Q-4747 Quizartinib, Free Base, >99%

Synonyms : [AC220] [AC010220]

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  • 1 mg
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  • 5 mg
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  • 10 mg
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  • 25 mg
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  • 50 mg
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  • 100 mg
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  • 200 mg
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  • 250 mg
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  • 500 mg
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  • 1 g
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  • M.W. 560.67
  • C29H32N6O4S
  • [950769-58-1]

Storage: Store at or below -20 ºC. Solubility: Soluble in DMSO at 200 mg/mL; very poorly soluble in ethanol; very poorly soluble in water; maximum solubility in plain water is estimated to be about 10-20 µM; buffers, serum, or other additives may increase or decrease the aqueous solubility. Disposal: A.

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  • Quizartinib, also known as AC-220, is a second-generation FLT3 receptor tyrosine kinase inhibitor.
  • Quizartinib has high affinity for FLT3 in a binding assay (Kd = 1.6 nM) and is a potent inhibitor in cellular autophosphorylation assays (IC50 = 1.1 nM for FLT3-ITD and 4.2 nM for wt FLT3). It inhibits the growth of human leukemia cell line MV4-11 (IC50 = 0.56 nM) which is FLT3 dependent and contains a homozygous FLT3-ITD mutation, and A375 cells (IC50 > 10,000 nM) which are not FLT3 dependent and contain an activating mutation in BRAF. Quizartinib inhibits FLT3 activity in subcutaneous MV4-11 tumor xenografts. Treatment with quizartinib at 10 mg/kg in MV4-11 tumor xenografts results in rapid and complete regression of tumors. Quizartinib prolongs the survival of mice injected with MV4-11 cells in a dose-dependent manner. Zarrinkar, P.P., et al. "AC220 is a uniquely potent and selective inhibitor of FLT3 for the treatment of acute myeloid leukemia (AML)." Blood 114: 2984-2992 (2009).
  • Quizartinib inhibited the autophosphorylation of wt FLT3 and FLT3/ITD with IC50 values of 5 and 1 nM, respectively. However, the cytotoxic effect of quizartinib was not exclusively dependent on inhibition of FLT3 autophosphorylation. It depended on the clinical status of acute myoloid leukemia and FLT3-mutant allelic burden. Relapsed samples and samples with a high mutant allelic burden were more sensitive to the cytotoxic effect from FLT3 inhibition by quizartinib compared with the samples obtained at diagnosis or those with a low mutant allelic burden. Pratz, K.W., et al. "FLT3-mutant allelic burden and clinical status are predictive of response to FLT3 inhibitors in AML." Blood 115: 1425-1432 (2010).
  • Quizartinib has demonstrated significant promise in early phases of clinical investigation with patients with acute myeloid leukemia (AML), and is now in more advanced clinical trials. Fathi, A.T. and Chabner, B.A. "FLT3 Inhibition as Therapy in Acute Myeloid Leukemia: A Record of Trials and Tribulations." The Oncologist 16: 1162-1174 (2011).
  • Quizartinib has demonstrated significant promise in early phases of clinical investigation with patients with acute myeloid leukemia (AML), and is now in more advanced clinical trials. Fathi, A.T. and Chabner, B.A. "FLT3 Inhibition as Therapy in Acute Myeloid Leukemia: A Record of Trials and Tribulations." The Oncologist 16: 1162-1174 (2011).
  • Related CAS numbers: 1132827-21-4 for the quizartinib dihydrochloride.
  • Sold for laboratory or manufacturing purposes only; not for human, veterinary, food, or household use.
  • This product is offered for R&D use in accordance with (i) 35 USC 271(e)+A13(1) in the U.S.; (ii) Section 69.1 of Japanese Patent Law in Japan; (iii) Section 11, No. 2 of the German Patent Act of 1981 in Germany; (iv) Section 60, Paragraph 5b of the U.K. Patents Act of 1977 in the U.K.; (v) Sections 55.2(1) and 55.2(6) and other common law exemptions of Canadian patent law; (vi) Section 68B of the Patents Act of 1953 in New Zealand together with the amendment of same by the Statutes Amendment Bill of 2002; (vii) such related legislation and/or case law as may be or become applicable in the aforementioned countries; and (viii) such similar laws and rules as may apply in various other countries.
  • Not available in some countries; not available to some institutions; not available for some uses.
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