Zero human trials, zero randomised trials.
A 2023 paper reports it maintains cardioprotection in a model system. Model-system evidence.
The design intent. Untested in people, and hypotension remains listed as a theoretical effect.
No human protocol exists at all. Anyone selling a dosing schedule invented it.
Grades describe how much human evidence exists for that specific claim, not whether it will work for you or whether it is safe.
Pros and cons
- • The anti-fibrotic target is genuinely important — fibrosis is what makes organ damage permanent
- • Relaxin biology is well characterised and the receptor biology is real
- • Simpler and cheaper to manufacture than full relaxin, which was a real obstacle
- • Zero human trials — grade D on the site's own ladder and preclinical in reality
- • No human dosing protocol exists, so any dose being sold was made up
- • Measured half-life of around six minutes for the native peptide
- • Theoretical hypotensive effect, which is the relaxin family's known problem
- • The full-length parent, serelaxin, failed its large clinical trials
When to stop
- • Lightheadedness, faintness or a measured blood pressure drop
- • Injection-site reaction that spreads
- • Honestly: before starting, given there is no human dosing basis at all
Interactions
The relaxin family lowers blood pressure. Additive hypotension is the predictable concern.
Same direction, compounded.
Relaxin is a pregnancy hormone with major effects on connective tissue. Introducing an analog is entirely unstudied.
There is no human interaction literature whatsoever for this compound.
Absence of documented interactions here reflects absence of study, not safety.
Is this for you?
- • Laboratory research. There is no human context for this compound yet
- • You have low blood pressure or unstable cardiovascular status
- • You are pregnant or nursing
- • You want a dose you can trust — none exists
The one number
Sources for the claims above
- Maintains the cardioprotective effects of relaxin in a model system
- Single-chain peptide agonists of relaxin receptors
- Peptide design and delivery context
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Tracked alongside B7-33
Same goal, different aisle — each graded on its own evidence in the Pepdex catalog.
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