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Anti-Inflammatory Effects of Oral NLRP3 Inhibition With Ruvonoflast Among Individuals at Elevated Cardiovascular

Kausik K Ray¹, Nicholas Clarke², Peter Thornton²

¹Department of Primary Care and Public Health, Imperial College London, London, United Kingdom; Imperial Clinical Trials Unit-Global, Imperial College London, London, United Kingdom.

Journal of the American College of Cardiology

|May 26, 2026

Summary

Ruvonoflast, an oral NLRP3 inhibitor, significantly reduced C-reactive protein (CRP) and other inflammatory biomarkers in individuals with high cardiovascular risk. Further trials will explore its therapeutic potential.

Keywords:

fibrinogen high-sensitivity C-reactive protein inflammation interleukin-1β interleukin-6 residual risk

Related Experiment Videos

Area of Science:

Cardiovascular Disease Research
Inflammation and Immunology
Pharmacology

Background:

The NLRP3 inflammasome plays a crucial role in non-communicable diseases, including atherosclerotic cardiovascular disease.
Ruvonoflast, an oral NLRP3 inhibitor, has shown potential in reducing systemic and central nervous system inflammation biomarkers.

Purpose of the Study:

To evaluate the anti-inflammatory efficacy and safety of ruvonoflast in patients with residual inflammatory risk and high atherosclerotic cardiovascular disease (ASCVD) risk.
To assess the impact of ruvonoflast on C-reactive protein (CRP) levels and other inflammatory markers.

Main Methods:

A double-blind, randomized Phase 1b trial involving 63 participants with elevated hsCRP and cardiovascular risk factors.
Participants received oral ruvonoflast (225mg twice daily) or placebo, alongside a controlled diet.
Primary endpoint: change in hsCRP at Day 28, analyzed using Bayesian methods; secondary endpoints included inflammatory biomarkers and body weight.

Main Results:

Ruvonoflast demonstrated a >99% probability of superiority in reducing hsCRP compared to placebo by Day 28 (82.2% vs 37.2% reduction).
Significant reductions in interleukin-6 (IL-6) and fibrinogen were observed with ruvonoflast.
While serious adverse events were similar, 10% of ruvonoflast participants discontinued due to transient side effects.

Conclusions:

Oral NLRP3 inhibition with ruvonoflast effectively reduced hsCRP and other inflammatory biomarkers in individuals at elevated inflammatory risk.
Larger, longer-duration Phase 2 trials are underway to further define the therapeutic role of ruvonoflast.