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Quizartinib, AC-220

(CAS No:950769-58-1)
Quizartinib (AC220) is a second-generation FLT3 inhibitor for Flt3(ITD/WT) with IC50 of 1.1 nM/4.2 nM in MV4-11 and RS4;11 cells, respectively, 10-fold more selective for Flt3 than KIT, PDGFRα, PDGFRβ, RET, and CSF-1R. Phase 3.
CAS No:950769-58-1
Molecular Weight(MW):560.67
Purity:99.00%
Specification:500MG;1G;5G;10G;50G;100G
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QC Documents
　COA 　MSDS 　HPLC 　NMR
ChemicalInfomation
CAS No: 950769-58-1
Molecular formula(MF) C29H32N6O4S
Molecular Weight(MW): 560.67
Alias
Solubility
In vitro DMSO 33.2 mg/mL (59.21 mM)
Water <0.3 mg/mL
Ethanol <0.5 mg/mL
In vivo 15% Captisol 30 mg/mL
Biological Activity
Description Quizartinib (AC220) is a second-generation FLT3 inhibitor for Flt3(ITD/WT) with IC50 of 1.1 nM/4.2 nM in MV4-11 and RS4;11 cells, respectively, 10-fold more selective for Flt3 than KIT, PDGFRα, PDGFRβ, RET, and CSF-1R. Phase 3.
Features The most potent cellular FLT3-ITD inhibitor.
Targets
FLT3 (ITD) [1]
(MV4-11 cells)		 FLT3 (WT) [1]
(RS4;11 cells)
1.1 nM 4.2 nM
In vitro

AC220, a unique, potent and selective inhibitor of FLT3, has high affinity for FLT3 with a Kd value of 1.6 nM. AC220 inhibits the autophosphorylation of FLT3 in the human leukemia cell lines MV4-11 which harbor a homozygous FLT3-ITD mutation and is FLT3 dependent, and RS4;11 which expresses wild-type FLT3 with IC50 values of 1.1 nM and 4.2 nM, respectively. AC220 is the most potent cellular FLT3-ITD inhibitor, leading to the most significant inhibition of MV4-11 cell proliferation with IC50 of 0.56 nM compared to all other FLT3 inhibitors whose IC50 values range from 0.87 nM to 64 nM. AC220 has no inhibitory activity against the proliferation of A375 cells which harbor an activating mutation in BRAF and are not FLT3 dependent, indicating a large window between FLT3 inhibition and general cytotoxic effects. [1]
Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
HL60/VCR Function Assay 0.1-10 μM 30 min enhances uptake of substrates of ABCG2 and ABCB1 in a concentration-dependent manner 23967177
K562/ABCB1 Function Assay 0.1-10 μM 30 min enhances uptake of substrates of ABCG2 and ABCB1 in a concentration-dependent manner 23967177
8226/MR20  Function Assay 0.1-10 μM 30 min enhances uptake of substrates of ABCG2 and ABCB1 in a concentration-dependent manner 23967177
K562/ABCG2 Function Assay 0.1-10 μM 30 min enhances uptake of substrates of ABCG2 and ABCB1 in a concentration-dependent manner 23967177
MCF-7 FLV1000 Kinase Assay 0–30 µM 5 min decreases [125I]-IAAP photolabeling of ABCB1 at IC50 of 3.3 μM 23967177
MCF-7 FLV1000 Kinase Assay 0–30 µM 5 min decreases [125I]-IAAP photolabeling of ABCB2 at IC50 of 0.07 μM 23967177
K562/ABCG2 Cell Viability Assays 0.1/0.5/1 µM 96 h sensitizes K562/ABCG2 cells to mitoxantrone topotecan  23967177
8226/MR20 Cell Viability Assays 0.1 µM 96 h sensitizes K562/ABCG2 cells to mitoxantrone topotecan  23967177
HMC1.1 Growth Inhibition Assay IC50=14 nM 23497317
HMC1.2 Growth Inhibition Assay IC50=1727 nM 23497317
p815 Growth Inhibition Assay IC50=445 nM 23497317
Kasumi-1 Growth Inhibition Assay IC50=36 nM 23497317
M-07e + SCF Growth Inhibition Assay IC50=77 nM 23497317
EOL-1 Growth Inhibition Assay IC50=1 nM 23497317
MV4;11 Growth Inhibition Assay IC50< 1 nM 23497317
MOLM14 Growth Inhibition Assay IC50< 1 nM 23497317
Pat.221 Growth Inhibition Assay IC50=675 nM 23497317
Pat.279 Growth Inhibition Assay IC50=3434 nM 23497317
Pat.299 Growth Inhibition Assay IC50=7248 nM 23497317
Pat.305 Growth Inhibition Assay IC50=7079 nM 23497317
Pat.375 Growth Inhibition Assay IC50=503 nM 23497317
Pat.379 Growth Inhibition Assay IC50=806 nM 23497317
Pat.368 Growth Inhibition Assay IC50=2700 nM 23497317
Pat.601 Growth Inhibition Assay IC50=1153 nM 23497317
HMC1.1 Apoptosis Assay IC50=31 nM 23497317
p815 Apoptosis Assay IC50=341 nM 23497317
Kasumi-1 Apoptosis Assay IC50=67 nM 23497317
M-07e + SCF Apoptosis Assay IC50=78 nM 23497317
EOL-1 Apoptosis Assay IC50< 1 nM 23497317
MV4;11 Apoptosis Assay IC50=2 nM 23497317
MOLM14 Apoptosis Assay IC50=3 nM 23497317
GIST822 Apoptosis Assay IC50=109 nM 23497317
Pat.368 Apoptosis Assay IC50=2998 nM 23497317
Pat.601 Apoptosis Assay IC50=876 nM 23497317
MV4-11 Growth Inhibition Assay 72 h IC50=0.3 nM 23412931
MOLM-14 Growth Inhibition Assay 72 h IC50=0.1 nM 23412931
SEM-K2 Growth Inhibition Assay 72 h IC50=0.4 nM 23412931
RS4;11 Growth Inhibition Assay 72 h IC50>10,000 nM 23412931
THP-1 Growth Inhibition Assay 72 h IC50>10,000 nM 23412931
MV4-11 Apoptosis Assay 8/24 h induces significant and dose-dependent PARP cleavage and accumulation of sub-2N DNA 23412931
MOLM-14 Apoptosis Assay 8/24 h induces significant and dose-dependent PARP cleavage and accumulation of sub-2N DNA 23412931
SEM-K2 Apoptosis Assay 8/24 h induces significant and dose-dependent PARP cleavage and accumulation of sub-2N DNA 23412931
MV4-11 Growth Inhibition Assay 72 h IC50=0.56 ± 0.3 nM 19654408
A375 Growth Inhibition Assay 72 h IC50> 10 000 nM 19654408

... Click to View More Cell Line Experimental Data
In vivo Oral administration of AC220 (10 mg/kg) induces time-dependent inhibition of FLT3 autophosphorylation in the FLT3-ITD–dependent MV4-11 tumor xenograft mouse model; the inhibition being 90% at 2 hours and 40% at 24 hours. AC220 significantly extends survival in a mouse model of FLT3-ITD AML with doses as low as 1 mg/kg given orally once a day. Treatment with AC220 at 10 mg/kg for 28 days results in rapid and complete regression of tumors in all mice with no tumor regrowth during the 60-day posttreatment period. AC220 displays more significant efficacy compared to sunitinib treatment which causes tumors to shrink slowly and resume growth immediately upon discontinuation of treatment in all but one of the mice. [1]
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