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Peptide Profile

Relaxin

Relaxin-2 · RLN2 · H2 relaxin · human relaxin

Relaxin (relaxin-2; serelaxin; RLX030) is a 53-residue two-chain polypeptide hormone structurally related to insulin, produced primarily by the corpus luteum during pregnancy and by the heart during cardiac stress, that acts…

Reproductive & HormonalInvestigationalResearch Only
Half-life
~7–8 h (terminal, serelaxin/rh-relaxin-2)
Routes
subcutaneous, intravenous

Educational research information — not medical advice. Review primary sources and consult a qualified professional before any decision.

Educational research tools — not medical advice.

Overview

What Relaxin is

About Relaxin

Binds RXFP1 receptor, activating adenylyl cyclase and cAMP/PKA pathway. Upregulates matrix metalloproteinases (MMPs) to degrade excess collagen. Inhibits TGF-β fibrotic signaling. Promotes cervical softening and pelvic ligament compliance.

Relaxin (relaxin-2; serelaxin; RLX030) is a 53-residue two-chain polypeptide hormone structurally related to insulin, produced primarily by the corpus luteum during pregnancy and by the heart during cardiac stress, that acts through RXFP1 receptors to promote vasodilation, reduce systemic vascular resistance, increase renal perfusion, and attenuate fibrotic signaling — properties that made it a compelling candidate for acute decompensated heart failure, where peripheral vasoconstriction and organ hypoperfusion are central pathophysiological features. RXFP1 activation stimulates cAMP/PKA and nitric oxide signaling to acutely reduce systemic and renal vascular resistance, increase cardiac output without directly affecting heart rate, and suppress TGF-beta-mediated fibrotic remodeling; these hemodynamic and organoprotective mechanisms distinguished relaxin mechanistically from existing vasodilators and diuretics. The RELAX-AHF Phase 3 randomized controlled trial, published in The Lancet (2013), demonstrated that serelaxin significantly improved dyspnea and reduced cardiovascular mortality at 180 days versus placebo in acute heart failure patients; however, the subsequent confirmatory RELAX-AHF-2 Phase 3 trial failed to meet its co-primary endpoint of cardiovascular death reduction, and regulatory applications in the US and Europe were not approved. Serelaxin has no FDA approval and no approved indication in any jurisdiction; the clinical development program was discontinued following the RELAX-AHF-2 results; endogenous relaxin and its RXFP1 pathway remain active areas of basic research in fibrosis biology and obstetric physiology, but no injectable formulation is currently available outside of clinical trials.

Relaxin Benefits & Research Areas

connective tissue remodelinganti-fibroticpelvic floor supportfertility support
Pharmacokinetics

Relaxin half-life calculator

Compound & timing

Half-lifefrom PeptideBase data
Source: "~7–8 h (terminal, serelaxin/rh-relaxin-2)" · Relaxin (PeptideBase)
to show amount remaining
8 h
0%25%50%75%100%08.317253342time since dose (h)
Plasma decay curve for Relaxin: 45% to 50% remaining at 8 h after the dose.
range (~7–8 h (terminal, serelaxin/rh-relaxin-2))slower half-life
45%–50%remaining in plasmaat 8 h after the dose
Half-life
7 – 8 h
~97% cleared after
40 h

Model: single-dose, first-order (single-compartment) estimate. Real clearance is multi-compartment and varies by individual and route.

The Research

What the evidence says about Relaxin

Research Evidence

based on 5 studies · 2 RCTs · most recent 2026

Regulatory Status

Availability Status
Research Only
FDA Status
Investigational

Regulatory status reflects publicly available information and may change. This is not legal or medical advice.

Research Sources

5 sources cited · 2 strong · 1 moderate · 2 weak

2 RCTs · 1 Cohort · 1 Review · 1 Animal

  • Development of a long-acting relaxin for the treatment of pulmonary hypertension.

    Br J Pharmacol · 2026

    # Summary Research found that TX000045, a long-acting relaxin therapeutic engineered by fusing human relaxin-2 to an immunoglobulin Fc domain, demonstrated an extended half-life of 2–3 weeks and was well-tolerated in early human studies while reducing pulmonary hypertension markers in animal models. This study demonstrated that TX45's pharmacokinetic and pharmacodynamic properties—including vasodilatory effects on renal plasma flow and reductions in cardiac hypertrophy and pulmonary arterial changes—were consistent with preclinical predictions, supporting its advancement toward clinical evaluation for pulmonary hypertension treatment.

    RCTStrongPMID 42173817
  • Serelaxin, recombinant human relaxin-2, for treatment of acute heart failure (RELAX-AHF): a randomised, placebo-controlled trial

    Lancet · 2013

    The RELAX-AHF trial of 1,161 patients demonstrated that serelaxin (recombinant human relaxin-2, 30 μg/kg/day IV) significantly improved the dyspnoea VAS AUC primary endpoint (p=0.007) and reduced 180-day all-cause mortality (HR 0.63, p=0.019) in acute heart failure, establishing the systemic vasodilatory and organ-protective pharmacology of recombinant relaxin-2 in humans and supporting its broader therapeutic relevance as a peptide hormone.

    RCTn=1,161StrongPMID 23141816
  • Association of Relaxin-1 Levels with Mortality in Sepsis and Septic Shock.

    J Clin Med · 2026

    CohortModeratePMID 42355830
Show 2 more sources
  • Serelaxin has greater anti-fibrotic potential than perindopril but maintains its anti-fibrotic efficacy in the presence of perindopril in normotensive mouse models of heart disease.

    Life Sci · 2026

    # Research Summary Research found that serelaxin demonstrated greater anti-fibrotic effects than the ACE inhibitor perindopril in mouse models of heart disease, while maintaining its anti-fibrotic efficacy when combined with perindopril treatment. This study demonstrated that serelaxin could serve as an effective adjunct therapy to standard ACE inhibitor treatment without compromising its therapeutic benefits.

    AnimalWeakPMID 42176886
  • [Advances in targeted pharmacotherapies for pulmonary hypertension associated with left heart disease].

    Zhonghua Yi Xue Za Zhi · 2026

    # Summary Research found that novel therapeutic agents, including activin signaling inhibitors and long-acting relaxin analogs, demonstrated potential benefits in preliminary studies for treating pulmonary hypertension associated with left heart disease. This study highlighted that these agents with distinct mechanisms may offer new treatment avenues for this prevalent form of pulmonary hypertension, where current PAH-targeted therapies have not shown proven efficacy and safety benefits.

    ReviewTheoreticalPMID 42135043

Relaxin Side Effects & Safety Considerations

Research-use compound with limited human data. Evidence strength varies — see the Evidence section.

No established clinical contraindications. This is an investigational compound with limited human data and has not been evaluated by the FDA for safety in this context. Consult a qualified clinician.

Consult a qualified healthcare professional before making any health decisions. This information is educational only and does not constitute medical advice.

Frequently Asked Questions — Relaxin

Relaxin (relaxin-2; serelaxin; RLX030) is a 53-residue two-chain polypeptide hormone structurally related to insulin, produced primarily by the corpus luteum during pregnancy and by the heart during cardiac stress, that acts through RXFP1 receptors to promote vasodilation, reduce systemic vascular resistance, increase renal perfusion, and attenuate fibrotic signaling — properties that made it a compelling candidate for acute decompensated heart failure, where peripheral vasoconstriction and organ hypoperfusion are central pathophysiological features. RXFP1 activation stimulates cAMP/PKA and nitric oxide signaling to acutely reduce systemic and renal vascular resistance, increase cardiac output without directly affecting heart rate, and suppress TGF-beta-mediated fibrotic remodeling; these hemodynamic and organoprotective mechanisms distinguished relaxin mechanistically from existing vasodilators and diuretics.

connective tissue remodeling, anti-fibrotic, pelvic floor support, fertility support, cardiac protection.

Research on Relaxin primarily documents effects related to connective tissue remodeling and anti-fibrotic and pelvic floor support and fertility support and cardiac protection. These are areas covered in preclinical and clinical literature — individual response varies and effects depend on context of use.

For Relaxin, its FDA status is investigational (not FDA-approved), and it is designated for research use only. Regulatory status reflects publicly available information and may change. This is not legal or medical advice.

# Summary Research found that TX000045, a long-acting relaxin therapeutic engineered by fusing human relaxin-2 to an immunoglobulin Fc domain, demonstrated an extended half-life of 2–3 weeks and was well-tolerated in early human studies while reducing pulmonary hypertension markers in animal models. This study demonstrated that TX45's pharmacokinetic and pharmacodynamic properties—including vasodilatory effects on renal plasma flow and reductions in cardiac hypertrophy and pulmonary arterial changes—were consistent with preclinical predictions, supporting its advancement toward clinical evaluation for pulmonary hypertension treatment.

Access

How to get Relaxin

Where to buy Relaxin

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