B7-33
RXFP1 receptor agonist. Selectively activates the pERK pathway, degrading excessive collagen (fibrosis) without causing systemic vasodilation (which caused tumours with the original Relaxin).
- Reversal of fibrosis (internal scarring)
- Improved heart function (post-infarction)
- Treatment of liver/pulmonary fibrosis
- Superior vascular safetyReversal of fibrosis (internal scarring)
- Superior vascular safety
- Unknown in humans.
- Local irritation.Unknown in humans.
- Local irritation.
B7-33 is a functional short-chain peptide derived from human Relaxin-2, specifically designed to isolate the anti-fibrotic and vasodilatory properties without the unwanted hormonal effects of full relaxin.
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What it is (in plain language)
- It is an 'anti-scarring' agent for the internal organs. B7-33 helps reverse and prevent fibrosis (the hardening of tissues) in the heart, lungs and kidneys. It signals the body to break down excessive collagen that accumulates after injuries or chronic inflammation, restoring tissue elasticity.
Why do you appear online so much
- It is one of the greatest promises for cardiovascular health and organ longevity. Biohackers and researchers are focusing on it as a tool for reversing damage to the myocardium after heart attacks or for treating the arterial stiffness associated with ageing, being much safer than native relaxin.
How it is framed today (pragmatic view)
- 1) Evidence: Strong evidence in models of heart failure and chronic kidney disease. 2) Objective: Reversal of systemic fibrosis and protection of vital organs. 3) Risk: Excellent safety profile, but still restricted to advanced research contexts.
How to use this form
- See the references section to understand the mechanism of activation of the RXFP1 receptor.
- Quick profile (curated by Subject 157)
- Class: Repair
- Status: Verified
- Use case: Longevity
- Route: Injectable
- Tags: Injectable|Scar Tissue|Fibrosis
- Half-life: Short
- Start: Fast
- Duration: ~24 hours
- Mechanism (high level)
RXFP1 receptor agonist. Selectively activates the pERK pathway, degrading excessive collagen (fibrosis) without causing systemic vasodilation (which caused tumours with the original Relaxin).
- Evidence (what the literature covers)
RESEARCH RANGE (Experimental, Non-prescriptive):
Very positive animal studies.
Level of Evidence: C.
- Safety and harm-reduction (non-prescriptive)
Risks: Unknown in humans.
Local irritation.
Interactions: Antihypertensives (theoretical).
- References (anchors)
- Hossain, M. A. (2016) - B7-33, a functionally selective relaxin agonist - https://doi.org/10.1016/j.chembiol.2016.05.013
- PubMed:27345432
Note: Educational/research content. Does not constitute medical advice, diagnosis or prescription.
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