Novartis has agreed to acquire Boston-based clinical-stage biopharmaceutical company Anthos Therapeutics for an upfront payment of $925m.
The transaction includes $2.15bn of potential additional payments, contingent on regulatory and sales milestones.
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It is anticipated to close in the first half of 2025.
The acquisition aligns with Novartis’ growth strategy and therapeutic area focus, capitalising on the company’s established strengths in the cardiovascular domain.
Novartis Development president and chief medical officer Shreeram Aradhye stated: “We are excited to join forces to advance the development of abelacimab, a potential first-in-class treatment and safer approach for stroke prevention in atrial fibrillation as well as cancer-associated thrombosis.
“Welcoming Anthos Therapeutics strengthens our focus in the cardiovascular space and complements our portfolio of life-changing treatments, comprehensive clinical programmes and strategic collaborations that help thousands of patients with heart disease around the world.”
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By GlobalDataLaunched in 2019 by Novartis and Blackstone Life Sciences, Anthos has been developing abelacimab, a highly selective and fully human monoclonal antibody.
Licenced from Novartis, the therapy targets Factor XI to achieve anticoagulation without compromising haemostasis.
Phase II trials have demonstrated a significant decrease in bleeding events in subjects with atrial fibrillation treated with the antibody against those receiving standard direct-oral anticoagulants.
Three Phase III trials are currently underway, investigating abelacimab for arterial and venous clots across various subject groups.
The US Food and Drug Administration granted fast track status to the antibody in July 2022 for the treatment of thrombosis associated with cancer.
In September 2022, it received fast track designation for the prevention of stroke and systemic embolism in atrial fibrillation patients.
Abelacimab’s mechanism of action involves binding to Factor XI and blocking its activation, thereby preventing the formation of Factor XIa.
This approach is inspired by the natural deficiency of Factor XI, which is known to protect against thromboembolic conditions.
