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What are the current treatment options for patients with KRAS-mutated colorectal cancer who have progressed on first-line therapy? 

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Patients with KRAS-mutated colorectal cancer who have progressed on first-line therapy have several treatment options. Targeted therapies like BRAF inhibitors and immune checkpoint inhibitors show promise for patients without KRAS and PIK3CA mutations . Specifically, inhibitors like Adagrasib and Sotorasib are effective against KRAS G12C mutations, with ongoing development of new inhibitors for other KRAS mutations . Additionally, regorafenib, a multikinase inhibitor, has shown efficacy as a second-line therapy for RAS-mutant metastatic colorectal cancer, prolonging overall survival . Furthermore, the emergence of resistance to direct inhibitors can be addressed with combination therapies involving indirect pathway inhibition and immunotherapy . These treatment options represent significant advancements in managing KRAS-mutated colorectal cancer post first-line therapy progression.

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Combination therapies involving KRAS G12C inhibitors, CDK46 inhibitors like palbociclib, and other targeted agents are promising for KRAS-mutated colorectal cancer patients who have progressed on first-line therapy.
Current second-line treatment for patients with RAS-mutant colorectal cancer after progression on first-line therapy includes regorafenib monotherapy, showing manageable toxicity and potential benefit in selected patients with favorable features.
Emerging therapies for KRAS-mutated colorectal cancer post first-line treatment include novel agents targeting KRAS G12C mutation, signifying a significant advancement in managing affected patients.
Current treatment options for KRAS-mutated colorectal cancer post first-line therapy include KRAS G12C inhibitors like Sotorasib and Adagrasib, combination therapies with chemotherapies, immunotherapies, and pan-pathway inhibitors.
Patients with KRAS-mutated colorectal cancer post first-line therapy have limited targeted options, including specific KRAS G12C inhibitors for a small subset and potential benefit from combination therapies with PI3K inhibitors.

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