TEAD Precision Therapeutic
CDK2-Cyclin E Precision Therapeutic
Innate Immune Precision Therapeutic
Additional Precision Therapeutics
TEAD Precision Therapeutic Preclinical
CDK2-Cyclin E Precision Therapeutic Preclinical
Innate Immune Precision Therapeutic Discovery
Additional Precision Therapeutics Discovery

Conditional Inhibitors

About Cedilla’s TEAD Program

TEAD (Transcriptional Enhanced Associate Domain) is a key component of the Hippo signaling pathway, which is aberrantly regulated in solid tumors such as mesothelioma and certain squamous cell carcinomas. TEAD is also increasingly implicated in resistance to targeted therapies, including those for the treatment of EGFR-mutated and KRAS-mutated lung cancer.

Cedilla’s program is designed to inhibit the function of TEAD by preventing a post-translational modification required for full function. 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.

About Cedilla’s CDK2 Program

CDK2 (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. In addition, Cyclin E amplification drives genetically defined subsets of ovarian, uterine, stomach and esophageal cancers. . The CDK2-Cyclin E cancer node has remained inaccessible due to challenges in achieving selectivity over other CDKs, particularly CDK1, and Cyclin E isoforms. Cedilla has developed a unique series of inhibitors that bind to a previously unreported site on the CDK2-Cyclin E complex with unprecedented selectivity, potentially offering a substantial advance over two decades of industry efforts. Preclinical characterization suggests that the exquisite selectivity of Cedilla’s inhibitor could result in a better safety profile compared to traditional kinase inhibitors, particularly with respect to dose-limiting hematological toxicities.