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Association details:
| Biomarker: | RAS mutation |
|---|---|
| Cancer: | Pancreatic Ductal Adenocarcinoma |
| Drug: | IMM-6-415 (MEK inhibitor) |
| Direction: | Sensitive |
Evidence:
Source:
Title:
449 Cyclic disruption of the mitogen-activated protein kinase (MAPK) pathway by the dual MEK inhibitor, IMM-6-415, enhances PD1 and CTLA4 checkpoint blockade in RAS mutant tumors
Published date:
11/08/2022
Excerpt:
Humanized 3D tumor models revealed a promising sensitivity profile for IMM-6-415 in RAS-mutant CRC and PDAC….We demonstrate that IMM-6-415 displays single-agent activity in multiple RAS-mutant models, has a 0.3h half-life, is well tolerated in mice, and when combined at sub-MTD levels with either PD1 or CTLA4 checkpoint inhibitors, significantly improved responses in the CT-26 model (p-value < 0.05).
DOI:
10.1136/jitc-2022-SITC2022.0449
Source:
Title:
449 Cyclic disruption of the mitogen-activated protein kinase (MAPK) pathway by the dual MEK inhibitor, IMM-6-415, enhances PD1 and CTLA4 checkpoint blockade in RAS mutant tumors
Published date:
11/08/2022
Excerpt:
Humanized 3D tumor models revealed a promising sensitivity profile for IMM-6-415 in RAS-mutant CRC and PDAC….We demonstrate that IMM-6-415 displays single-agent activity in multiple RAS-mutant models, has a 0.3h half-life, is well tolerated in mice, and when combined at sub-MTD levels with either PD1 or CTLA4 checkpoint inhibitors, significantly improved responses in the CT-26 model (p-value < 0.05).
Secondary therapy:
PD1 inhibitor; CTLA4 inhibitor
DOI:
10.1136/jitc-2022-SITC2022.0449
