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divarasib + bevacizumab + FOLFIRI
- Development stage
- Unknown
- Lead developer
- Genentech
- Modality
- Classical Binding Small Molecules → Small Molecules, Covalent Small Molecules → Small Molecules, Nucleic Acid-Directed Small Molecules → Small Molecules, Monoclonal Antibodies → Antibody-Based Therapeutics
- Administration
- Intravenous, Oral
01
Overview
This is a combination regimen consisting of **divarasib** (a selective, oral KRAS G12C inhibitor), **bevacizumab** (a recombinant humanized monoclonal antibody targeting vascular endothelial growth factor A, VEGF-A), and **FOLFIRI** (a chemotherapy regimen including folinic acid [leucovorin], fluorouracil [5-FU], and irinotecan). - Divarasib inhibits the KRAS G12C mutation, impairing oncogenic signal transduction in tumors harboring this mutation. - Bevacizumab inhibits angiogenesis by binding and neutralizing VEGF-A, preventing new blood vessel formation required for tumor growth and metastasis. - FOLFIRI acts via three agents: fluorouracil is a pyrimidine antagonist incorporated into RNA/DNA and is an irreversible thymidylate synthase inhibitor, irinotecan inhibits topoisomerase I, leading to DNA damage, and folinic acid enhances fluorouracil efficacy by stabilizing its binding to thymidylate synthase. The combination is under clinical development for metastatic colorectal cancer, particularly KRAS G12C-mutated cases, and may be used in other advanced gastrointestinal malignancies.
- Brand names
- Avastin + FOLFIRI
- Other names
- divarasib + bevacizumab + leucovorin + fluorouracil + irinotecan
02
Targets
KRASG12C (Kirsten rat sarcoma viral oncogene homolog G12C)TOP1 (DNA Topoisomerase I)VEGFA (Vascular endothelial growth factor A)TS (Thymidylate synthase)
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