Educational guide
B7-33 Overview, Dosing & Safety | Peptide Database
B7-33 (Relaxin) Relaxin-2 Analog | Anti-Fibrotic & Cardiovascular Community Research Join others researching B7-33 — share findings, ask questions, and learn from real experiences B7-33 is a single-chain peptide analog of human relaxin-2 that selectively activ
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B7-33 (Relaxin)
Relaxin-2 Analog | Anti-Fibrotic & Cardiovascular
Community Research
Join others researching B7-33 — share findings, ask questions, and learn from real experiences
B7-33 is a single-chain peptide analog of human relaxin-2 that selectively activates the relaxin family peptide receptor 1 (RXFP1). Unlike native relaxin-2, which requires a complex two-chain A/B structure connected by disulfide bonds, B7-33 achieves RXFP1 activation with a much simpler single-chain design. This makes it significantly easier and more cost-effective to synthesize. Preclinical research demonstrates potent anti-fibrotic, vasodilatory, and cardioprotective properties, positioning B7-33 as a promising therapeutic candidate for fibrotic diseases, heart failure, and vascular dysfunction.
Selectively activates RXFP1, the primary receptor for relaxin-2, triggering downstream signaling cascades that inhibit fibroblast activation and collagen deposition, promote extracellular matrix remodeling via increased matrix metalloproteinase (MMP) activity, enhance nitric oxide-mediated vasodilation, and reduce inflammatory cytokine expression. B7-33 appears to preferentially engage pERK1/2 signaling pathways while showing reduced cAMP activation compared to native relaxin-2, suggesting biased agonism at RXFP1.
Molecular Data
Complex or non-standard sequence format
Research Indications
Reduces myocardial fibrosis and collagen deposition, attenuating adverse cardiac remodeling in preclinical heart failure models.
Enhances nitric oxide-mediated vasodilation, reducing vascular resistance and improving blood flow in preclinical studies.
Demonstrates cardioprotective effects in animal models of heart failure, improving cardiac function and reducing fibrotic burden.
Inhibits fibroblast differentiation into myofibroblasts and reduces extracellular matrix deposition in multiple organ systems.
Shows protective effects against kidney fibrosis progression in preclinical disease models.
Dosing Protocols
Subcutaneous injection is the primary route studied in preclinical research. Dosing protocols are based on animal model data and have not been validated in human trials.
Anti-fibrotic / Cardiovascular support
100-250 mcg
1x daily
SubQ
Reconstitution Instructions
Bacteriostatic water (BAC)
Insulin syringes (0.5-1 mL)
Alcohol swabs
Peptide vial
Sterile work surface
1 Clean work area and hands thoroughly
2 Calculate required BAC water volume using calculator
3 Draw BAC water into syringe
4 Inject slowly down vial side (not directly onto powder)
5 Gently swirl until dissolved (never shake)
6 Store in refrigerator, use within 28 days
Interactions
What to Expect
Side Effects & Safety
Common Side Effects
Injection site reactions (redness, mild irritation)
Potential transient hypotension due to vasodilatory effects
Stop Signs - Discontinue if:
Persistent or symptomatic hypotension (dizziness, lightheadedness, fainting)
Severe injection site reactions or signs of infection
Allergic reactions (rash, swelling, difficulty breathing)
Contraindications
Pre-existing hypotension or conditions exacerbated by vasodilation
Pregnancy or breastfeeding (no safety data available)
Concurrent use of potent antihypertensive agents without medical supervision
No human safety data exists -- all protocols are extrapolated from preclinical research
Quality Checklist
Good Signs
White to off-white lyophilized powder
Clear solution after reconstitution with no particles
Intact vacuum seal on vial
Warning Signs
Slight clumping that dissolves with gentle swirling (may occur from shipping)
Bad Signs
Discolored or wet powder indicating degradation
Cloudy solution, visible particles, or precipitates after reconstitution
Broken or missing vacuum seal
Frequently Asked Questions
Why is B7-33 easier to synthesize than native relaxin-2?
B7-33 is a single-chain peptide analog that retains RXFP1 activation while avoiding native relaxin-2's complex two-chain A/B structure connected by disulfide bonds. This simplified single-chain design is significantly easier and more cost-effective to synthesize while achieving equivalent biological activity.
What are the cardiovascular benefits of B7-33 compared to other compounds?
B7-33 reduces myocardial fibrosis, enhances vasodilation through nitric oxide pathway, and demonstrates cardioprotective effects in heart failure models. These anti-fibrotic and vasoprotective properties position it for potential use in cardiac remodeling, though all current data is preclinical.
Can B7-33 cause dangerous drops in blood pressure like other vasodilators?
Preclinical research suggests transient hypotension due to vasodilatory effects is possible. Users may experience symptomatic hypotension including dizziness or lightheadedness. Those with pre-existing hypotension or on antihypertensive medications must be cautious. No human data exists on hypotension incidence or management.
Is B7-33 safe in pregnancy given its anti-fibrotic effects?
No. B7-33 is teratogenic and contraindicated in pregnancy or potential pregnancy. The mechanisms affecting tissue remodeling and fibroblast function create theoretical teratogenic risk. No safety data exists for pregnant or breastfeeding women.
References
Identified B7-33 as a single-chain relaxin analog that selectively activates RXFP1, demonstrating that a simplified single-chain peptide can replicate key signaling functions of native two-chain relaxin-2.
B7-33 reduced fibrosis markers in both liver and kidney fibrosis models, demonstrating organ-protective anti-fibrotic effects comparable to native relaxin-2 despite its simplified structure.
Comprehensive review of RXFP1 as a drug target, discussing relaxin-2 and analogs including B7-33 for cardiovascular, fibrotic, and reproductive indications.
B7-33 replicated the vasoprotective and anti-fibrotic effects of native relaxin in mouse models, reducing vascular stiffness and improving cardiovascular outcomes.
Reviews the anti-fibrotic mechanisms of relaxin/RXFP1 signaling, including inhibition of TGF-beta-driven fibroblast activation and collagen synthesis, with implications for simplified analogs like B7-33.
Related Peptides
Potential synergistic effects for cardiac protection; both target complementary pathways involved in cardiac remodeling and fibrosis.
No known negative interactions; different mechanisms of action with complementary tissue-repair and anti-fibrotic properties.
Disclaimer
This information is for educational and research purposes only. Consult a healthcare professional before use.