Quizartinib | Selective FLT3 Inhibitor
NMR (Conforms)
Available Options
| Size: | Price | Quantity | |
|---|---|---|---|
| 5 mg | $50.00 | ||
| 25 mg | $130.00 |
Quizartinib (950769-58-1) is a potent and selective inhibitor of FLT3 (Kd = 1.6nM, IC50 = 0.56 nM MV4-11 cells).1 It is in clinical trials for treatment of Acute Myelogenous Leukemia (AML).2,3 Quizartinib priming resulted in prevention of myelosuppression in mice treated with 5-FU and Gemcitabine.4 Quizartinib showed significant reversal of ABCG2-mediated multidrug resistance (@ 3 µM) via antagonism of drug efflux function.5,6
References/Citations:
1) Chao et al. (2009) Identification of N-(5-tert-butyl-isoxazol-3-yl)-N’-{4-[7-(2-morpholin-4-yl-ethoxy)imidazo[2,1-b][1,3]benzothiazol-2-yl]phenyl}urea dihydrochloride (AC220), a uniquely potent, selective, and efficacious FMS-like tyrosine kinase-3 (FLT3) inhibitor; J. Med. Chem. 52 7808
2) Zarrinkar et al. (2009); AC220 is a uniquely potent and selective inhibitor of FLT3 for the treatment of acute myeloid leukemia(AML); Blood 114 2984
3) Fathi and Chen (2017); The role of FLT3 inhibitors in the treatment of FLT3-mutated acute myeloid leukemia; Eur. J .Haematol. 98 330
4) Taylor and Langdon (2017); Hitting the snooze button: Inducing quiescence with the FLT3 inhibitor quizartinib protects hematopoietic progenitors from chemotherapy; Mol. Cell Oncol. 4 e1378156
5) Li et al. (2017); Quizartinib (AC220) reverses ABCG2-mediated multidrug resistance: In vitro and In vivo studies; Oncotarget 8 93785
6) Bhullar et al. (2013) The FLT3 inhibitor quizartinib inhibits ABCG2 at pharmacologically relevant concentrations, with implications for both chemosensitization and adverse drug reactions; PLoS One 8 e71266
NMR (Conforms)
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Product Data Sheet:
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Quizartinib (950769-58-1) is a potent and selective inhibitor of FLT3 (Kd = 1.6nM, IC50 = 0.56 nM MV4-11 cells).1 It is in clinical trials for treatment of Acute Myelogenous Leukemia (AML).2,3 Quizartinib priming resulted in prevention of myelosuppression in mice treated with 5-FU and Gemcitabine.4 Quizartinib showed significant reversal of ABCG2-mediated multidrug resistance (@ 3 µM) via antagonism of drug efflux function.5,6
References/Citations:
1) Chao et al. (2009) Identification of N-(5-tert-butyl-isoxazol-3-yl)-N’-{4-[7-(2-morpholin-4-yl-ethoxy)imidazo[2,1-b][1,3]benzothiazol-2-yl]phenyl}urea dihydrochloride (AC220), a uniquely potent, selective, and efficacious FMS-like tyrosine kinase-3 (FLT3) inhibitor; J. Med. Chem. 52 7808
2) Zarrinkar et al. (2009); AC220 is a uniquely potent and selective inhibitor of FLT3 for the treatment of acute myeloid leukemia(AML); Blood 114 2984
3) Fathi and Chen (2017); The role of FLT3 inhibitors in the treatment of FLT3-mutated acute myeloid leukemia; Eur. J .Haematol. 98 330
4) Taylor and Langdon (2017); Hitting the snooze button: Inducing quiescence with the FLT3 inhibitor quizartinib protects hematopoietic progenitors from chemotherapy; Mol. Cell Oncol. 4 e1378156
5) Li et al. (2017); Quizartinib (AC220) reverses ABCG2-mediated multidrug resistance: In vitro and In vivo studies; Oncotarget 8 93785
6) Bhullar et al. (2013) The FLT3 inhibitor quizartinib inhibits ABCG2 at pharmacologically relevant concentrations, with implications for both chemosensitization and adverse drug reactions; PLoS One 8 e71266
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