Gilead and Kymera Partner on Novel CDK2 Molecular Glue Degrader for Cancer Treatment
Key Insights
Gilead Sciences and Kymera Therapeutics (search) have entered into an exclusive option and license agreement to develop novel molecular glue degraders targeting CDK2 (search) for cancer treatment.
The collaboration focuses on CDK2 (search)-directed molecular glue degraders that selectively remove the CDK2 protein from cells rather than just inhibiting its function, potentially offering more precise cancer treatments.
Kymera is eligible to receive up to $750 million in total payments, including up to $85 million in upfront and potential option exercise payments, plus tiered royalties on net product sales.
Gilead Sciences and Kymera Therapeutics (search) have announced an exclusive option and license agreement to accelerate the development and commercialization of a novel molecular glue degrader (MGD) program targeting cyclin-dependent kinase 2 (CDK2 (search)) with broad oncology treatment potential including in breast cancer and other solid tumors.
Revolutionary Approach to Cancer Treatment
CDK2 (search)-directed MGDs represent a new type of drug designed to remove CDK2 – a key contributor in tumor growth – rather than just inhibiting its function. Traditional inhibitors of CDK2 prevent it from working but often interfere with similar proteins, which can cause undesired side effects. MGDs have the potential to provide more precise, safe and effective treatments for cancers that rely on CDK2 activity by selectively removing this protein from cells.
"MGDs are opening exciting new possibilities in cancer research by offering a way to eliminate disease-driving proteins rather than just blocking them. This mechanism aligns within our oncology scientific framework where we evaluate therapeutic agents that selectively target and kill cancer cells with minimal impact on healthy tissue," said Flavius Martin, MD, Executive Vice President, Research, Gilead Sciences.
Compelling Preclinical Profile
Kymera's highly specific, orally active, CDK2 (search) molecular glue degraders have demonstrated a compelling preclinical profile and have the potential to transform the therapeutic landscape for breast cancer patients and other tumor types with high unmet medical need.
"We are excited to announce this strategic collaboration with Gilead Sciences, highlighting our dedication to innovation in the field with our first disclosed molecular glue program. We are committed to developing highly selective, potent, oral degrader medicines that address key disease-causing proteins and pathways that are undrugged or inadequately drugged by existing technologies," said Nello Mainolfi, PhD, Founder, President and CEO, Kymera Therapeutics (search).
Financial Terms and Development Structure
Under the terms of the agreement, Kymera is eligible to receive up to $750 million in total payments, including up to $85 million in upfront and potential option exercise payments. In addition, Kymera may also receive tiered royalties ranging from high single-digit to mid-teens on net product sales under the collaboration.
Kymera will lead all research activities for the CDK2 (search) program. If Gilead exercises its option to exclusively license the program, Gilead will have global rights to develop, manufacture and commercialize all products resulting from the collaboration.
The transaction is expected to reduce Gilead's GAAP and non-GAAP 2025 EPS by approximately $0.02 - $0.03, as Gilead does not exclude acquired IPR&D expenses from its non-GAAP financial measures.
Addressing Unmet Medical Needs
The collaboration aims to advance this novel oral program with the potential to drive meaningful improvements in the standard of care for patients living with breast cancer and other cancers that are inadequately served with existing therapies. The partnership represents Kymera's first disclosed molecular glue program and highlights both companies' commitment to developing innovative cancer treatments that target previously undruggable or inadequately drugged proteins and pathways.