A novel long-acting relaxin-2 fusion, AZD3427, improves cardiac performance in non-human primates with cardiac dysfunction
Open accessAbstract
Aims: Relaxin-2, a well-known human hormone primarily associated with pregnancy, has shown promising cardiovascular benefits in both pre-clinical models and clinical trials. However, its therapeutic potential has been limited due to the short half-life and the short duration of treatment. To address this, we developed AZD3427, a novel long-acting relaxin-2 analogue, and assessed its efficacy during prolonged treatment in a large animal model with cardiac dysfunction. Methods and results: Extensive protein engineering resulted in AZD3427, a novel fusion protein, which closely mimics the natural hormone's structure and consists of a single relaxin-2 and the Fc fragment of human IgG1 to extend its half-life. AZD3427 exhibits an improved pharmacokinetic profile, allowing for weekly or less frequent, subcutaneous dosing, and maintains the pharmacology profile of relaxin-2 with signalling via relaxin family peptide receptor 1 (RXFP1) in cell systems. The effects of chronic RXFP1 agonism with AZD3427 were investigated in a non-human primate (NHP) model with systolic dysfunction and metabolic syndrome. Administration of AZD3427 over a 21-week period led to significant improvements in cardiac function, as evidenced by increased ejection fraction, cardiac output, and stroke volume, as well as reduced systemic vascular resistance. Importantly, no adverse events related to treatments were observed and there were no concomitant changes in heart rate or blood pressure. During the 18-week washout period, the observed effects gradually disappeared. Conclusion: Prolonged administration of AZD3427, a long-acting relaxin receptor RXFP1 agonist, resulted in remarkable improvement in cardiac function in a NHP model. Findings of this study are an important translational step to developing future therapies and support further clinical development of AZD3427 as a novel treatment for patients with heart failure.
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Papworth et al showed improvement in LVEF starting from week-5 and progressively further improving throughout the 21-week treatment without a sign of reaching a plateau.
“Papworth et al clearly showed improvement in LVEF starting from week-5 and progressively further improving throughout the 21-week period of treatment without a sign of reaching a plateau.6”
From Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseases (2025) · cites this paper as [6]
The Results (page unavailable) report improved ejection fraction in treated non-human primates at 21 weeks, and the Discussion says EF had not reached a pharmacodynamic steady state by then, supporting the no-plateau point. The Methods list an assessment at Week 5, but our copy does not state that improvement began then or that EF increased progressively at every assessment through Week 21. (LLM, conf=0.86)
Experimental — accuracy not yet measuredThe study was a randomized and double-blind drug trial.
“this study was a randomized and double-blind drug trial.”
From Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseases (2025) · cites this paper as [6]
Methods, ‘NHP study cohort and design,’ says the non-human primates were randomized to vehicle or AZD3427 treatment groups. Methods, ‘Imaging and HDO,’ says assessors were blinded to treatment assignment, but does not establish that the study was double-blind. (LLM, conf=0.90)
Experimental — accuracy not yet measuredAZD3427 treatment significantly improves stroke volume in monkeys.
“The significant improvement in LVEF and stroke volume (SV), together with reduction in the peripheral vascular resistance in AZD3427-treated monkeys is convincing”
From Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseases (2025) · cites this paper as [6]
The Results section (page unavailable) reports a notable increase in stroke volume in AZD3427-treated monkeys with cardiac dysfunction. It explicitly calls the improvement in ejection fraction significant, but does not establish statistical significance for stroke volume, as the claim does. (LLM, conf=0.84)
Experimental — accuracy not yet measuredPapworth et al found no evidence for improvement of renal parameter UACR by AZD3427 treatment in the NHP model.
“Papworth et al found no evidence for either heart rate increment or improvement of renal parameter urinary albumin creatinine ratio (UACR) by AZD3427 treatment in the NHP model.6”
From Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseases (2025) · cites this paper as [6]
Papworth et al reported a therapeutic effect of AZD3427 in a non-human primate model of HFrEF.
“Papworth et al reported on the therapeutic effect of a novel long-acting relaxin analogue AZD3427 in a non-human primate (NHP) model of HF with reduced left ventricular ejection fraction (LVEF).6”
From Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseases (2025) · cites this paper as [6]
The study included an 18-week washout observation, which is helpful to confirm the efficacy of AZD3427.
“the authors astutely included an 18-week period of washout observation, which is helpful to confirm the efficacy of AZD3427.”
From Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseases (2025) · cites this paper as [6]
LVEF exhibited a slow and progressive decline during the 18-week washout period towards the pre-treatment baseline.
“Likewise, LVEF exhibited a slow and progressive decline during the 18-week washout period towards the pre-treatment baseline.6”
From Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseases (2025) · cites this paper as [6]
AZD3427 treatment significantly improves LVEF in monkeys.
“The significant improvement in LVEF and stroke volume (SV), together with reduction in the peripheral vascular resistance in AZD3427-treated monkeys is convincing”
From Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseases (2025) · cites this paper as [6]
Papworth et al found no evidence for heart rate increment by AZD3427 treatment in the NHP model.
“Papworth et al found no evidence for either heart rate increment or improvement of renal parameter urinary albumin creatinine ratio (UACR) by AZD3427 treatment in the NHP model.6”
From Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseases (2025) · cites this paper as [6]
A HFrEF model was developed in aged NHPs by 2-year high-fat-diet feeding, leading to phenotypes simulating clinical conditions, including LV systolic dysfunction and comorbidities (obesity, dyslipidaemia, early signs of hypertension and diabetes).
“a HFrEF model was developed in aged NHPs by 2-year high-fat-diet feeding, leading to phenotypes simulating clinical conditions, including LV systolic dysfunction and presence of comorbidities (e.g.obesity, dyslipidaemia, and early signs of hypertension and diabetes).”
From Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseases (2025) · cites this paper as [6]
AZD3427 treatment reduces peripheral vascular resistance in monkeys.
“The significant improvement in LVEF and stroke volume (SV), together with reduction in the peripheral vascular resistance in AZD3427-treated monkeys is convincing”
From Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseases (2025) · cites this paper as [6]
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- Authors
- Papworth, M., Kulkarni, S., Antonsson, M., Sermadiras, I., Hovdal, D., Connolly, K., Olsson, J., Shukla, A., Cotton, P., Althage, M., Paterson, J., Martin, E., Wolny, M., Ferraro, F., Sadowska, A., Hao, W., Larsson, N., Backmark, A., Marlow, T., Perez, R., Jermutus, L., Omar, S., George, R. T., Gabrielsen, A., Pettersen, D., & Jennbacken, K.
- Affiliations
- AstraZeneca (United Kingdom) (GB)
- AstraZeneca (Sweden) (SE)
- Biologics Engineering, Oncology R&D, AstraZeneca , Cambridge ,
- AstraZeneca (United States) (US)
- Kunming Biomed International , No. 4571 Boda Road, Yuhua Area, Chenggong, Kunming 650500 ,
- Corresponding author
- Jennbacken, Karin
- ORCID
- Venue
- Cardiovascular Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2025-03-03
- Volume
- 121
- Issue
- 6
- Pages
- 871-881
- ISSN
- 0008-6363 (ISSN-L)
- 1755-3245
- PMC
- PMC12160805
- OpenAlex
- W4408129079
- Cited by
- 8
- References
- 40
- Citations by year
- 2026: 5 · 2025: 3
- FWCI
- 7.28
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Cardiovascular Research (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Apollo (University of Cambridge) (submittedVersion, cc-by-nc)
- Funders
- AstraZeneca
- Topics
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Pregnancy-related medical research
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Failure Treatment and Management
- Keywords
- relaxin-2, Fc fusion protein, cardiac dysfunction, systolic dysfunction, metabolic syndrome, heart failure, nonhuman primate model, pharmacokinetics, cardiac function, systemic vascular resistance
- MeSH terms
- Animals, Disease Models, Animal, Female, Humans, Immunoglobulin Fc Fragments, Macaca fascicularis, Macaca mulatta, Male, Recombinant Fusion Proteins, Relaxin, Stroke Volume, Time Factors, Signal Transduction, Ventricular Function, Left, Receptors, Peptide, Receptors, G-Protein-Coupled
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