Pipeline

ProgramIndicationsDiscoveryPreclinicalINDClinical
TEAD Precision Therapeutic
Oncology
CDK2-Cyclin E Precision Therapeutic
Oncology
Additional Precision Therapeutics
Oncology
Additional Precision Therapeutics
Oncology
IndicationStage
TEAD Precision Therapeutic Preclinical
CDK2-Cyclin E Precision Therapeutic Preclinical
Additional Precision Therapeutics Discovery
Additional Precision Therapeutics Discovery

Conditional Inhibitors

Cedilla’s conditional inhibitors are small molecules that are unlocking historically undruggable cancer targets for therapeutic development. Our asset-by-asset approach is not one-size-fits-all. We start by developing a deep understanding of the disease biology and contextual biochemistry of the target. 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. The first two targets that Cedilla has selected for the development of conditional inhibitors are TEAD and CDK2.

Learn more about our approach to conditional inhibition »

About Cedilla’s TEAD Program

TEAD (Transcriptional Enhanced Associate Domain) is a key component of the Hippo signaling pathway. In certain cancer states such as mesothelioma and certain squamous cell carcinomas, the Hippo pathway is dysregulated, resulting in hyperactivation. 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 disrupt this hyperactivated state 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. Selectively inhibiting CDK2 has historically been challenging because of the conserved function and structures of the CDK family of proteins, particularly CDK1, and Cyclin E isoforms.

Cedilla is leveraging the condition of CDK2 in complex with its binding partner, Cyclin E, to target a previously unreported binding site and develop inhibitors of CDK2 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.