Major press releases from ESC and MHH; multiple media articles (MedicalXpress, Cardiovascular News); LinkedIn expert discussions; presented as first randomized RNA therapy trial in HF; high social shares in cardiology community.
CDR132L did not significantly improve left ventricular end-systolic volume index at 6 months compared to placebo in patients with reduced ejection fraction after myocardial infarction.
RCT
1:1:1
Double-blind
Yes
Does the microRNA inhibitor CDR132L improve left ventricular end-systolic volume index in patients with recent myocardial infarction and left ventricular systolic dysfunction?
294 patients (280 in modified intention-to-treat population, 245 men and 35 women) with recent myocardial infarction (MI) and left ventricular (LV) systolic dysfunction, randomized within 3-14 days after MI. Multinational.
CDR132L (synthetic antisense oligonucleotide miR-132 inhibitor) 5 mg/kg or 10 mg/kg as three intravenous doses at 4-week intervals plus guideline-directed therapy
Matching placebo as three intravenous doses at 4-week intervals plus guideline-directed therapy
Percentage change in LV end-systolic volume index at 6 monthssurrogate
The microRNA-132 inhibitor CDR132L was safe but did not significantly improve left ventricular reverse remodeling at 6 months compared to placebo in patients with recent MI and LV systolic dysfunction.
Abstract MicroRNA-132 (miR-132) is a central regulator of adverse cardiac remodeling. Here we evaluated CDR132L, a synthetic antisense oligonucleotide miR-132 inhibitor, in a multinational, randomized, double-blind, placebo-controlled phase 2 trial (HF-REVERT) in patients with recent myocardial infarction (MI) and left ventricular (LV) systolic dysfunction. Within 3–14 days after MI, 294 patients were randomized to receive CDR132L 5 mg kg −1 , CDR132L 10 mg kg −1 or placebo as three intravenous doses at 4-week intervals plus guideline-directed therapy. In total, 280 patients (245 men and 35 women) who received at least one dose of the study drug were included in the modified intention-to-treat population. CDR132L was well tolerated, with no hepatic, renal, hematologic or cardiac toxicity signals. The primary endpoint—the percentage change in LV end-systolic volume index at 6 months—improved in all groups but did not differ significantly between the CDR132L groups (5 mg kg −1 and 10 mg kg −1 ) and the placebo group. Secondary endpoints, including LV ejection fraction, global longitudinal strain and N-terminal pro B-type natriuretic peptide, were also not significantly different between the CDR132L and placebo groups. Prespecified exploratory analyses suggested potential benefits of CDR132L treatment in patients with advanced adverse remodeling at baseline, supporting further evaluation of CDR132L, including in chronic heart failure conditions. ClinicalTrials.gov: NCT05350969 .
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Johann Bauersachs
Scott D. Solomon
S D Anker
Nature Medicine
Harvard University
Brigham and Women's Hospital
National and Kapodistrian University of Athens
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Bauersachs et al. (Sun,) conducted a rct in Reduced left ventricular ejection fraction after myocardial infarction (n=294). CDR132L vs. Placebo was evaluated on Percentage change in left ventricular end-systolic volume index (LVESVI) at 6 months (LSM difference -2.14%, p=0.26). CDR132L did not significantly improve left ventricular end-systolic volume index at 6 months compared to placebo in patients with reduced ejection fraction after myocardial infarction.
www.synapsesocial.com/papers/6a02701c19750436f6cb5985 — DOI: https://doi.org/10.1038/s41591-026-04408-4