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Getting the latest healthcare news for you

A highly anticipated phase III trial testing pelacarsen — a drug designed to lower lipoprotein(a) levels — has failed to reduce major cardiovascular events. Novartis's Lp(a)HORIZON trial enrolled over 8,300 patients with established CVD and elevated Lp(a), but found no benefit over placebo. The results are now prompting cardiologists to rethink Lp(a)'s role in cardiovascular prevention.
The cardiology world got a sobering reality check this week. Novartis announced that its phase III Lp(a)HORIZON trial — testing pelacarsen, an investigational antisense oligonucleotide — failed to meet its primary endpoint. Despite successfully lowering lipoprotein(a) levels in patients, the drug did not reduce the combined risk of cardiovascular death, nonfatal MI, nonfatal stroke, or urgent coronary revascularization compared to placebo.
The trial enrolled more than 8,300 patients with established cardiovascular disease (CVD) and elevated Lp(a) — a lipid particle long considered an independent, largely genetically determined risk factor for ASCVD and calcific aortic stenosis. The failure raises a critical question: does lowering Lp(a) actually translate into fewer cardiac events?
Key Takeaways:
Why it matters: These back-to-back trial failures — first the inflammatory hypothesis, now the Lp(a) hypothesis — are prompting cardiologists to reconsider long-held assumptions about cardiovascular risk management. For clinicians and patients alike, the results underscore that lowering a biomarker doesn't always mean lowering risk.