Quizartinib (AC220)

Catalog No.S1526

Quizartinib (AC220) Chemical Structure

Molecular Weight(MW): 560.67

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.

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Cited by 22 Publications

7 Customer Reviews

  • Western analysis of the indicated proteins in parental BaF3 cells transfected with empty plasmid (Empty) and in these expressing FLT3(ITD) after 24 hrs incubation with 10 nM AC220 or vehicle in the presence of IL-3.

    Blood, 2018, 132(1):67-77.. Quizartinib (AC220) purchased from Selleck.

    Immunofluorescence staining of stably transduced Ba/F3 cells expressing FLT3-WT, FLT3-ITD or empty vector with or without AC220 treatment. WGA (wheat germ agglutinin). Scale bar: 10 μm.

    Leukemia, 2018, 32(2):313-322. Quizartinib (AC220) purchased from Selleck.

  • B. MOLM-14 cells were treated with PBS (control) or FLT3 inhibitor (100 nM) for 16 h, and were then stained for LC3B-FITC and analysed by flow cytometry. Histograms represent the percentages of LC3B-FITC medium fluorescence intensity (MFI) of cells treated with FLT3 inhibitor, normalized to PBS-treated cells (n=3 ± SEM). The FLT3 inhibitor is quizartinib.

    Oncogene, 2018, 37(6):787-797. Quizartinib (AC220) purchased from Selleck.

    Cotreatment with JQ1 and AC220 synergistically induces apoptosis of FLT3-ITD–expressing AML cells. MV4-11 cells were treated with the indicated concentrations of AC220 and/or JQ1 for 24 hours. At the end of treatment, immunoblot analyses were conducted as indicated. The numbers beneath the blots represent densitometry analysis conducted on representative blots.

    Mol Cancer Ther 2014 13(10), 2315-27. Quizartinib (AC220) purchased from Selleck.

  • The effect of the FLT3 inhibitor AC220 (2nM) on the expression of MYC and E2F1 in MOLM-13 and MV4;11 cells. Cells were treated with vehicle and the FLT3 specific inhibitor AC220 for 24 hM, and then the mRNA and protein levels of MYC and E2F1 were tested.

    Leuk Lymphoma, 2017, 58(10):2426-2438. Quizartinib (AC220) purchased from Selleck.

    Crude membranes from High-Five insect cells expressing ABCB1 and MCF-7 FLV1000 cells expressing ABCG2 were incubated with 0–30 uM quizartinib for 5 minutes at 21–23°C in 50 mM Tris-HCl, pH 7.5 and 3–6 nM [125I]-IAAP (2200 Ci/mmole) was added. Representative autoradiograms from one experiment are shown in the upper panels; similar results were obtained in two additional experiments. In the lower panels, incorporation of [125I]-IAAP (from autoradiogram, Y-axis) into the ABCB1 and ABCG2 bands was plotted as a function of quizartinib concentration (X-axis). Quizartinib inhibited [125I]-IAAP binding to ABCB1 and ABCG2 with IC50’s of 3.3 uM and 0.07 uM, respectively, and the latter correspond to a therapeutically relevant plasma concentration. Values are from a representative experiment among three independent experiments.

    PLoS One 2013 8(8), e71266. Quizartinib (AC220) purchased from Selleck.

  • Effect of AC220 on the sensitivity of KB-C2 cells to paclitaxel. The figure showes the survival curves of cells at different concentrations of paclitaxel with or without AC220.  Cell viability was determined by MTT Assay.  KB-3-1 is epidermoid carcinoma cell line while KB-C2 is ABCB1 (P-gp) overexpressing drug (cholchicine) selected cell line. VERA (Verapamil) was used as a positive control of ABCB1 inhibitor.

    Quizartinib (AC220) purchased from Selleck.

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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 M{m1ZWZ2dmO2aX;uJGF{e2G7 M33uOlAvOS1zMDFOwG0> MkLDN|AhdWmw M{TGXIVvcGGwY3XzJJVxfGGtZTDv[kB{fWK|dILheIV{KG:oIFHCR2czKGGwZDDBRmNDOSCrbjDhJINwdmOnboTyZZRqd25vZHXw[Y5l\W62IH3hco5meg>? MY[yN|k3PzF5Nx?=
K562/ABCB1 MVnGeY5kfGmxbjDBd5NigQ>? M3\WdVAvOS1zMDFOwG0> MVmzNEBucW5? Ml7V[Y5p[W6lZYOgeZB1[WunIH;mJJN2[nO2cnH0[ZMhd2ZiQVLDS|Ih[W6mIFHCR2IyKGmwIHGgZ49v[2WwdILheIlwdi2mZYDlcoRmdnRibXHucoVz MYeyN|k3PzF5Nx?=
8226/MR20  MXjGeY5kfGmxbjDBd5NigQ>? M3TnN|AvOS1zMDFOwG0> MYizNEBucW5? NFzqU3FmdmijbnPld{B2eHSja3Wgc4Yhe3Wkc4TyZZRmeyCxZjDBRmNIOiCjbnSgRWJESjFiaX6gZUBkd26lZX70doF1cW:wLXTldIVv\GWwdDDtZY5v\XJ? MX[yN|k3PzF5Nx?=
K562/ABCG2 NH\DZVRHfW6ldHnvckBCe3OjeR?= MmnKNE4yNTFyIN88US=> MW[zNEBucW5? NUj4[5Vn\W6qYX7j[ZMhfXC2YXvlJI9nKHO3YoP0doF1\XNib3[gRWJETzJiYX7kJGFDS0JzIHnuJIEh[2:wY3XueJJifGmxbj3k[ZBmdmSnboSgcYFvdmW{ MljTNlM6PjdzN{e=
MCF-7 FLV1000 MYPLbY5ie2ViQYPzZZk> Moj1NQKBmzNyINM1US=> MU[1JI1qdg>? Mn24[IVkemWjc3XzJHsyOjWLXT3JRWFRKHCqb4TvcIFj\Wyrbnegc4YhSUKFQkGgZZQhUUN3MDDv[kA{NjNizszN MnraNlM6PjdzN{e=
MCF-7 FLV1000 M1\YOWtqdmG|ZTDBd5NigQ>? NYOySZgyOOLCk{OwJOK2VQ>? NFnIdVU2KG2rbh?= M33CdoRm[3KnYYPld{BcOTJ3SW2tTWFCWCCyaH;0c4xi[mWuaX7nJI9nKEGEQ1KyJIF1KEmFNUCgc4YhOC5yNzFOwG0> Ml;SNlM6PjdzN{e=
K562/ABCG2 MWDD[YxtKF[rYXLpcIl1gSCDc4PhfZM> NF[0eFMxNjFxMD61M|EhyrWP M3m0UVk3KGh? MVzz[Y5{cXSrenXzJGs2PjJxQVLDS|Ih[2WubIOgeI8hdWm2b4jhcpRzd26nIITvdI91\WOjbtMg NXLnd2xVOjN7NkexO|c>
8226/MR20 M1Tv[2NmdGxiVnnhZoltcXS7IFHzd4F6ew>? NE\lWpIxNjFiwsXN NXrVR|NIQTZiaB?= MX7z[Y5{cXSrenXzJGs2PjJxQVLDS|Ih[2WubIOgeI8hdWm2b4jhcpRzd26nIITvdI91\WOjbtMg NG\ENoYzOzl4N{G3Oy=>
HMC1.1 NF3wOYxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXPJR|UxRTF2IH7N MUKyN|Q6PzNzNx?=
HMC1.2 NYHNS|lqT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MX3JR|UxRTF5Mkegcm0> MXmyN|Q6PzNzNx?=
p815 NVW4Vm5zT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHnPeVFKSzVyPUS0OUBvVQ>? NXrVfGsxOjN2OUezNVc>
Kasumi-1 NE\m[XJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkLzTWM2OD1|NjDuUS=> MnTiNlM1QTd|MUe=
M-07e + SCF MWrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIjMcodKSzVyPUe3JI5O NVnlcHZPOjN2OUezNVc>
EOL-1 NXzjXWVXT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4LETmlEPTB;MTDuUS=> M3zYU|I{PDl5M{G3
MV4;11 M{GyTGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVLQWVJ4UUN3MEygNUBvVQ>? NYjTN49sOjN2OUezNVc>
MOLM14 MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2j4T2lEPTB:IEGgcm0> MUOyN|Q6PzNzNx?=
Pat.221 M3\DPWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MX3JR|UxRTZ5NTDuUS=> MUmyN|Q6PzNzNx?=
Pat.279 Mm\US5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXXJR|UxRTN2M{Sgcm0> MVyyN|Q6PzNzNx?=
Pat.299 MVvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnjJTWM2OD15MkS4JI5O NGS2SWczOzR7N{OxOy=>
Pat.305 NYLySIN3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGLIbIJKSzVyPUewO|khdk1? MX6yN|Q6PzNzNx?=
Pat.375 M3TRXmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mn;0TWM2OD13MEOgcm0> M2nFVVI{PDl5M{G3
Pat.379 NIjhenNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYrEdIw6UUN3ME24NFYhdk1? NV;3XFlXOjN2OUezNVc>
Pat.368 NWT1bGNJT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmrQTWM2OD1{N{CwJI5O MWSyN|Q6PzNzNx?=
Pat.601 MWfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUHJR|UxRTFzNUOgcm0> MmTaNlM1QTd|MUe=
HMC1.1 M1L4[WFxd3C2b4Ppd{BCe3OjeR?= MljaTWM2OD1|MTDuUS=> NWrtVHRjOjN2OUezNVc>
p815 NU[5dZFjSXCxcITvd4l{KEG|c3H5 M3nUU2lEPTB;M{SxJI5O NWDZRphZOjN2OUezNVc>
Kasumi-1 NWnScGJRSXCxcITvd4l{KEG|c3H5 NH;VXnJKSzVyPU[3JI5O Mn7qNlM1QTd|MUe=
M-07e + SCF M4LUfmFxd3C2b4Ppd{BCe3OjeR?= NIfnTHJKSzVyPUe4JI5O NEfGO3MzOzR7N{OxOy=>
EOL-1 M2DU[GFxd3C2b4Ppd{BCe3OjeR?= M1SyZWlEPTB:IEGgcm0> NWH3[YY4OjN2OUezNVc>
MV4;11 M1zxZ2Fxd3C2b4Ppd{BCe3OjeR?= Ml;TTWM2OD1{IH7N MUCyN|Q6PzNzNx?=
MOLM14 MY\BdI9xfG:|aYOgRZN{[Xl? NWW4bnk{UUN3ME2zJI5O NY\v[ox6OjN2OUezNVc>
GIST822 MX3BdI9xfG:|aYOgRZN{[Xl? NYO4fVIxUUN3ME2xNFkhdk1? MmGyNlM1QTd|MUe=
Pat.368 MULBdI9xfG:|aYOgRZN{[Xl? NV7E[YszUUN3ME2yPVk5KG6P MXKyN|Q6PzNzNx?=
Pat.601 M3LnUmFxd3C2b4Ppd{BCe3OjeR?= NFf6WXVKSzVyPUi3OkBvVQ>? M3f1XlI{PDl5M{G3
MV4-11 NEe1NWVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVu3NkBp MkLaTWM2OD1yLkOgcm0> NF;jenUzOzRzMkmzNS=>
MOLM-14 NEj3SpFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NESwbWI4OiCq NIHJOVJKSzVyPUCuNUBvVQ>? M1e5Z|I{PDF{OUOx
SEM-K2 MYTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYe3NkBp M4fuZWlEPTB;MD60JI5O M1HCTlI{PDF{OUOx
RS4;11 MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1PGOFczKGh? MWPJR|UxRjFyLECwNEBvVQ>? NGfwfnEzOzRzMkmzNS=>
THP-1 NEjleZRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnfqO|IhcA>? NV;4SYQ3UUN3ME6xNEwxODBibl2= MWeyN|QyOjl|MR?=
MV4-11 NEHQb4JCeG:ydH;zbZMhSXO|YYm= MnjvPE8zPCCq MVfpcoR2[2W|IIPp[45q\mmlYX70JIFv\CCmb4PlMYRmeGWwZHXueEBRSVKSIHPs[YF3[WenIHHu[EBi[2O3bYXsZZRqd25ib3[gd5VjNTKQIFTORS=> NVfQdWF2OjN2MUK5N|E>
MOLM-14 NULqOXFkSXCxcITvd4l{KEG|c3H5 NEnPN4k5NzJ2IHi= MmPDbY5lfWOnczDzbYdvcW[rY3HueEBidmRiZH;z[U1l\XCnbnTlcpQhWEGUUDDjcIVifmGpZTDhcoQh[WOldX31cIF1cW:wIH;mJJN2[i1{TjDEUmE> NVjqOGtHOjN2MUK5N|E>
SEM-K2 MXrBdI9xfG:|aYOgRZN{[Xl? NEnUbGw5NzJ2IHi= NEfYc3BqdmS3Y3XzJJNq\26rZnnjZY51KGGwZDDkc5NmNWSncHXu[IVvfCCSQWLQJINt\WG4YXflJIFv\CCjY3P1cZVt[XSrb36gc4Yhe3WkLULOJGRPSQ>? MmfuNlM1OTJ7M{G=
MV4-11 MUjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3K0WlczKGh? M1vhbWlEPTB;MD61OkDDuSByLkOgcm0> NFjseXEyQTZ3NESwPC=>
A375 NETKN3hIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVH3WFVmPzJiaB?= MkHkTWM2OD5iMUCgNFAxKG6P M{jWbFE6PjV2NEC4

... 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]

Protocol

Kinase Assay:[1]
+ Expand

Inhibition of FLT3 autophosphorylation:

To measure inhibition of FLT3 autophosphorylation, MV4-11 or RS4;11 cells are cultured in low serum media (0.5% FBS) overnight and seeded at a density of 400 000 cells per well in a 96-well plate the following day. The cells are incubated with different concentrations of AC220 for 2 hours at 37 °C. To induce FLT3 autophosphorylation in RS4;11 cells, 100 ng/mL FLT3 ligand is added for 15 minutes after the 2-hour AC220 incubation. Cell lysates are prepared and incubated in 96-well plates precoated with a total FLT3 capture antibody. The coated plates are incubated with either a biotinylated antibody against FLT3 to detect total FLT3 or an antibody against phosphotyrosines to detect FLT3 autophosphorylation. In both cases, a SULFO-tagged streptavidin secondary antibody is used for electrochemiluminescence detection on the Meso Scale Discovery platform. The concentration of AC220 that inhibits FLT3-ITD or TLT3-WT autophosphorylation by 50% represents IC50 value
Cell Research:[1]
+ Expand
  • Cell lines: MV4-11 and RS4;11 cells
  • Concentrations: Dissolved in DMSO, final concentration ~20 μM
  • Incubation Time: 72 hours
  • Method: Cells are cultured overnight in low serum media (0.5% FBS), seeded in a 96-well plate at 40 000 cells per well and exposed to AC220 for 72 hours at 37 °C. Cell viability is measured using the Cell Titer-Blue Cell Viability Assa
    (Only for Reference)
Animal Research:[1]
+ Expand
  • Animal Models: Female NU/NU or severe combined immunodeficient mice implanted with MV4-11 cells
  • Formulation: Formulated in 22% hydroxypropyl-β-cyclodextrin
  • Dosages: ~10 mg/kg
  • Administration: Oral gavage
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 33 mg/mL (58.85 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
15% Captisol
For best results, use promptly after mixing.
30 mg/mL

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 560.67
Formula

C29H32N6O4S

CAS No. 950769-58-1
Storage powder
in solvent
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03735875 Recruiting Acute Myeloid Leukemia With FLT3/ITD Mutation|FLT3 Gene Mutation|FLT3 Internal Tandem Duplication|Recurrent Acute Myeloid Leukemia|Refractory Acute Leukemia M.D. Anderson Cancer Center|National Cancer Institute (NCI) January 25 2019 Phase 1|Phase 2
NCT03735875 Recruiting Acute Myeloid Leukemia With FLT3/ITD Mutation|FLT3 Gene Mutation|FLT3 Internal Tandem Duplication|Recurrent Acute Myeloid Leukemia|Refractory Acute Leukemia M.D. Anderson Cancer Center|National Cancer Institute (NCI) January 25 2019 Phase 1|Phase 2
NCT03723681 Recruiting Acute Myeloid Leukemia (AML) Daiichi Sankyo Co. Ltd.|Daiichi Sankyo Inc. November 5 2018 Phase 1
NCT03723681 Recruiting Acute Myeloid Leukemia (AML) Daiichi Sankyo Co. Ltd.|Daiichi Sankyo Inc. November 5 2018 Phase 1
NCT03661307 Recruiting Acute Myeloid Leukemia With FLT3/ITD Mutation|Blasts More Than 10 Percent of Bone Marrow Nucleated Cells|Blasts More Than 10 Percent of Peripheral Blood White Cells|Myelodysplastic Syndrome|Recurrent Acute Myeloid Leukemia|Recurrent Myelodysplastic Syndrome M.D. Anderson Cancer Center|National Cancer Institute (NCI) October 31 2018 Phase 1|Phase 2
NCT03661307 Recruiting Acute Myeloid Leukemia With FLT3/ITD Mutation|Blasts More Than 10 Percent of Bone Marrow Nucleated Cells|Blasts More Than 10 Percent of Peripheral Blood White Cells|Myelodysplastic Syndrome|Recurrent Acute Myeloid Leukemia|Recurrent Myelodysplastic Syndrome M.D. Anderson Cancer Center|National Cancer Institute (NCI) October 31 2018 Phase 1|Phase 2

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

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Frequently Asked Questions

  • Question 1:

    Is it possible to alter the captisol concentration to make it more dissolvable i.e 20% or 25% captisol ?

  • Answer:

    In 15% Captisol, the compound forms s suspension at 30mg/ml. Increasing the percentage of Captisol will not convert the mixture into solution. You can use suspension for oral gavage feeding.

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID