B7-33
Relaxin-2 Analog · Anti-Fibrotic & Cardiovascular
Analog of human relaxin-2 built as a single chain, activating relaxin family peptide receptor 1 (RXFP1) selectively. Where native relaxin-2 depends on two chains, A and B, held together by disulfide bonds in a complex structure, B7-33 achieves the same RXFP1 activation from one simple chain — synthesis is far easier and far cheaper for it. Anti-fibrotic, vasodilatory, and cardioprotective properties are potent in preclinical research, which puts B7-33 forward as a promising therapeutic candidate for heart failure, fibrotic diseases, and vascular dysfunction.
Overview
Analog of human relaxin-2 built as a single chain, activating relaxin family peptide receptor 1 (RXFP1) selectively. Where native relaxin-2 depends on two chains, A and B, held together by disulfide bonds in a complex structure, B7-33 achieves the same RXFP1 activation from one simple chain — synthesis is far easier and far cheaper for it. Anti-fibrotic, vasodilatory, and cardioprotective properties are potent in preclinical research, which puts B7-33 forward as a promising therapeutic candidate for heart failure, fibrotic diseases, and vascular dysfunction.
RXFP1 — relaxin-2's primary receptor — is activated selectively, and the downstream cascades that follow hold back fibroblast activation and collagen deposition, push extracellular matrix remodeling through raised matrix metalloproteinase (MMP) activity, strengthen nitric oxide-mediated vasodilation, and lower inflammatory cytokine expression. Engagement of pERK1/2 signaling pathways appears preferential, with cAMP activation reduced relative to native relaxin-2, which points to biased agonism at RXFP1.
Research indications
What the compound has been studied for, grouped by body system. Effect size is the reported magnitude where it was measured — not a recommendation.
Cardioprotection appears in animal heart failure models, where cardiac function improves and fibrotic burden drops.
Myocardial fibrosis and collagen deposition both fall, which attenuates adverse cardiac remodeling in preclinical models of heart failure.
Nitric oxide-mediated vasodilation is strengthened; preclinical studies report lower vascular resistance and better blood flow.
Differentiation of fibroblasts into myofibroblasts is blocked, and extracellular matrix deposition falls across multiple organ systems.
Protection against the progression of kidney fibrosis appears in preclinical disease models.
- Class
- Single-chain peptide
- Research status
- Emerging
- Molecular weight
- 4000 Da
- Typical dose
- 100–250 µg
- Frequency
- Once daily
- Cycle length
- 4–8 weeks (preclinical extrapolation)
- Storage
- Lyophilized: freezer long-term. Reconstituted: 2-8 C for up to 28 days
Molecular data
- Type
- Single-chain peptide
- Molecular weight
- 4000 Da
Dosing reference
Doses reported in the literature and by suppliers. These are a record of what has been used in research — reference, never instruction.
| Context | Route | Amount | Frequency |
|---|---|---|---|
| Anti-fibrotic / Cardiovascular support | SubQ | 100-250 mcg | 1x daily |
Interactions
Cardiac protection may be synergistic here; complementary pathways in cardiac remodeling and fibrosis are targeted by both.
No negative interactions known; the mechanisms of action differ, with tissue-repair and anti-fibrotic properties that complement.
What to expect
Safety
Mechanistic flags — properties of the pathway, not observed adverse events.
- Reactions at the injection site — redness, mild irritation
- Transient hypotension possible, from the vasodilatory effects
- Hypotension that persists or turns symptomatic (dizziness, lightheadedness, fainting)
- Severe reactions where injected, or signs of infection
- Allergic reactions such as rash, swelling, or difficulty breathing
- Hypotension already present, or conditions that vasodilation exacerbates
- Pregnancy or breastfeeding (safety data absent)
- Potent antihypertensive agents used concurrently without medical supervision
- Human safety data do not exist; every protocol is an extrapolation from preclinical research
Quality checklist
What to confirm before trusting a batch of research material. A verification aid — not an endorsement of any supplier.
- Third-party Certificate of AnalysisIndependent lab · dated · lot-matched.
- HPLC purity ≥ 98%Reverse-phase trace included.
- Mass-spec confirms 4000 g/molMALDI-TOF or ESI-MS.
- Counterion stated (acetate ≫ TFA)TFA salts can confound bioassays.
- Endotoxin / sterility statementRelevant once reconstituted.
- Lyophilised · cold-chain shippedStored −20 °C, shipped on ice.
- Labelled “research use only”No therapeutic or dosing claims.
Recorded signals for this compound · 7
- ✓After reconstitution: solution clear, no particles
- ✓Vacuum seal on the vial intact
- ✓Lyophilized powder, white to off-white
- !Slight clumping that a gentle swirl dissolves (shipping can cause it)
- ×Powder discolored or wet, a sign of degradation
- ×After reconstitution: cloudiness, visible particles, precipitates
- ×Vacuum seal broken or absent
FAQ
Why is synthesis of B7-33 simpler than that of native relaxin-2?
As a single-chain peptide analog, B7-33 keeps RXFP1 activation but sidesteps the two-chain A/B structure of native relaxin-2, whose chains are joined by disulfide bonds. That simplification makes synthesis significantly easier and more cost-effective, and biological activity remains equivalent.
How do B7-33's cardiovascular benefits compare with those of other compounds?
Myocardial fibrosis is reduced, vasodilation is enhanced through the nitric oxide pathway, and cardioprotective effects appear in heart failure models. Anti-fibrotic and vasoprotective properties of that kind position it for potential use in cardiac remodeling, though all current data are preclinical.
Does B7-33 drop blood pressure dangerously, as other vasodilators can?
Preclinical research points to possible transient hypotension from the vasodilatory effects. Symptomatic hypotension, dizziness or lightheadedness included, may occur. Caution is required where hypotension already exists or antihypertensive medication is in use. Incidence and management in humans are undocumented.
Given the anti-fibrotic effects, is B7-33 safe during pregnancy?
No. Teratogenicity makes B7-33 contraindicated where pregnancy exists or may exist. The mechanisms acting on tissue remodeling and fibroblast function are the source of that theoretical teratogenic risk. Safety data are absent for women who are pregnant or breastfeeding.
References
- 1A single-chain peptide derived from the relaxin B-chain selectively activates RXFP1Hossain, M.A., et al. · Chemical Science · 2016
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.
Review · inferredPubMed 28058093 ↗ - 2B7-33 replicates the vasoprotective effects of relaxin in mouse models of cardiovascular diseaseMarshall, S.A., et al. · Annals of the New York Academy of Sciences · 2017
B7-33 replicated the vasoprotective and anti-fibrotic effects of native relaxin in mouse models, reducing vascular stiffness and improving cardiovascular outcomes.
Meta-analysisPubMed 28500779 ↗ - 3The role of relaxin and its receptor (RXFP1) in the pathogenesis and treatment of fibrotic diseasesSamuel, C.S., et al. · Molecular and Cellular Endocrinology · 2017
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.
In vitro · inferredPubMed 27838392 ↗ - 4The relaxin receptor as a therapeutic target -- perspectives from evolution and drug targetingBathgate, R.A.D., et al. · Pharmacology & Therapeutics · 2018
Comprehensive review of RXFP1 as a drug target, discussing relaxin-2 and analogs including B7-33 for cardiovascular, fibrotic, and reproductive indications.
Review · inferredPubMed 29378218 ↗ - 5The single-chain relaxin mimetic, B7-33, maintains anti-fibrotic activity in liver and kidney fibrosis modelsHossain, M.A., et al. · British Journal of Pharmacology · 2020
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.
ReviewPubMed 31789427 ↗