Novo Nordisk to Acquire Corvidia Therapeutics for Up to $2.1 Billion to Expand Cardiovascular Pipeline with IL-6 Inhibitor Ziltivekimab

News Event

Today, the Danish pharmaceutical company Novo Nordisk announced that it will acquire the U.S. private pharmaceutical company Corvidia for $725 million. If all goes well, its shareholders could receive up to $2.1 billion in proceeds. Corvidia’s core asset is ziltivekimab, a long-acting fully human IL-6 antibody currently in Phase II clinical trials for reducing cardiovascular events in patients with chronic kidney disease (CKD). Corvidia also has an ApoC drug, COR-003, in preclinical development, aimed at lowering triglycerides. Founded in 2015, Corvidia previously raised a total of $86 million in Series A and B financing rounds.

Drug Source Analysis

Novo Nordisk is a traditional diabetes company that has long thrived on successive generations of insulin. However, several years ago, it announced the discontinuation of incremental insulin innovations to focus on new product development, with its most significant achievement being the portfolio of GLP-1 receptor agonists. GLP-1 receptor agonists are the only glucose-lowering drugs, aside from SGLT2 inhibitors, that have demonstrated cardiovascular benefits; unfortunately, the mechanism underlying this cardiovascular benefit remains unclear, making further optimization challenging. Progress in another key therapeutic area, hemophilia, has been unsatisfactory. In March of this year, three mid-to-late stage clinical trials of concizumab were halted due to safety concerns. Additionally, their preclinical bispecific antibody mimicking factor VIII, Mim8, lags far behind Roche’s already marketed Hemlibra.

Like many chronic diseases, chronic kidney disease (CKD) and cardiovascular disease have pathological components involving immune abnormalities. Controlling inflammation is considered the third pillar of management, alongside controlling blood pressure and lipid levels. A few years ago, Novartis conducted the CANTOS trial, a large-scale study involving 10,000 participants using the IL-1β antibody canakinumab. Although it significantly reduced mortality in cardiovascular patients with inflammation, the FDA rejected the label expansion due to safety concerns. Professor Ridker from Harvard University, the principal investigator of the CANTOS trial, believes that while blocking IL-1β shows efficacy, IL-6 is the real culprit. IL-6 is a major component of cytokine storms, and both IL-6 and IL-6 receptor antibodies have already been approved for rare diseases associated with cytokine storms, such as CAR-T-related CRS and juvenile arthritis caused by HLH. In this year’s COVID-19 infections, some severe cases showed significantly elevated levels of IL-1 and IL-6, so IL-6 antibodies are also being tested in clinical trials for COVID-19. Corvidia believes that ziltivekimab is the most potent IL-6 antibody and therefore has the greatest potential to offer an adequate safety window.

IL-1 and IL-6 are key cytokines in the immune response; inhibiting their activity has systemic implications. Although these cytokines may be involved in the pathogenesis of many diseases, identifying indications with a sufficient therapeutic window for blocking agents requires highly complex evaluation and selection mechanisms. This may explain why existing antibody drugs have only been approved for rare diseases lacking standard therapies, and it is also a challenge facing the development of other agents with similar mechanisms, such as NLRP3 inhibitors. Canakinumab has demonstrated promising efficacy in gout and cardiovascular disease, but its benefits do not sufficiently outweigh the side effects; consequently, it has not yet received approvals for these common conditions. Ziltivekimab faces similar challenges. A few years ago, Novartis promoted the concept of “specializing common diseases” for canakinumab, proposing to stratify common diseases into subtypes with varying sensitivities to different therapies. This approach could make Novartis’s earlier pathway-based drug discovery model more practical. This model posits that a given mechanism should first target rare diseases with a broader therapeutic window, and then expand to common diseases sharing the same pathway abnormalities.