AstraZeneca Pays $50 Million Up-Front for Cancer Drug


Merck and AstraZeneca recently announced a worldwide licensing agreement for Merck’s oral small molecule inhibitor of WEE1 kinase (MK-1775). MK-1775 is currently being evaluated in Phase IIa clinical studies in combination with standard-of-care therapies for the treatment of patients with certain types of ovarian cancer.

WEE1 helps to regulate the cell-division cycle. The WEE1 inhibitor MK-1775 is designed to cause certain tumor cells to divide without undergoing normal DNA repair processes, ultimately leading to cell death. Preclinical evidence suggests that the combination of MK-1775 and DNA damage-inducing chemotherapy agents can enhance anti-tumor properties, in comparison to chemotherapy alone.

Under the terms of the agreement, AstraZeneca will pay Merck a $50 million up-front fee. In addition, Merck will be eligible to receive future payments tied to development and regulatory milestones, plus sales-related payments and tiered royalties. AstraZeneca will be responsible for all future clinical development, manufacturing, and marketing.

“MK-1775 is a strong addition to AstraZeneca’s growing oncology pipeline, which already includes a number of inhibitors of the DNA damage response,” said Susan Galbraith, Head of AstraZeneca’s Oncology Innovative Medicines Unit. “The compound has demonstrated encouraging clinical efficacy data, and we intend to study it in a range of cancer types in which there is a high unmet medical need.”

“Merck is committed to advancing potentially meaningful therapeutic options promptly for patients with cancer,” said Iain D. Dukes, Senior Vice President and Head of Licensing and External Scientific Affairs, Merck. “We are pleased to enter this agreement with AstraZeneca to realize the potential of MK-1775 while we focus on advancing our later stage oncology programs, MK-3475 and vintafolide.”

The agreement is contingent on expiration or termination of the waiting period under the Hart Scott-Rodino Antitrust Improvement Act.

WEE1 is a cell cycle checkpoint protein regulator. Preclinical data indicate that disruption of WEE1 may enhance the cell killing effects of some anticancer agents. MK-1775 is an investigational orally available inhibitor of the cell cycle checkpoint protein WEE1. MK-1775 is being evaluated in Phase IIa clinical trials for the treatment of patients with P53-deficient ovarian cancer.