C4 Therapeutics Presents Preclinical Data on CFT7455, a Novel IKZF1/3 Degrader for the Treatment of Hematologic Malignancies, at the AACR Annual Meeting 2021

– CFT7455 Demonstrated High Cereblon Binding Affinity and Rapid, Deep IKZF1/3 Degradation Enabling Activity across a Panel of Multiple Myeloma Cell Lines Including IMiD-Resistant Models –

– CFT7455 Promotes Sustained Degradation of IKZF1/3 and Durable Anti-tumor Response, Including Regressions in an IMiD-Insensitive Myeloma Tumor Xenograft Model –

– CFT7455 Phase 1/2 Trial in Multiple Myeloma and Non-Hodgkin Lymphomas On Track for 1H 2021 Initiation –

WATERTOWN, Mass., April 10, 2021 (GLOBE NEWSWIRE) -- C4 Therapeutics, Inc. (C4T) (Nasdaq: CCCC), a biopharmaceutical company pioneering a new class of small-molecule medicines that selectively destroy disease-causing proteins through degradation, today presented preclinical data for CFT7455, the Company’s lead program, a MonoDAC^TM degrader targeting IKZF1/3 for the treatment of hematologic malignancies. These results, which support clinical evaluation of CFT7455 in multiple myeloma, were delivered as a late-breaking oral presentation during the first session of the American Association for Cancer Research (AACR) Annual Meeting 2021.

“IKZF1/3 proteins are critical dependencies of B cell malignancies including multiple myeloma and subsets of non-Hodgkin’s lymphoma,” said Stewart Fisher, Ph.D., chief scientific officer of C4 Therapeutics. “We are pleased to share preclinical data demonstrating that potent catalytic IKZF1/3 degradation activity of CFT7455, coupled with optimized pharmacological properties, can result in regression of multiple myeloma xenograft tumors not responsive to approved IMiD therapies. We are optimistic that the in vitro and in vivo data we saw preclinically will translate into improved, clinically meaningful outcomes for patients and we look forward to initiating our CFT7455 Phase 1/2 clinical trial in the first half of this year.”

Summary of Results

C4T conducted in vitro studies to confirm CFT7455’s intended mechanism. Notable observations include:

• CFT7455 binds with high affinity to the E3 ligase adapter protein, cereblon (Kd = 0.9 nM);
• In vitro, CFT7455 treatment results in deep, rapid degradation of IKZF1/3 proteins, resulting in apoptotic cell death; and
• CFT7455 demonstrated broad, potent anti-proliferative activity in a panel of multiple myeloma cell lines.