About Cedilla’s CDK2 ProgramĬDK2 (Cyclin-Dependent Kinase 2) has been a major target of interest for cancer indications driven by amplification or high levels of Cyclin E, including in roughly half of patients with CDK4/6-resistant breast cancer. The company’s portfolio of TEAD inhibitors encompasses multiple chemotypes with different effects on TEAD isoforms and cofactors, providing Cedilla with a range of starting points for selecting a candidate with an optimal profile for effective and combinable TEAD inhibition.
#E edge pipeline full
TEAD is also increasingly implicated in resistance to targeted therapies, including those for the treatment of EGFR-mutated and KRAS-mutated lung cancer.Ĭedilla’s program is designed to disrupt this hyperactivated state by preventing a post-translational modification required for full function. In certain cancer states such as mesothelioma and certain squamous cell carcinomas, the Hippo pathway is dysregulated, resulting in hyperactivation. TEAD (Transcriptional Enhanced Associate Domain) is a key component of the Hippo signaling pathway. Learn more about our approach to conditional inhibition » About Cedilla’s TEAD Program The first two targets that Cedilla has selected for the development of conditional inhibitors are TEAD and CDK2. We then deploy cutting-edge technologies in a focused and directed manner, leveraging the knowledge and insight our team has gained along the way, to find new and non-obvious binding sites and mechanisms of action. We start by developing a deep understanding of the disease biology and contextual biochemistry of the target. Our asset-by-asset approach is not one-size-fits-all. Cedilla’s conditional inhibitors are small molecules that are unlocking historically undruggable cancer targets for therapeutic development.
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