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|Therapy Name||PLX4720 + Ponatinib|
|Drug Name||Trade Name||Synonyms||Drug Classes||Drug Description|
|PLX4720||PLX-4720|PLX 4720||BRAF Inhibitor 20||PLX4720 is a 7-azaindole derivative and RAF kinase inhibitor with greater affinity for BRAF V600E than BRAF wild-type, which may induce cell cycle arrest and apoptosis, and lead to tumor growth inhibition and regression (PMID: 18287029).|
|Ponatinib||Iclusig||AP24534||ABL Inhibitor (pan) 9 BCR-ABL Inhibitor 28 DDR1 Inhibitor 8 DDR2 inhibitor 7 FGFR Inhibitor (Pan) 22 FLT3 Inhibitor 57 KIT Inhibitor 52 PDGFR-alpha Inhibitor 9 RET Inhibitor 43 SRC Inhibitor 31 VEGFR Inhibitor (Pan) 33||Iclusig (ponatinib) inhibits the Bcr-Abl fusion, and other tyrosine kinases, such as RET, DDR, VEGFR, FGFR, KIT, and FLT3 (PMID: 23526464, PMID: 25284748, PMID: 19878872). Iclusig (ponatinib) is FDA approved for chronic myeloid leukemia (CML) and Philadelphia chromosome positive acute lymphoblastic leukemia (Ph positive ALL) as well as ABL1 T315I CML and ABL1 T315I Ph positive ALL (FDA.gov).|
|Molecular Profile||Indication/Tumor Type||Response Type||Therapy Name||Approval Status||Evidence Type||Efficacy Evidence||References|
|BRAF V600E||thyroid gland cancer||sensitive||PLX4720 + Ponatinib||Preclinical - Cell line xenograft||Actionable||In a preclinical study, Iclusig (ponatinib) and PLX4720 treatment demonstrated synergy, and inhibited Erk, Mek, and c-jun phosphorylation, reduced cell proliferation, colony formation, and migration, and induced apoptosis in thyroid cancer cells harboring BRAF V600E and in PLX4720-resistant cells harboring BRAF V600E in culture, and inhibited tumor growth, reduced lung and liver metastases, and increased survival in cell line xenograft models (PMID: 31937621).||31937621|
|Clinical Trial||Phase||Therapies||Title||Recruitment Status||Covered Countries||Other Countries|