Therapy Detail
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| Therapy Name | GMI-1359 + Sorafenib |
| Synonyms | |
| Therapy Description | |
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| Drug Name | Trade Name | Synonyms | Drug Classes | Drug Description |
|---|---|---|---|---|
| GMI-1359 | GMI1359|GMI 1359 | CXCR4 Inhibitor 15 | GMI-1359 is a dual inhibitor of Cxcr4 and E-selectin, which may inhibit leukemia cell adhesion and lead to apoptosis (Blood 2015 126(23):3790, PMID: 31877673, PMID: 31431613). | |
| 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). |
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| Molecular Profile | Indication/Tumor Type | Response Type | Therapy Name | Approval Status | Evidence Type | Efficacy Evidence | References |
|---|---|---|---|---|---|---|---|
| FLT3 exon 14 ins | leukemia | predicted - sensitive | GMI-1359 + Sorafenib | Preclinical - Cell culture | Actionable | In a preclinical study, combination of GMI-1359 with Nexavar (sorafenib) enhanced apoptosis compared to Nexavar (sorafenib) alone (48.9% vs 36.6%) in leukemia cell lines harboring FLT3 internal tandem duplication (ITD) mutations (Blood 2015 126(23):3790). | detail... |
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| Clinical Trial | Phase | Therapies | Title | Recruitment Status | Covered Countries | Other Countries |
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