Cardiac miR-132 activation leads to adverse remodelling and pathological hypertrophy. CDR132L is a synthetic lead-optimized oligonucleotide inhibitor with proven preclinical efficacy and safety in heart failure (HF) early after myocardial infarction (MI). In a chronic model of post-MI HF monthly intravenous (IV) treatments of CDR132L significantly improved cardiac function and reversed cardiac remodeling. In a world-wide first clinical trial of an antisense drug in HF patients, CDR132L was shown to be safe and well tolerated, confirmed linear plasma pharmacokinetics with no signs of accumulation, and suggested cardiac functional improvements. Further phase 2 studies aiming to confirm the beneficial CDR132L pharmacodynamic effects for the treatment of HF will start soon.