Delving into the Latest Updates on Serelaxin with Synapse

Overview

Basic Info

Drug Type

Peptide Hormone

Synonyms

ConXn, Human relaxin 2 (relaxin h2), Human relaxin recombinant

+ [13]

Target

RXFP1

Action

agonists

Mechanism

RXFP1 agonists(Relaxin receptor 1 agonists)

Therapeutic Areas

Cardiovascular Diseases

Active Indication

Heart Failure

Inactive Indication

Acute decompensated heart failureChronic heart failureCompensated cirrhosis+ [9]

Originator Organization

The Florey Institute of Neuroscience & Mental Health

Active Organization-

Inactive Organization

Novartis Pharmaceuticals Corp.

Novartis Pharmaceuticals Canada, Inc.

Corthera, Inc.

+ [4]

License Organization-

Drug Highest PhaseApproved

First Approval Date

Russia (01 Jan 2015),

Heart Failure

Regulation-

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Structure/Sequence

Sequence Code 43631

Source: *****

Sequence Code 1320151

Source: *****

Portal hypertension (an increase in blood pressure in the portal vein that carries the blood from the intestine and spleen to the liver) underlies most of the serious complications of liver cirrhosis. This randomised placebo controlled study in people with liver cirrhosis evaluates the acute effects serelaxin (RLX030) infusion on portal hypertension and liver blood flow.

Start Date18 Oct 2017

Sponsor / Collaborator

The University of Edinburgh

[+2]

NCT02625922

/ TerminatedPhase 2

A Multicenter, Randomized, Double-blind, Crossover Placebo-controlled Phase II Study to Assess the Effect of Serelaxin Versus Placebo on High-sensitivity Cardiac Troponin I (Hs-cTnI) Release in Patients With Chronic Heart Failure After Exercise When Used in Addition to Standard of Care

This was a multicenter, randomized, double-blind, crossover, placebo-controlled, Phase II clinical study that evaluated the effect of serelaxin versus placebo (both in addition to SoC) on the release of hs-cTnI, in patients with CHF after an exercise testing session.

Start Date05 Feb 2016

Sponsor / Collaborator

Novartis Pharmaceuticals Corp.

PER-023-15

/ CompletedPhase 3

A MULTICENTER, RANDOMIZED, DOUBLE BLIND, PLACEBO- CONTROLLED PHASE IIIB STUDY TO EVALUATE THE EFFICACY, SAFETY AND TOLERABILITY OF SERELAXIN WHEN ADDED TO STANDARD THERAPY IN ACUTE HEART FAILURE PATIENTS

Start Date22 Oct 2015

Sponsor / Collaborator-

100 Clinical Results associated with Serelaxin

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100 Translational Medicine associated with Serelaxin

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100 Patents (Medical) associated with Serelaxin

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293

Literatures (Medical) associated with Serelaxin

01 Aug 2026·British Journal of Pharmacology

EXPRESSION OF CONCERN: Serelaxin‐Mediated Signal Transduction in Human Vascular Cells: Bell‐Shaped Concentration–Response Curves Reflect Differential Coupling to G Proteins

01 Aug 2026·British Journal of Pharmacology

Development of a long‐acting relaxin for the treatment of pulmonary hypertension

Article

Author: Thulasiraman, Sarulatha ; Ruddy, Marcella ; Ghosh, Susmita ; West, Mary ; Soni, Hitesh ; Lacy, Alisa ; Darce, Jaime ; Booe, Jason ; MacBain, Zachary ; Muslin, Anthony J. ; Milton, Mark ; Diener, John ; Knihtila, Ryan ; Denney, William ; Bencsics, Craig ; McNamara, Peter

Abstract:

Background and Purpose:

Relaxin is a naturally occurring peptide hormone with significant cardiovascular effects, particularly during the adaptation to pregnancy. A short‐acting peptide therapeutic previously demonstrated pharmacological effects in acute heart failure. TX000045 (‘TX45’) is a long‐acting relaxin being developed for the treatment of pulmonary hypertension.

Experimental Approach:

TX45 is human relaxin‐2 fused to the C‐terminus of the Fc domain of human IgG1, wherein the B and A chains of human relaxin are connected by a peptide linker. Protein engineering optimized the biophysical properties through adjustment of the isoelectric point. Preclinical animal models confirmed extended half‐life and known pharmacodynamic (PD) vasodilator effects on renal plasma flow. TX45 decreased inflammation, cardiac hypertrophy and pulmonary arterial muscularization in a monocrotaline (MCT) rat pulmonary hypertension model. First‐in‐human studies evaluated pharmacokinetic (PK) and PD in a double‐blind, placebo‐controlled, single ascending dose study in healthy subjects.

Key Results:

TX45 significantly improved biophysical and PK/PD properties, relative to unmodified versions. TX45 clearly decreased pulmonary hypertension in the MCT rat model. In healthy human subjects, TX45 was well‐tolerated with a terminal elimination half‐life of 2–3 weeks and increased renal plasma flow. Repeated measures of renal plasma flow after single doses of TX45 were used to create an exposure–response model that enabled Phase 2 dose selection.

Conclusions and Implications:

TX45 is an extended half‐life relaxin with PK and PD properties consistent with a relaxin mimetic. TX45 was well tolerated in early clinical studies. Preclinical PK/PD data predicted human PK/PD.

01 Aug 2026·LIFE SCIENCES

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

Article

Author: Wang, Chao ; Ferens, Dorota ; Salimova, Ekaterina ; Samuel, Chrishan S ; Widdop, Robert E ; She, Gang ; Gaspari, Tracey A ; Wang, Ziqiao

AIMS:

Serelaxin (RLX), the drug form of human gene-2 relaxin, has potent anti-fibrotic properties that are currently being clinically-evaluated for the treatment of heart failure (HF). Whilst these effects can potentially be antagonised by angiotensin receptor blocker co-administration, this study determined if RLX was a suitable adjunct therapy to angiotensin converting enzyme inhibitor (ACEi) treatment. In particular, the anti-fibrotic effects of RLX were compared to or combined with the clinically-used ACEi, perindopril, in murine models of isoprenaline (ISO)-induced cardiomyopathy and surgically-induced myocardial infarction (MI).

METHODS:

The dose-response effects of perindopril (1, 2 or 4 mg/kg/day) on systolic blood pressure (SBP) and left ventricular (LV) fibrosis were first assessed in ISO-injured mice, after 7- or 14-days of treatment. The therapeutic effects of RLX (0.5 mg/kg/day) on SBP, LV fibrosis and LV functional parameters (ejection fraction, fractional shortening, stroke volume, cardiac output) were then compared to or combined with perindopril (2 mg/kg/day) pre-treatment (7-days prior) or co-administration (over 7-days) in ISO-injured mice; or perindopril co-administration (over 21-days) in MI-injured mice.

KEY FINDINGS:

Perindopril attenuated the ISO-induced LV fibrosis at 2 or 4 mg/kg/day, but induced significant hypotension at 4 mg/kg/day. RLX reduced the ISO- or MI-induced LV fibrosis, and restored measures of LV dysfunction, to a greater extent than perindopril (2 mg/kg/day), in the absence of BP regulation. These effects were maintained in the presence of perindopril pre-treatment or co-administration.

SIGNIFICANCE:

These findings confirmed that RLX had greater anti-fibrotic potential than perindopril, but could be applied as a rapidly-acting adjunct therapy to ACEi.

13

News (Medical) associated with Serelaxin

31 Aug 2026

·firstwordpharma.com

ESC26: AstraZeneca's AZD5462 may revive hopes for relaxin in heart failure

Early-stage study data suggest an oral relaxin receptor agonist being developed by AstraZeneca led to improvements in cardiac remodeling and haemodynamics in patients with chronic heart failure (HF), potentially offering a new glimmer of hope for a treatment approach that has stumbled before.Results from the Phase IIb LUMINARA study, presented at the European Society of Cardiology (ESC) and published simultaneously in Circulation, showed that AZD5462 was well tolerated on top of guideline-directed HF therapy, with effects observed across a range of left ventricular ejection fractions (LVEFs).The trial randomised 375 chronic HF patients to once-daily AZD5462 at 20 mg, 80 mg or 360 mg, or placebo. The study included 235 patients with LVEF ≤35% (cohort A) and 140 with LVEF of 41% to 55% (cohort B).The primary endpoint in cohort A was change in end systolic volume index from baseline to week 24, a measure of adverse cardiac remodelling. The lowest dose produced the most benefit on this metric, with a placebo-adjusted change of −5.4 mL/m² (p=0.054). Effects on secondary endpoints, including change in LVEF, were also greatest at the lowest dose.For cohort B, the primary endpoint looked at change in systemic vascular resistance index from baseline to week 24, a measure of the resistance the heart has to pump against. AZD5462 significantly lowered the index across all three doses, by 19%, 21% and 15% at the 20-, 80- and 360-mg doses, respectively (all p≤0.021)."The observed effects on cardiac remodeling in heart failure with reduced ejection fraction and vascular resistance in patients with heart failure with mildly reduced/preserved ejection fraction suggest that oral relaxin family peptide receptor 1 (RXFP1) agonism may have relevance across multiple heart failure phenotypes," the study authors said.Past challengesThe peptide hormone relaxin-2 acts on RXFP1, leading to effects that may be beneficial in HF in terms of vasodilation, easing the heart's workload, and reducing inflammation and myocardial fibrosis.However, the authors noted that the history of relaxin-based therapies has yielded a "disconnect between short-term physiological promise and long-term clinical efficacy and safety."Earlier studies of Novartis' short-acting relaxin analogue serelaxin generated encouraging signals in acute HF, though subsequent trials failed to demonstrate longer-term clinical benefit. That spurred the development of longer-acting RXFP1 agonists, though a Phase II HF study of one of these, Eli Lilly's volenrelaxin (LY3540378), was terminated early last year after patients with preserved ejection fraction showed worsening fluid buildup and no significant kidney benefit.The overall incidence of adverse events in the LUMINARA study was comparable between the pooled AZD5462 and placebo groups. Investigators noted a "modest blood pressure–lowering effect" that was in line with what was seen in Phase I. "The clinical significance of this finding is unclear; notably there were no imbalances in clinically reported AEs of hypotension in cohort A despite extensive background [guideline-directed medical therapy]," they said.

Phase 2Clinical ResultAHA

10 Feb 2026

·www.fiercebiotech.com

AstraZeneca relaxed about relaxin drug\'s poor efficacy in phase 2 heart failure trial

AstraZeneca shared news it cut AZD3427 from its pipeline alongside the removal of two other new molecular entities.\n AstraZeneca executives have told Fierce Biotech they still see potential in harnessing the relaxin hormone to treat heart failure despite abandoning work on one of two clinical-stage candidates. As part of its full-year 2025 financial results (PDF), the U.K.-based Big Pharma revealed that it removed a long-acting relaxin-2 analog called AZD3427 from its pipeline, citing underwhelming efficacy in a phase 2 trial.There is a history of studying relaxin in cardiovascular settings—Novartis started a phase 3 heart failure trial of a recombinant relaxin-2 peptide in 2013—but preclinical evidence of the molecule’s vasodilatory, anti‐inflammatory and antifibrotic effects has yet to translate into clinical success.AstraZeneca identified the short half-lives of earlier candidates as a potential cause of the failures. To fix the problem, the company created a relaxin-2 mimic fusion protein and attached a fragment to create a candidate with a half-life measured in days rather than hours. However, AstraZeneca has now stopped development of AZD3427 after completing a phase 2 trial in 260 people with heart failure. While AZD3427 has been sunk by efficacy, the company is continuing to develop the oral relaxin drug candidate AZD5462. AstraZeneca has called (PDF) the candidate the first small molecule targeting relaxin biology to enter clinical trials. Data from a phase 2b trial of stable patients with chronic heart failure are due in the second half of 2026.During a press conference this morning, Sharon Barr, Ph.D., executive vice president of biopharmaceuticals R&D at AstraZeneca, told Fierce the company is moving forward with AZD5462 “because we think this is a potentially important molecule.”“One of the things that we have learned from competitor studies is that dosing matters,” Barr continued. “You really have to find that perfect space between efficacy and congestion, and we think we\'ve put in the hard yards to really understand the posology there, and we\'re moving forward with our existing program.”AstraZeneca CEO Pascal Soriot also told Fierce during the call that work on the relaxin program is a case study of “what is so exciting in this industry at this present time.”Soriot pointed to the likes of ACE inhibitors and SGLT2 drugs as examples of the progress made in recent years to treat specific groups of cardiovascular patients.“There\'s more and more of those technologies, and we need just to pick the right products to really help patients with heart disease,” the CEO added. AstraZeneca disclosed its discontinuation of AZD3427 alongside the removal of two other new molecular entities from the pipeline. The drugmaker confirmed the removal of AZD0233, a CX3CR1 modulator that was in development as a treatment for dilated cardiomyopathy. AstraZeneca terminated a phase 1 trial of the candidate last month over an adverse finding in a nonclinical, chronic toxicology study.The company also revealed it had axed a COVID-19 vaccine program. AstraZeneca moved the mRNA viruslike particle vaccine program into phase 1 in late 2023. Recently, the company reported that a vaccine candidate was well tolerated compared to Pfizer and BioNTech’s Comirnaty and generated similar immunogenicity at one-third of the dosage.

$AstraZeneca relaxed about relaxin drug\'s poor efficacy in phase 2 heart failure trial$

VaccinePhase 2Phase 1Financial Statement

19 Nov 2025

·thryvtrx.com

Amy Rudolph, PhD, Joins Thryv Therapeutics’ Board of Directors to Support Portfolio Progression into Heart Failure

Montreal, Quebec – November 19, 2025 – Thryv Therapeutics Inc., a clinical-stage biotechnology company advancing a series of novel serum glucocorticoid inducible kinase 1 (SGK1) inhibitors for inherited cardiac arrhythmias, cardiometabolic diseases, and cardiomyopathies, today announced that new preclinical data will be presented at the American Heart Association’s Scientific Sessions 2025, taking place November 8–10 in New Orleans, Louisiana. The American Heart Association’s Scientific Sessions bring together global experts to exchange the latest advancements in cardiovascular science, clinical care, and research. Thryv Therapeutics is honored to contribute to this important dialogue with its recent research highlighting the potential of SGK1 inhibition as a novel therapeutic strategy for cardiovascular disease, including heart failure. Dr. Rudolph currently serves as Head of Global Medical Affairs and Cross-TA Medical Affairs at Boehringer Ingelheim, where she leads a global transformation to build a market-leading Medical Affairs organization focused on external engagement, digital/AI integration, evidence generation, advanced analytics, and learning. “We are thrilled to welcome Amy Rudolph to our Board of Directors,” said Paul Truex, Chairman and CEO of Thryv Therapeutics. “Her extensive experience in medical affairs, evidence generation, and cross-functional drug development will be invaluable as we progress our SGK1 inhibitor pipeline toward late-stage clinical studies.” “We are also deeply grateful to Scott Weiner for his many contributions to the Board of Directors,” added Truex. “We’re pleased that he will remain closely involved with Thryv in an advisory capacity.” Prior to joining Boehringer Ingelheim, Dr. Rudolph held leadership roles at Novartis Pharmaceutical Corporation, where she served as Head of HCS (Healthcare Systems) Partnerships in Global Drug Development and Head of Evidence and Launch Excellence in Global Medical Affairs. Earlier in her career, she held key positions at Pfizer Inc., where she was responsible for the atherosclerosis and stroke platforms, early development, and licensing/technology evaluations, and began her scientific career with G.D. Searle/Pharmacia/Pfizer. Over the course of her career, Dr. Rudolph has played key roles in the development and launch of multiple cardiovascular therapies, including Inspra, Eliquis, Lipitor, Diovan, Diovan/HCT, Exforge, Tekturna, and Entresto, as well as in the development of Serelaxin and Amturnide. Dr. Rudolph earned her Ph.D. in Biochemistry and Molecular Biology from Washington University in St. Louis and is an inventor on 13 patents and numerous scientific publications spanning preclinical research, drug development, and real-world evidence. “I am honored to join Thryv Therapeutics’ Board of Directors,” said Amy Rudolph. “Thryv’s science and patient-centered mission resonate deeply with me, and I look forward to supporting the company’s continued progress in addressing serious cardiovascular conditions.” Dr. Rudolph joins the Board of Directors as Scott Weiner, who has served as a valued member since 2021, transitions to an observer role. Mr. Weiner will remain on the Board of Directors of the company’s subsidiary, Thryv Therapeutics USA, Inc., while also serving as an advisor to the company. About Thryv’s SGK1 Inhibitor Platform Thryv Therapeutics is advancing a portfolio of potent and selective SGK1 (serum and glucocorticoid-regulated kinase 1) inhibitors that target the fundamental mechanisms driving electrical and structural remodeling in the heart. THRV-1268, the company’s lead clinical candidate, is a best-in-class, highly selective SGK1 inhibitor with the potential to transform the treatment landscape for Long QT Syndrome (LQTS), heart failure (HF), and atrial fibrillation (AFib)—three serious cardiac conditions with urgent unmet medical needs. About Thryv Therapeutics Inc. Thryv Therapeutics Inc. is a privately owned company based in Montreal, Quebec, Canada. Thryv is pioneering a precision medicine approach to treat genetic channelopathies, cardiometabolic diseases, and cardiomyopathies with potent and highly selective inhibitors of serum glucocorticoid inducible kinase 1 (SGK1). For more information, please visit www.thryvtrx.com. Media Inquiries brittany@thryvtrx.com | 514 973 0915

Executive ChangeAHA

100 Deals associated with Serelaxin

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External Link

KEGG	Wiki	ATC	Drug Bank
D10488	Serelaxin	C01DX21	DB05794

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Heart Failure	Russia	-	01 Jan 2015

Developing

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Acute decompensated heart failure	Phase 3	Austria	Novartis Pharmaceuticals Corp.	31 Jan 2014
Acute decompensated heart failure	Phase 3	Belgium	Novartis Pharmaceuticals Corp.	31 Jan 2014
Acute decompensated heart failure	Phase 3	Bulgaria	Novartis Pharmaceuticals Corp.	31 Jan 2014
Acute decompensated heart failure	Phase 3	Croatia	Novartis Pharmaceuticals Corp.	31 Jan 2014
Acute decompensated heart failure	Phase 3	Czechia	Novartis Pharmaceuticals Corp.	31 Jan 2014
Acute decompensated heart failure	Phase 3	Estonia	Novartis Pharmaceuticals Corp.	31 Jan 2014
Acute decompensated heart failure	Phase 3	Finland	Novartis Pharmaceuticals Corp.	31 Jan 2014
Acute decompensated heart failure	Phase 3	France	Novartis Pharmaceuticals Corp.	31 Jan 2014
Acute decompensated heart failure	Phase 3	Germany	Novartis Pharmaceuticals Corp.	31 Jan 2014
Acute decompensated heart failure	Phase 3	Greece	Novartis Pharmaceuticals Corp.	31 Jan 2014

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Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT01979614 (Pubmed) Manual	Phase 2	Coronary Artery Disease	51	serelaxin	gkgimdkmqy(husdyjhqkv) = wkzweclpzx szohqdltot (yrgphzxaho ) View more	Positive	01 Jan 2021
				Placebo	gkgimdkmqy(husdyjhqkv) = xspdjhlhsd szohqdltot (yrgphzxaho ) View more
NCT02669875 (STOPP, Pubmed \| Trials)	Phase 2	Fibrosis	15	Serelaxin	ruaeqpficj(kazzqnprii) = dnjfuolxbx myxnesbecy (spgrgxthvf, ±3.5)	-	12 Mar 2020
NCT01870778 (RELAX-AHF-2, Pubmed \| Br Dent J \| N Engl J Med) Manual	Phase 3	Heart Failure	6,545	Serelaxin	vwlzctuldv(duwlureenw) = kypfowdxts wudgjoofvm (oynrjsrblt ) View more	Negative	22 Aug 2019
				Placebo	vwlzctuldv(duwlureenw) = kjqfrtdxdi wudgjoofvm (oynrjsrblt ) View more
NCT01979614 (CTgov)	Phase 2	Coronary Artery Disease	58	Serelaxin (Serelaxin)	gkcibordou(ueujxthmgc) = knjipfhbkc ygvtfxlusp (mgbxlhwamu, ixovczuljt - kjgtucocxf) View more	-	01 Jul 2019
				Placebo (Placebo)	gkcibordou(ueujxthmgc) = vaingnbmwb ygvtfxlusp (mgbxlhwamu, akwtjdhteh - tkbkszucvn) View more
NCT02151383 (RELAX-PEDS-PK, CTgov)	Phase 2	Heart Failure	12	Serelaxin (Serelaxin: Cohort 1)	vqcagswhhy = xnwepsnksp shfbeilxjh (bplqulxxvy, gxuumiuwqm - bwlfsbquis) View more	-	25 Jun 2019
				Serelaxin (Serelaxin: Cohort 2)	vqcagswhhy = sfurqngttf shfbeilxjh (bplqulxxvy, uyedfphiqs - gsamcmckda) View more
NCT02064868 (RELAX-AHF-EU, CTgov)	Phase 3	Acute decompensated heart failure	2,666	Standard of Care+Serelaxin (Serelaxin + Standard of Care)	sinrbfgdph = hgxwvqayme vapnqfodlh (miedbxzozp, diwymdkywt - cpmlybfopt) View more	-	22 Mar 2019
				Standard of Care (Standard of Care (SOC))	sinrbfgdph = uqcgcuxpvl vapnqfodlh (miedbxzozp, ebhwlprapt - caslrngogm) View more
NCT02064868 (RELAX-AHF-EU, Pubmed \| Eur J Heart Fail) Manual	Phase 3	Heart Failure	2,666	standard of care+serelaxin	nloupijtmm(tmwvnpyczj) = qubimboeky lqpypxawwz (idaryslsbk )	Positive	01 Mar 2019
				standard of care	nloupijtmm(tmwvnpyczj) = fauxxtdiwb lqpypxawwz (idaryslsbk )
NCT02625922 (RELAX-Cardio, CTgov)	Phase 2	Chronic heart failure	26	Serelaxin (Serelaxin)	puzcaablpy(nykowuayzv) = soxzvyqjfs oypcjojdpm (ulengpovku, 0.64893) View more	-	21 Sep 2018
				placebo (Placebo)	puzcaablpy(nykowuayzv) = bxqvbdgxto oypcjojdpm (ulengpovku, 0.60192) View more
NCT01870778 (RELAX-AHF-2, CTgov)	Phase 3	Heart Failure	6,600	RLX030 (Serelaxin (RLX030))	sxrnczbyml = sherhxxgkn ymzxbmaxiw (iqafleiyro, uvnljccnik - ympzqiecep) View more	-	30 Mar 2018
				Placebo (Placebo)	sxrnczbyml = atibphpslu ymzxbmaxiw (iqafleiyro, pelufmdwac - pyelssqsen) View more
NCT01979614 (ESC2017)	Phase 2	Coronary Artery Disease	62	IV serelaxin (30 Î¼g/kg/24 h)	pwihfrfscy(xhcxviopgr) = ddrbnhrcry vllxwcpqoz (sbqqdsjfeh ) View more	Negative	27 Aug 2017
				Placebo	pwihfrfscy(xhcxviopgr) = sxqrekxnyd vllxwcpqoz (sbqqdsjfeh ) View more

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