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B7-3326 residuesVIKLSGRELVRAQIAISGMSTWSKRSLEach bubble = one amino acid. Size = residue mass. Color = chemical class.Also known as: single-chain relaxin mimetic, RXFP1 biased agonist
Infarct size cut nearly in half. That's what B7-33 did in mouse hearts after ischemia-reperfusion injury, dropping damage from 45.3% to 22.0% in the Devarakonda 2020 study [1]. B7-33 is a single-chain relaxin-2 analog, a simplified version of the two-chain H2 relaxin hormone that costs a fraction to produce. It targets the RXFP1 receptor with biased agonism, activating pERK1/2 over cAMP. That matters because cAMP drove prostate tumor growth in relaxin studies; B7-33 avoids it. Zero human data exists. All dosing comes from rodent models. The 6-minute serum half-life is a real limitation, and twice-daily injections are likely the minimum for meaningful receptor engagement.
Infarct size dropped from 45.3% to 22.0% (P=0.02) in mice receiving B7-33 after cardiac ischemia-reperfusion. That single data point from Devarakonda and colleagues (n=8-10 per group)[1] captures why this peptide interests fibrosis researchers. B7-33 (CAS: not yet assigned; molecular formula derived from relaxin-2 B-chain residues 7-33) is a synthetic single-chain peptide first described in 2016 by Hossain's group at the Florey Institute and Monash University [2]. Native H2 relaxin requires two chains and three disulfide bonds, an insulin-like architecture that makes production expensive and difficult. B7-33 sidesteps all of that. It's a linear peptide, largely unstructured in solution, that folds into the correct conformation only when it contacts RXFP1. The mechanism is what separates B7-33 from its parent hormone. It preferentially activates pERK1/2 signaling over cAMP through RXFP1-AT2R heterodimers. This biased agonism drives collagen degradation via MMP-2 upregulation and suppresses TGF-beta1/Smad-mediated fibrosis. In mouse cardiomyopathy models, 7 days of B7-33 reversed left ventricular fibrosis faster than the ACE inhibitor perindopril [3]. It also replicated the vasoprotective effects of serelaxin in rat mesenteric arteries at equimolar doses [4]. The catch: roughly 11-13 papers exist, predominantly from one research group at Monash/Florey. Independent replication is minimal. No human has received B7-33 in any clinical or pharmacokinetic study. The in vitro serum half-life sits at approximately 6 minutes, and a lipidated derivative with 10x stability improvement [5] isn't commercially available. This is a preclinical research compound, full stop.
B7-33 binds RXFP1, a leucine-rich repeat-containing G protein-coupled receptor that normally responds to H2 relaxin. The difference is selectivity. Native relaxin activates both cAMP and pERK1/2 through RXFP1. B7-33 preferentially triggers pERK1/2 with minimal cAMP accumulation in cells that endogenously express the receptor. The anti-fibrotic pathway runs through RXFP1-AT2R heterodimers. When B7-33 engages these receptor complexes, downstream signaling activates protein phosphatases via pERK1/2. This cascade upregulates MMP-2, a collagen-degrading enzyme that breaks down excess extracellular matrix. At the same time, B7-33 suppresses TGF-beta1/Smad signaling. That blocks myofibroblast differentiation and stops new collagen deposition. The result is a two-pronged attack on fibrosis: clearing existing collagen while preventing new deposits. In blood vessels, B7-33 stimulates nitric oxide production through endothelial NOS activation. Smooth muscle relaxes. Blood pressure drops. This accounts for the vasoprotective effects confirmed in rat mesenteric artery preparations [4]. During ischemic injury, B7-33 also reduces endoplasmic reticulum stress and limits cardiomyocyte apoptosis. The biased signaling profile (pERK1/2 over cAMP) is the entire therapeutic premise; cAMP-mediated RXFP1 activation expanded prostate size by over 150% in mouse models with native relaxin. B7-33 showed no prostate growth effect [2].
Anti-fibrotic and cardioprotective in rodent models via RXFP1 biased agonism (pERK1/2 over cAMP). Reduces myocardial infarct size ~50% (45.3% → 22.0%), reverses established LV fibrosis faster than perindopril, replicates serelaxin vasoprotection. Zero human data.
Devarakonda et al. 2020 (PMID 32295457): mouse ischemia-reperfusion MI model; B7-33 reduced infarct size from 45.3% to 22.0% (P=0.02) and preserved fractional shortening at 7 days
~11-13 papers total, predominantly from one Monash/Florey Institute group with minimal independent replication; zero human PK or safety data; 6-min in vitro serum t½ limits SC exposure window; no in vivo PK published; lipidated formulation (10× stability improvement) not commercially available
No self-experimentation community exists for B7-33. Zero Reddit threads found (search: r/Peptides, r/nootropics, general Reddit). Discussed only in academic literature and occasionally in bodybuilding forums as a theoretical anti-fibrotic without reported personal use.
B7-33 has no community self-experimentation base. All data originates from academic preclinical research. The 6-min serum half-life and extreme niche status have prevented any measurable community adoption.
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 100mcg | Daily |
| Moderate | 250mcg | Daily |
| Aggressive | 500mcg | Daily |
Your first vial of B7-33 will likely be 2 mg. Add 2 mL of bacteriostatic water and you get 1 mg/mL (1000 mcg/mL). On a standard insulin syringe, 10 units equals 100 mcg (beginner dose) and 25 units equals 250 mcg (moderate dose). If you find a 5 mg vial, adding 2 mL gives you 2.5 mg/mL; then 100 mcg is 4 units and 250 mcg is 10 units. The thing most people miss with B7-33 is the dosing frequency. The 6-minute serum half-life means once-daily injection is almost certainly not enough. The published mouse protocol used 0.25 mg/kg twice daily, 12 hours apart. If you're only injecting once a day, you're probably not getting meaningful RXFP1 engagement throughout the day. Reconstituted B7-33 degrades fast at room temperature. Keep it at 2-8 degrees C and use it within 7-10 days. Prepare only the dose you need per session. The short half-life reflects real susceptibility to proteolysis; this isn't a peptide that tolerates sloppy storage. Request an HPLC/MS Certificate of Analysis from your vendor, 98% purity minimum. Degraded B7-33 looks identical to active peptide without mass spectrometry analysis.
No established cycling protocol exists for B7-33 in any species. Animal studies used continuous daily dosing for 7-14 day treatment windows (e.g., days 7-14 post-injury in cardiomyopathy models). The 8-on/4-off suggestion is a conservative placeholder based on general peptide cycling conventions. Researchers should follow study-specific dosing timelines.
No receptor desensitization, antibody formation, or tachyphylaxis data exists for B7-33 in any species. The 8-week on / 4-week off convention in peptides.ts is a conservative precautionary placeholder based on general peptide cycling conventions. Published animal studies used continuous dosing for 7-14 day treatment windows: no long-duration cycling studies have been conducted. Cycling is recommended as a safety precaution to allow monitoring breaks, not because tolerance has been observed.
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Expected: Unknown in humans. Mouse studies show measurable anti-fibrotic effect at 7-14 days. Human fibrosis resolution (via MMP-2 upregulation / TGF-β suppression) expected to require weeks to months.
Monitor: Monitor blood pressure: vasodilatory effects (NO-mediated eNOS activation) are expected. No other validated monitoring parameters exist for human use.
Gather your supplies: B7-33 vial (lyophilized), bacteriostatic water, alcohol swabs, insulin syringe (29-31 gauge).
For a 2 mg vial, add 2 mL of bacteriostatic water slowly down the side of the vial. Do not shake. Swirl gently until dissolved. This gives you 1 mg/mL (1000 mcg/mL).
At 1 mg/mL concentration: 100 mcg equals 10 units on an insulin syringe. 250 mcg equals 25 units. 500 mcg equals 50 units (half the syringe on a 100-unit insulin syringe).
Pull the plunger to the correct unit marking.
Pinch a fold of skin, insert the needle at a 45-degree angle, inject slowly. Rotate injection sites with each dose.
The published mouse protocol calls for dosing every 12 hours (twice daily). Morning and evening injections, roughly 12 hours apart, best approximate the validated animal schedule.
Store reconstituted vial at 2-8 degrees C immediately after use. Do not leave at room temperature. Use within 7-10 days. Discard if the solution becomes cloudy or shows particles.
Monitor blood pressure at baseline, after the first dose, and weekly. Sit or lie down for 10-15 minutes post-injection if you experience lightheadedness.
Oral dosing every 72h over 4 weeks showed anti-fibrotic efficacy ≥ perindopril in murine cardiomyopathy model (PMID 41382190). Standard unconjugated B7-33 has no oral bioavailability.
Requires conjugation to glycinated superparamagnetic iron oxide nanoparticles (SPION). Mechanism: phagocytosis by RXFP1-expressing dendritic cells enables sustained intracellular delivery. Not purchasable: research synthesis only. Do not attempt oral dosing with standard research-vendor B7-33.
In vitro half-life extended from 6 to 60 minutes via albumin binding (10× improvement, PMID 37047588). In vivo PK data not yet published.
Exists only in published Monash group synthesis protocols. No vendor sells this formulation. Standard B7-33 from research vendors is the only purchasable form.
Complementary anti-fibrotic mechanisms: BPC-157 promotes angiogenesis and GABAergic healing via non-RXFP1 pathways; B7-33 targets RXFP1-mediated MMP-2 collagen degradation. Theoretical synergy for cardiac or organ fibrosis context. No animal or human combination data exists.
Thymosin beta-4 promotes actin polymerization, angiogenesis, and tissue repair. Theoretical complementary stacking with B7-33 for cardiac remodeling. No combination data in any species.
B7-33 activates RXFP1-AT2R heterodimers, modulating the renin-angiotensin system. Additive hypotension risk and potentially altered AT2R signaling dynamics.
B7-33 upregulates endothelial NO via eNOS activation. Combined with nitrate donors, risk of excessive vasodilation and hypotensive crisis.
Do not combineOverlapping vasodilatory mechanisms. Additive blood pressure reduction; hypotension risk particularly at higher B7-33 doses.
No human has ever received B7-33 in a clinical setting. Every safety inference below comes from animal pharmacology or from the known profile of serelaxin (recombinant H2 relaxin), which targets the same receptor but with different signaling bias. Treat all of this as theoretical risk assessment, not documented adverse events. The primary pharmacological risk is hypotension. B7-33 activates endothelial NOS, producing nitric oxide and vasodilation. If you're on ACE inhibitors, ARBs, calcium channel blockers, or nitrate medications, additive blood pressure drops are a real concern. Serelaxin in human heart failure trials (RELAX-AHF) caused mild nausea, headache, and hypotension. B7-33's signaling profile differs, but RXFP1-mediated vasodilation is shared. The 6-minute in vitro serum half-life is actually a double-edged consideration for safety. Systemic exposure after each subcutaneous injection is brief, which may limit adverse effects. But it also means any sustained effect requires twice-daily dosing, doubling injection site exposure. Injection site reactions are expected with repeated subcutaneous administration of any research peptide. B7-33's immunogenicity is completely uncharacterized. Persistent nodules, erythema, or induration at injection sites warrant stopping. Long-term toxicology studies have not been published for B7-33 in any species. The total preclinical literature is roughly 11-13 papers, predominantly from one research group. MMP-2 upregulation (the anti-fibrotic mechanism) could theoretically affect vascular integrity if sustained at high levels; the interaction with anticoagulants is uncharacterized. Reproductive safety is unknown. Relaxin signaling plays a role in gestational physiology, and exogenous RXFP1 activation during pregnancy could disrupt normal processes. B7-33 is contraindicated in pregnancy and breastfeeding. For anyone with active malignancy: although B7-33 avoided prostate tumor promotion unlike native relaxin, the safety profile in cancer contexts is not established. The 6 papers showing no tumor growth were conducted in specific prostate models, not across cancer types. When to stop: symptomatic hypotension (dizziness, presyncope, lightheadedness), progressive injection site reactions, or any unexpected systemic symptoms. Given zero human safety data, the threshold for stopping should be low.
Verify B7-33 dosing and safety with a second opinion
Niche compound with a small vendor pool. The 6-min serum t½ means degraded peptide is functionally indistinguishable from active peptide without LC-MS analysis. Storage missteps before or during shipping directly impact dosing reliability. Independent third-party CoA availability varies by vendor.
| Test | When | Target |
|---|---|---|
| Blood pressure (manual cuff or ambulatory monitor) | Baseline, then after first dose, then weekly during the dosing period | Systolic >90 mmHg seated; stop use immediately if symptomatic hypotension occurs |
| Injection site assessment | Each injection; weekly visual inspection | — |
B7-33 promotes NO-dependent vasodilation via eNOS activation and RXFP1-AT2R signaling. Hypotension is the primary expected pharmacological risk in any human use context.
Repeated SC injections of an immunologically uncharacterized peptide carry unknown local reaction risk. Persistent nodules, erythema, or induration may indicate local immune response.
No observable effects expected at this stage; peptide exposure establishing in tissue. Based on animal model timelines.
In mouse MI models, measurable cardioprotection (reduced infarct size, preserved fractional shortening) was evident by day 7 post-treatment.
In cardiomyopathy models, 7 days of B7-33 treatment (days 7-14) reduced left ventricular fibrosis and inflammation, matching the efficacy of native relaxin.
Continued anti-fibrotic remodeling expected with sustained dosing; collagen degradation via MMP-2 upregulation is a gradual process.
In implant studies, 6 weeks of B7-33 release produced a 49% reduction in fibrotic capsule thickness. Maximum anti-fibrotic benefit likely requires sustained multi-week exposure.
Days 1-3, Establishing RXFP1 exposure: Don't expect to feel or see anything anti-fibrotic at this stage. Receptor occupancy starts with each dose, but tissue-level collagen remodeling hasn't begun. The one thing that is pharmacologically immediate is vasodilation from NO production. Some blood pressure reduction and warmth are plausible within hours of injection, especially at higher doses or if you're on antihypertensives. Days 3-7, Early cardioprotective window: In the mouse MI model [1], measurable cardioprotection was already evident by day 7 of treatment. Infarct size was reduced, fractional shortening preserved. Human timing is completely unknown and likely substantially longer. Injection site reactions may start appearing with repeated dosing. Weeks 1-2, Anti-fibrotic activity phase: The mouse cardiomyopathy study [3] treated animals from days 7-14 post-injury. Seven days of B7-33 significantly reduced left ventricular fibrosis and outperformed perindopril. Translating rodent fibrotic remodeling to human timelines is speculative; human fibrosis resolution occurs over weeks to months, not days. Immunogenicity risk (uncharacterized) increases with continued administration. Weeks 4-8, Sustained remodeling phase: The implant coating study [6] needed 6 weeks of continuous B7-33 release to achieve that 49.2% reduction in fibrotic capsule thickness. The oral nanoparticle study [7] dosed every 72 hours for 4 weeks and matched perindopril's anti-fibrotic efficacy. MMP-2-mediated collagen degradation is a gradual biological process. If B7-33 works in humans at all, the full effect likely requires sustained multi-week exposure that the 6-minute half-life makes challenging to achieve with standard subcutaneous injection.
Receptor occupancy begins with each dose. No measurable tissue-level anti-fibrotic effects expected at this stage based on mouse model timelines. Vasodilation (NO-dependent) is pharmacologically immediate.
No community data. Vasodilatory effects (warmth, mild blood pressure reduction) are theoretically plausible within hours of dosing.
In mouse MI (ischemia-reperfusion) models, measurable cardioprotection, reduced infarct size and preserved fractional shortening, was evident by day 7 post-treatment start (PMID 32295457). Timing in humans completely unknown.
No community data.
7 days of B7-33 in mouse isoprenaline-induced cardiomyopathy (treatment days 7-14 post-injury) significantly reduced LV fibrosis and inflammation, outperforming the ACE inhibitor perindopril (PMID 36753958). Human fibrotic remodeling occurs over weeks to months.
No community data.
PLGA implant coating studies showed 49.2% reduction in fibrotic capsule thickness at 6 weeks with continuous B7-33 release (PMID 31713411). MMP-2-mediated collagen degradation and TGF-β/Smad suppression are gradual biological processes. Nanoparticle oral dosing every 72h showed anti-fibrotic efficacy ≥ perindopril over 4 weeks in mice (PMID 41382190).
No community data. Human fibrosis resolution timelines are substantially longer than rodent models.
Source: In vitro serum half-life of ~6 minutes reported in Hossain et al. 2016 (PMID 30155023) and confirmed by Dantas de Lucas et al. 2023 (PMID 37047588). No in vivo PK data published.
Loading the interactive decay curve.
B7-33 is classified as a research-only compound. It has no FDA approval, no Investigational New Drug application on record, and no clinical trials registered in any jurisdiction as of April 2026. It is not approved for human therapeutic use anywhere in the world. B7-33 is available from select research chemical vendors (Peptide Sciences, BiotechPeptides, Core Peptides, NovoPro Labs) labeled "for research purposes only" or "not for human consumption." Purchase and possession for legitimate research purposes is legal in most jurisdictions, but self-administration falls outside any regulatory framework. No WADA status has been established for B7-33. Athletes subject to anti-doping testing should assume any unapproved research peptide carries disqualification risk. This content is provided for educational and informational purposes only. It does not constitute medical advice, diagnosis, or treatment recommendations. Consult a qualified healthcare provider before making any decisions regarding peptide research compounds.
Peptide Schedule Research TeamReviewed Apr 20269 Citations
