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Authors | Bryan D. Smith, Molly M. Hood, Scott C. Wise, Michael D. Kaufman, Wei-Ping Lu, Thomas Rutkoski, Daniel L. Flynn and Michael C. Heinrich |
Title | Abstract 2690: DCC-2618 is a potent inhibitor of wild-type and mutant KIT, including refractory Exon 17 D816 KIT mutations, and exhibits efficacy in refractory GIST and AML xenograft models |
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URL | http://cancerres.aacrjournals.org/content/75/15_Supplement/2690 |
Abstract Text | Cancer Res August 1 2015 (75) (15 Supplement) 2690 |
Molecular Profile | Treatment Approach |
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Gene Name | Source | Synonyms | Protein Domains | Gene Description | Gene Role |
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Therapy Name | Drugs | Efficacy Evidence | Clinical Trials |
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Drug Name | Trade Name | Synonyms | Drug Classes | Drug Description |
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Gene | Variant | Impact | Protein Effect | Variant Description | Associated with drug Resistance |
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Molecular Profile | Indication/Tumor Type | Response Type | Therapy Name | Approval Status | Evidence Type | Efficacy Evidence | References |
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KIT D816Y | mast cell neoplasm | predicted - sensitive | Ripretinib | Preclinical - Cell culture | Actionable | In a preclinical study, Qinlock (ripretinib) inhibited proliferation of a mouse mastocytosis cell line expressing KIT K816Y in culture (Cancer Res 2015;75(15 Suppl):Abstract nr 2690). | detail... |
KIT N822K | acute myeloid leukemia | sensitive | Ripretinib | Preclinical - Pdx | Actionable | In a preclinical study, Qinlock (ripretinib) induced tumor regression in a patient-derived xenograft (PDX) model of acute myeloid leukemia harboring KIT N822K (Cancer Res 2015;75(15 Suppl):Abstract nr 2690). | detail... |