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Find Clinical Drug Pipeline Developments & Deals by C4 Therapeutics
The collaboration aims to exclusively discover two targeted protein degraders against critical oncogenic proteins that C4T has progressed within its internal discovery pipeline using its proprietary TORPEDO® platform.
The proceeds will be used to develop and commercialize CFT8919, an orally bioavailable BiDAC™ degrader designed to be potent and selective against EGFR L858R for non-small cell lung cancer patients, in Greater China.
Under the agreement, Merck will develop degrader-antibody conjugates (DACs), an emerging modality designed to selectively target and neutralize disease-causing proteins in cancer cells.
CFT7455 is an orally bioavailable MonoDAC degrader designed to be highly potent and selective against its intended targets of IKZF1 and IKZF3 and overcome shortcomings of currently approved therapies to treat multiple myeloma (MM) and non-Hodgkin’s lymphoma (NHL).
CFT8919 is an orally bioavailable allosteric BiDAC™ degrader that is designed to be potent and selective against EGFR bearing an oncogenic L858R mutation. In preclinical studies, CFT8919 is active in in vitro and in vivo models of L858R driven non-small cell lung cancer.
Under the terms of the agreement, Betta Pharmaceuticals will develop and commercialize CFT8919, an orally bioavailable BiDAC™ degrader designed to be potent and selective against EGFR L858R for non-small cell lung cancer patients, in Greater China.
CFT1946 is an orally bioavailable BiDAC™ degrader designed to be potent and selective against BRAF V600 mutant targets. C4T is advancing CFT1946 to the clinic to study treatment for BRAF V600 mutant solid tumors including NSCLC, colorectal cancer, and melanoma.
In pre-clinical studies, CFT1946 is active in vivo and in vitro in models with BRAF-V600E-driven disease and in the escape mutant BRAF models. C4T is advancing CFT1946 to the clinic to study treatment for BRAF-V600 mutant solid tumors including lung, colorectal or melanoma.
CFT8634 is a BiDAC™ degrader targeting BRD9 for the treatment of cancers that are dependent on BRD9, including synovial sarcoma and SMARCB1-null cancers.
Single agent CFT7455 induces deep and durable degradation of IKZF1/3 and meaningful decreases in serum-free light chain at doses lower than expected based on pre-clinical studies.
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