Our Pipeline of ADCs
Building drug conjugates with multimodal mechanisms of action to provide an impenetrable wall of activity.
Coromip: Unlocking the Full Potential of PI3K/mTOR Through ADC Delivery
- Warhead is PI3K/mTOR inhibitor Omipalisib
- Targets PI3K/mTOR-addicted tumors
- Systemically dose-limited > ADC-enabled
- Designed to unlock the next wave of targeted ADC efficacy
Axis-Based Dual Payload Discovery Programs leveraging Coromip backbone
Our Pipeline of Coromip ADCs
Indications
Lead
Discovery
In Vivo
Cyno Tox
Preclinical
ER+/HER2- BrCa*
mAb Target: TROP2
SacI-81
Ovarian/Endometrial*
mAb Target: TROP2
SacI-81
Therapeutic Discovery
EGFRmut NSCLC
mAb Target: TROP2
SacI-81
KRASmut NSCLC
mAb Target: TROP2
SacI-81
Therapeutic Discovery
TNBC
mAb Target: TROP2
SacI-81
HER+ R/R Enhertu BrCa*
mAb Target: HER2
Zan-81
Hematologic
mAb Target: CDH17
Lonca-81
Prostate
mAb Target: CD180
PSMA-81
Oncology & Non-Oncology
mAb Target: Various
Various
Target Validation
CMC, GMP, GLP
Clinical
Our Therapeutic Programs
CO-1024: First in Class of ADCs to Treat Solid Tumors
Despite considerable progress made in the treatment of Non-small Cell Lung Cancer (NSCLC), Colorectal Cancer (CRC), Gastric Cancer, and Pancreatic Cancers with immune therapy, only a fraction of these patients respond with durable responses. CO-1024-directed ADCs offer a new approach to the treatment of these malignancies with a high unmet medical need.
A Franchise of CO-1008 Directed Therapies
Patients with Acute Myeloid Leukemia (AML) currently have few therapeutic options that provide a durable response to tumors. Despite considerable progress in treatment for Non-Hodgkins Lymphoma (NHL), a significant population of Diffuse Large B Cell Lymphoma (DLBCL), Mantle Cell Lymphoma (MCL), and B Cell Acute Lymphoblastic Leukemia (B-ALL) tumors are either CD19-negative or relapse as CD19-negative tumors. CO-1008 ADC aims to resolve the unmet medical needs of patients diagnosed with AML, specifically in tumors with MLL/KMT2A fusions. CO-1008 target expression is driven by MLL/KMT2A fusion products and regulates the hyperinflammatory nature of these tumors. The CO-1008 target has low toxicity liabilities with expression absent in hematopoietic stem cells and common myeloid progenitors.