B7-33 Relaxin Analog
B7-33 is a single-chain peptide analog of human relaxin-2 (H2 relaxin), engineered as a 25-amino-acid linear peptide derived from the B-chain of native relaxin. Native relaxin is a two-chain disulfide-linked hormone produced primarily during pregnancy that mediates connective tissue remodeling, vasodilation, and anti-fibrotic signaling via the relaxin family peptide receptor 1 (RXFP1). B7-33 retains anti-fibrotic and pro-angiogenic activity but discards the cAMP-coupled vasodilatory and reproductive endocrine actions of full relaxin, producing a more focused therapeutic profile.
Inject any time of day. Reconstitute with bacteriostatic water. The 25-amino-acid linear peptide is more stable than disulfide-linked native relaxin - tolerates standard handling. Daily dosing is the typical research-community pattern given the relatively short half-life.
Start here. Every protocol below is ordered lowest-first. Begin at the smallest effective dose, hold about a week to assess tolerance, and step up only if needed.
B7-33 is a structurally simplified relaxin-2 analog that retains the binding affinity for relaxin family peptide receptor 1 (RXFP1) but produces biased signaling - favoring the ERK1/2 / TGF-β-antagonist / anti-fibrotic pathway over the cAMP-coupled vasodilatory and reproductive pathways of full-length relaxin.
B7-33 binds RXFP1, a G-protein coupled receptor expressed on cardiac fibroblasts, vascular smooth muscle, kidney mesangial cells, lung interstitial cells, and other connective tissue compartments.
B7-33 activates downstream pathways that antagonize TGF-β-driven fibroblast activation, reduce collagen I/III deposition, and promote matrix metalloproteinase (MMP) expression - net reducing extracellular matrix accumulation in chronically inflamed tissues.
Unlike full relaxin-2 (or serelaxin), B7-33 produces minimal cAMP elevation and minimal vasodilation. This eliminates the rapid hemodynamic effects (and side effects) of native relaxin while preserving the slower-onset structural anti-fibrotic action.
B7-33 maintains relaxin's pro-angiogenic effects via VEGF pathway signaling - useful in cardiac and renal repair contexts where neovascularization supports healing.
25-amino-acid linear peptide without the disulfide bridges of native relaxin - simpler synthesis and more stable in storage. No Met or Cys residues - chemistry-compatible with copper-conjugated peptides like GHK-Cu.
Week 1-4: minimal subjective effect. Anti-fibrotic action is silent at the cellular level.
Week 4-8: rodent-model fibrotic burden reductions emerge. Human translational data unavailable.
Week 8-12+: peak theoretical anti-fibrotic effect. Without imaging or biomarker monitoring, clinical effect in off-label use is hard to assess.
Each reference below was re-fetched from its PubMed record, and the quoted sentence was confirmed to appear in that abstract and to support the claim it sits under. Follow any of them to read the source.
Mechanism: B7-33 binds RXFP1 and preferentially activates pERK over cAMP, with downstream MMP-2 signaling.
Here we report the design and synthesis of a H2 relaxin B-chain-only analogue, B7-33, which was shown to bind to RXFP1 and preferentially activate the pERK pathway over cAMP in cells that endogenously expressed RXFP1.
Evidence scope. In vitro receptor pharmacology plus preclinical rodent fibrosis models; mechanism-only claim, no human data.
Route/dose boundary: mice received B7-33 subcutaneously at 0.25 mg/kg/day; this does not validate the card’s absolute 100 mcg/day dose.
Adult male 129sv mice were subjected to isoprenaline (ISO; 25 mg/kg/day, s.c)-induced cardiomyopathy, then s.c-treated with either RLX (0.5 mg/kg/day), B7-33 (0.25 mg/kg/day; equivalent dose corrected for MW) or perindopril (1 mg/kg/day) from days 7-14 post-injury.
Evidence scope. Mouse, subcutaneous, isoprenaline-induced cardiomyopathy model; explicitly not used to validate human dosing.
Claims we could not support
No abstract we checked supports these for this molecule at this route. That is not the same as saying they are false — it marks where the evidence is missing.
Exact dose: 100 mcg SubQ daily. Only weight-based preclinical SubQ dosing was found; no abstract supports the displayed absolute human dose.
Primary safety concern / human safety. No human administration abstract was found.
Plasma (estimated; human PK not characterized)
SubQ
Functional anti-fibrotic effect window
subQ ~70% (estimated)
Daily dosing typical for chronic anti-fibrotic effect
Renal/hepatic peptidase
Storage. Lyophilized vial: refrigerate (2-8°C / 36-46°F) or freeze (-20°C) for long-term storage. After reconstitution with bacteriostatic water: refrigerate, use within 21-28 days. The linear peptide structure (no disulfides) is relatively stable. Light-sensitive. Discard if cloudy, discolored, or contains particulates.
Not FDA-approved for any indication. Has not entered human clinical trials. All evidence is rodent preclinical. Available only as a research chemical from peptide-supply vendors. WADA prohibited under class S2 (peptide hormones, growth factors, related substances). Sale for human use is prohibited by FDA regulation. The related compound serelaxin (recombinant relaxin-2) reached Phase 3 for acute heart failure but failed (RELAX-AHF-2) and was withdrawn from development.
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