India Pharma Outlook Team | Monday, 09 November 2026
Two major heart trials from Novartis and Novo Nordisk have delivered a sobering message for cardiovascular drug development.
Presented at the American Heart Association (AHA) meeting in Chicago, the studies showed that experimental medicines could successfully lower important biological risk markers without preventing heart attacks, strokes, or deaths.
The results surprised researchers who expected these treatments to translate into meaningful clinical benefits.
Despite strong improvements in cholesterol-related and inflammation markers, neither drug protected patients from major cardiovascular events, raising fresh questions about how scientists should approach heart disease treatment.
Novartis’ experimental drug pelacarsen targeted lipoprotein(a), or Lp(a), a genetically determined cardiovascular risk factor that affects approximately 20% of the global population. The trial enrolled more than 8,300 patients with previous cardiovascular events and followed them for a median of 4.7 years.
The findings marked the first major test of whether substantially lowering Lp(a) could prevent cardiovascular complications.
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Novo Nordisk’s ziltivekimab targeted inflammation through interleukin-6 (IL-6), a pathway associated with cardiovascular disease. The study included approximately 6,300 patients with heart disease, advanced kidney disease and systemic inflammation. Although ziltivekimab successfully lowered inflammation markers, it failed to reduce major adverse cardiovascular events, including deaths, heart attacks and strokes.
The setback followed earlier difficulties for the program. Novo had already discontinued two other late-stage ziltivekimab trials in patients with heart failure after an independent monitoring committee questioned their likelihood of success.
The results challenge the assumption that improving a biological risk marker automatically improves patient outcomes. Experts now face difficult questions about residual cardiovascular risk and whether these targets adequately address the underlying disease mechanisms. For patients with elevated Lp(a), the disappointment carries particular significance. No approved treatment currently addresses this genetic risk factor directly.
Other companies continue to test experimental Lp(a)-lowering medicines. Amgen expects Phase 3 results in early 2028, while Eli Lilly anticipates results in 2029. These upcoming studies could clarify whether different treatment approaches, patient populations, or stronger biological effects can deliver meaningful cardiovascular protection.
The failures highlight a critical lesson for future heart trials: biological success alone cannot establish clinical value. The question now remains whether targeting these pathways differently can finally prevent the cardiovascular events researchers hoped to eliminate.
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