• Breakthrough Therapy Designation was granted for the treatment of adult patients with KRAS G12C-mutated locally advanced or metastatic non-small cell lung cancer (NSCLC) who have had prior treatment with platinum-based chemotherapy and anti-PD-(L)1 antibody but have not been previously treated with a KRAS G12C inhibitor
• Orphan Drug Designation was granted for treatment of colorectal cancer (CRC) harboring KRAS G12C mutant protein.

D3 Bio, Inc, a clinical-stage oncology company focuses on discovery and development of precision oncology therapies, announced that the U.S. Food and Drug Administration (FDA) has granted a Breakthrough Therapy Designation to D3S-001, the company's next generation KRAS G12C-selective inhibitor, for the treatment of adult patients with KRAS G12C-mutated locally advanced or metastatic NSCLC who have received prior chemotherapy and immunotherapy but have not been previously treated with a KRAS G12C inhibitor. Additionally, D3S-001 has been granted Orphan Drug Designation for the treatment of adult patients with KRAS G12C-mutated locally advanced or metastatic CRC.

The Breakthrough Therapy and Orphan Drug Designations are based on clinical data from an ongoing Phase 1/2 study (NCT05410145) evaluating D3S-001 in patients with advanced solid tumors harboring a KRAS G12C mutation. Results from this ongoing clinical trial demonstrated highly compelling and durable efficacy according to RECIST (Response Evaluation Criteria in Solid Tumors) with a favorable safety and tolerability profile.

"We are very pleased to receive both Breakthrough Therapy and Orphan Drug Designations from the FDA for D3S-001, which highlights D3S-001's promising potential to address critical unmet needs in patients with KRAS G12C-mutated cancers," said George Chen, Founder and CEO of D3 Bio. "These designations also recognize D3S-001's novel profile as a next-generation KRAS G12C inhibitor. We look forward to bringing this exciting new treatment to patients with support and collaboration from health authorities."

KRAS mutations are among the most common oncogenic drivers in human cancers, found in approximately 25 to 30% of all tumors. The KRAS G12C mutation occurs in approximately 12% of NSCLC cases and 3 to 4% of CRC. Patients with KRAS G12C-mutated cancers often have more aggressive disease and limited responses to standard therapies, such as immunotherapy and/or chemotherapy.