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Therapy Name | Mirdametinib + Sorafenib |
Synonyms | |
Therapy Description | |
Drug Name | Trade Name | Synonyms | Drug Classes | Drug Description |
---|---|---|---|---|
Mirdametinib | Gomekli | PD0325901|PD 0325901|PD-901|PD-0325901 | MEK inhibitor (Pan) 26 MEK1 Inhibitor 26 MEK2 Inhibitor 24 | Gomekli (mirdametinib), a derivative of CI-1040, is a pan-MEK inhibitor, which inhibits activation of MAPK/ERK resulting in decreased tumor cell proliferation (PMID: 18952427, PMID: 32147669). Gomekli (mirdametinib) is FDA-approved for use in adult and pediatric patients 2 years and older with neurofibromatosis type 1 who have symptomatic plexiform neurofibromas (FDA.gov). |
Sorafenib | Nexavar | BAY 43-9006 | CSF1R Inhibitor 28 FLT3 Inhibitor 69 KIT Inhibitor 57 PDGFR-beta Inhibitor 14 RAF Inhibitor (Pan) 28 RET Inhibitor 53 VEGFR2 Inhibitor 37 | Nexavar (sorafenib) is a multikinase inhibitor with activity against several kinases, including RAF kinases, VEGFR2, VEGFR3, PDGFR-beta, KIT, FLT3, RET, and CSF1R, potentially resulting in decreased tumor growth (PMID: 18445656, PMID: 15466206, PMID: 21517818). Nexavar (sorafenib) is FDA approved for metastatic differentiated thyroid carcinoma, hepatocellular carcinoma, and renal cell carcinoma (FDA.gov). |
Molecular Profile | Indication/Tumor Type | Response Type | Therapy Name | Approval Status | Evidence Type | Efficacy Evidence | References |
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NRAS Q61L | acute myeloid leukemia | no benefit | Mirdametinib + Sorafenib | Preclinical - Cell culture | Actionable | In a preclinical study, addition of Nexavar (sorafenib) to Gomekli (mirdametinib) treatment did not demonstrate increased sensitivity compared to PD-0325901 alone in an acute myeloid leukemia cell line harboring NRAS Q61L in culture (PMID: 28923853). | 28923853 |
FLT3 exon 14 ins | acute myeloid leukemia | sensitive | Mirdametinib + Sorafenib | Preclinical - Patient cell culture | Actionable | In a preclinical study, Nexavar (sorafenib) and Gomekli (mirdametinib) synergistically induced apoptosis and inhibited proliferation of acute myeloid leukemia (AML) cell lines harboring FLT3 internal tandem duplication (ITD) mutations in culture, inhibited Erk phosphorylation in FLT3-ITD mutant AML patient cells, and reduced leukemic burden in a FLT3-ITD mutant AML cell line xenograft model (PMID: 28923853). | 28923853 |
Clinical Trial | Phase | Therapies | Title | Recruitment Status | Covered Countries | Other Countries |
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