Novartis, Amgen and Eli Lilly race to develop heart attack drugs targeting Lp(a)

Lp(a) has been hiding in plain sight for decades: a cholesterol-related particle discovered in 1963 by Norwegian geneticist Kåre Berg, largely set by genetics, and linked to heart disease even when standard cholesterol is under control. Now Novartis, Amgen and Eli Lilly and Company are all running late-stage trials to see whether lowering it can actually prevent heart attacks, a result that could reshape preventive cardiology and create a new blockbuster class of drugs.

The scale of the opportunity is hard to ignore. An estimated one in five people worldwide has elevated Lp(a), yet reviews still describe no widely available, well-established treatment that reliably lowers it in routine practice. That gap is what has made the current race so consequential: if the drugs work, drugmakers would not just be selling another lipid therapy, they would be trying to define a new standard of care for a risk factor that most patients have never been screened for.

Novartis’s Lp(a)HORIZON trial is active and not recruiting, with a last update posted April 1, 2026. The study is designed as a pivotal phase 3 trial to support an indication for reducing cardiovascular risk in patients with established cardiovascular disease and elevated Lp(a). Novartis is also running Lp(a)FRONTIERS CAVS, a separate phase 3 trial focused on the progression of calcific aortic valve stenosis, underscoring that the commercial and clinical case for Lp(a) reaches beyond heart attacks alone.

Amgen’s OCEAN(a)-Outcomes trial is also active and not recruiting, with a last update posted February 27, 2026. Its primary objective is to compare olpasiran with placebo on the risk of coronary heart disease death, myocardial infarction or urgent coronary revascularization in patients with atherosclerotic cardiovascular disease and elevated Lp(a). Lilly’s ACCLAIM-Lp(a) trial, updated April 20, 2026, is a phase 3 randomized, double-blind, placebo-controlled study in adults with elevated Lp(a) evaluating whether lepodisiran can reduce cardiovascular risk in people with cardiovascular disease or those at risk of a heart attack or stroke.

The science behind the push has been strengthening. Reviews describe Lp(a) as an independent and causal risk factor for atherosclerotic cardiovascular disease and calcific aortic stenosis, and note that its risk persists even after LDL cholesterol and apoB100 are lowered. Amgen has previously said olpasiran lowered Lp(a) by more than 90% in phase 2, while TIMI researchers reported a marked and durable reduction in pro-atherogenic oxidized phospholipids. But the industry’s real test is still ahead: phase 3 outcomes data must show fewer events, not just cleaner lab numbers.

That is why the practical questions matter now. Doctors will need to decide who gets tested first, insurers will have to decide whether screening and treatment belong in preventive care, and payers will judge whether an Lp(a)-targeted medicine can justify broad coverage. If the trials succeed, Lp(a) could become the next major franchise in cardiology. If they do not, the field will likely stay where it has been for years, full of biological promise but short on proven ways to change outcomes.