KRAS G12C Modulating Compound Combination Therapy
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Solution Overview
Problem
Current treatments for KRAS mutant cancers, particularly those with the G12C mutation, are inadequate, as direct targeting of KRAS has proven difficult and existing therapies do not effectively induce robust cell death or apoptosis, highlighting a need for improved combination therapies.
Innovation Solution
Administering a KRAS, HRAS, or NRAS G12C mutant modulating compound in combination with additional therapeutic agents such as EGFR inhibitors, PI3K inhibitors, or chemotherapeutic agents to synergistically inhibit mutant KRAS activity and induce apoptosis in cancer cells.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Measurement precision
If direct targeting of KRAS is attempted, then specific inhibition of mutant KRAS activity can be achieved, but robust cell death and apoptosis are not effectively induced
Solution Approach 1:
The patent combines a KRAS G12C modulating compound with additional therapeutic agents (such as EGFR inhibitors, PI3K inhibitors, or chemotherapeutic agents) to create a combination therapy that achieves both specific KRAS inhibition and robust cell death induction, resolving the contradiction between specificity and effectiveness
2Ease of operation
If existing therapies are used for KRAS mutant cancers, then treatment can be administered, but effective treatment options are lacking and survival chances remain extremely low
Solution Approach 1:
The patent changes the therapeutic parameter from monotherapy to combination therapy, incorporating a KRAS G12C modulating compound with additional therapeutic agents, which dramatically improves clinical outcomes and survival rates while maintaining ease of administration
3Productivity
If KRAS depletion is performed in cancer cells, then growth inhibition is observed, but robust induction of cell death or apoptosis does not occur
Solution Approach 1:
The patent introduces additional therapeutic agents as intermediaries that work in conjunction with the KRAS modulating compound to bridge the gap between growth inhibition and cell death induction, enabling robust apoptosis while maintaining growth suppression
Data Source
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AI summary
Combination therapies for treatment of cancers associated with mutations in the KRAS gene are provided. Compositions comprising therapeutic agents for treatment of cancers associated with mutations in the KRAS gene are also provided.