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 M3LEcGZ2dmO2aX;uJGF{e2G7 M4n2OlAvOS1zMDFOwG0> NWLyZ3ZOOzBibXnu M{j2e4VvcGGwY3XzJJVxfGGtZTDv[kB{fWK|dILheIV{KG:oIFHCR2czKGGwZDDBRmNDOSCrbjDhJINwdmOnboTyZZRqd25vZHXw[Y5l\W62IH3hco5meg>? MoroNlM6PjdzN{e=
K562/ABCB1 NX3yWIlmTnWwY4Tpc44hSXO|YYm= NXTxbGQ2OC5zLUGwJO69VQ>? NInuOow{OCCvaX6= MkDT[Y5p[W6lZYOgeZB1[WunIH;mJJN2[nO2cnH0[ZMhd2ZiQVLDS|Ih[W6mIFHCR2IyKGmwIHGgZ49v[2WwdILheIlwdi2mZYDlcoRmdnRibXHucoVz NUC2TIRqOjN7NkexO|c>
8226/MR20  MmTySpVv[3Srb36gRZN{[Xl? NGmyZnoxNjFvMUCg{txO MXGzNEBucW5? NF\UR|BmdmijbnPld{B2eHSja3Wgc4Yhe3Wkc4TyZZRmeyCxZjDBRmNIOiCjbnSgRWJESjFiaX6gZUBkd26lZX70doF1cW:wLXTldIVv\GWwdDDtZY5v\XJ? NX7ud4M6OjN7NkexO|c>
K562/ABCG2 MXPGeY5kfGmxbjDBd5NigQ>? NXf2RW52OC5zLUGwJO69VQ>? MoLxN|AhdWmw MoCw[Y5p[W6lZYOgeZB1[WunIH;mJJN2[nO2cnH0[ZMhd2ZiQVLDS|Ih[W6mIFHCR2IyKGmwIHGgZ49v[2WwdILheIlwdi2mZYDlcoRmdnRibXHucoVz NFTodGszOzl4N{G3Oy=>
MCF-7 FLV1000 NXfsRWVjU2mwYYPlJGF{e2G7 NVu3e|NTOOLCk{OwJOK2VQ>? MXO1JI1qdg>? MYDk[YNz\WG|ZYOgX|EzPUmfLVnBRXAheGixdH;sZYJmdGmwZzDv[kBCSkOEMTDheEBKSzVyIH;mJFMvOyEQvF2= MX6yN|k3PzF5Nx?=
MCF-7 FLV1000 NXz0PXNPU2mwYYPlJGF{e2G7 MWWw5qCUOzBiwsXN MlXHOUBucW5? MUPk[YNz\WG|ZYOgX|EzPUmfLVnBRXAheGixdH;sZYJmdGmwZzDv[kBCSkOEMjDheEBKSzVyIH;mJFAvODdizszN MX[yN|k3PzF5Nx?=
K562/ABCG2 MXjD[YxtKF[rYXLpcIl1gSCDc4PhfZM> M1PKfFAvOS9yLkWvNUDDvU1? MWe5OkBp MlrKd4Vve2m2aYrld{BMPTZ{L1HCR2czKGOnbHzzJJRwKG2rdH;4ZY51em:wZTD0c5BwfGWlYX9CpC=> NULXTVVKOjN7NkexO|c>
8226/MR20 NXnqPGRXS2WubDDWbYFjcWyrdImgRZN{[Xm| M1f2NVAvOSEEtV2= M1XVSFk3KGh? NGD5UJd{\W6|aYTpfoV{KEt3NkKvRWJETzJiY3XscJMhfG9ibXn0c5hidnS{b37lJJRweG:2ZXPhcuKh MX[yN|k3PzF5Nx?=
HMC1.1 MlLuS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVnuUJJCUUN3ME2xOEBvVQ>? MU[yN|Q6PzNzNx?=
HMC1.2 Ml6yS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXPRT5N3UUN3ME2xO|I4KG6P NXnxZZE4OjN2OUezNVc>
p815 NEnPO2pIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NUO2TZhFUUN3ME20OFUhdk1? NFnTOYEzOzR7N{OxOy=>
Kasumi-1 M1jNNGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlTxTWM2OD1|NjDuUS=> NXLiN5poOjN2OUezNVc>
M-07e + SCF M3nTdWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2nGdGlEPTB;N{egcm0> MnHkNlM1QTd|MUe=
EOL-1 NWXrWJA1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVPROJNKUUN3ME2xJI5O Ml7FNlM1QTd|MUe=
MV4;11 MXzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{fSTmlEPTB:IEGgcm0> NF;qZXAzOzR7N{OxOy=>
MOLM14 MXfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUXVSW1vUUN3MEygNUBvVQ>? NF;FdWYzOzR7N{OxOy=>
Pat.221 M1fHdGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NIjRepdKSzVyPU[3OUBvVQ>? NFOzbWwzOzR7N{OxOy=>
Pat.279 NGD4fo1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVv3Zm01UUN3ME2zOFM1KG6P Mn34NlM1QTd|MUe=
Pat.299 MXfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2\aTGlEPTB;N{K0PEBvVQ>? MX:yN|Q6PzNzNx?=
Pat.305 MVfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NILpZ41KSzVyPUewO|khdk1? MmO5NlM1QTd|MUe=
Pat.375 MnKxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUPJR|UxRTVyMzDuUS=> NX7ocJNzOjN2OUezNVc>
Pat.379 NVrvW5FyT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M2DmVWlEPTB;OEC2JI5O MYmyN|Q6PzNzNx?=
Pat.368 MnP2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1zTVWlEPTB;MkewNEBvVQ>? Mm\oNlM1QTd|MUe=
Pat.601 MoPsS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIHoeIZKSzVyPUGxOVMhdk1? M4f3SFI{PDl5M{G3
HMC1.1 MnXRRZBweHSxc3nzJGF{e2G7 M2HGSGlEPTB;M{Ggcm0> NYf0em9SOjN2OUezNVc>
p815 NIDuSYdCeG:ydH;zbZMhSXO|YYm= NV3vUGdwUUN3ME2zOFEhdk1? M2XOXlI{PDl5M{G3
Kasumi-1 MnPNRZBweHSxc3nzJGF{e2G7 NGe4[WFKSzVyPU[3JI5O NW\ndo1COjN2OUezNVc>
M-07e + SCF NF:5WVJCeG:ydH;zbZMhSXO|YYm= MlLoTWM2OD15ODDuUS=> NFyxVoUzOzR7N{OxOy=>
EOL-1 MnzTRZBweHSxc3nzJGF{e2G7 MUnJR|UxRCBzIH7N M1Hy[lI{PDl5M{G3
MV4;11 NV7jPZpDSXCxcITvd4l{KEG|c3H5 MVnJR|UxRTJibl2= NEDpbYczOzR7N{OxOy=>
MOLM14 M4S1dWFxd3C2b4Ppd{BCe3OjeR?= NG\zblVKSzVyPUOgcm0> MonINlM1QTd|MUe=
GIST822 M4\sVmFxd3C2b4Ppd{BCe3OjeR?= NFTGTlhKSzVyPUGwPUBvVQ>? MlzONlM1QTd|MUe=
Pat.368 MnXZRZBweHSxc3nzJGF{e2G7 M4K3e2lEPTB;Mkm5PEBvVQ>? MlftNlM1QTd|MUe=
Pat.601 M{SxWGFxd3C2b4Ppd{BCe3OjeR?= MYPJR|UxRTh5NjDuUS=> Mor5NlM1QTd|MUe=
MV4-11 M1zoV2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXzQfmVkPzJiaB?= NV\SS|NjUUN3ME2wMlMhdk1? MkHGNlM1OTJ7M{G=
MOLM-14 MnzjS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYGwfnEyPzJiaB?= MWXJR|UxRTBwMTDuUS=> MknJNlM1OTJ7M{G=
SEM-K2 NGWzdI1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYHFW2NGPzJiaB?= NVPkTY05UUN3ME2wMlQhdk1? MnOzNlM1OTJ7M{G=
RS4;11 MV7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NH;jdYs4OiCq NV7BU4hlUUN3ME6xNEwxODBibl2= MViyN|QyOjl|MR?=
THP-1 MVnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mkj4O|IhcA>? MVTJR|UxRjFyLECwNEBvVQ>? M{jKWFI{PDF{OUOx
MV4-11 MknpRZBweHSxc3nzJGF{e2G7 MkTtPE8zPCCq Mof1bY5lfWOnczDzbYdvcW[rY3HueEBidmRiZH;z[U1l\XCnbnTlcpQhWEGUUDDjcIVifmGpZTDhcoQh[WOldX31cIF1cW:wIH;mJJN2[i1{TjDEUmE> MoDBNlM1OTJ7M{G=
MOLM-14 MX3BdI9xfG:|aYOgRZN{[Xl? NYfad3BOQC9{NDDo NWLxeolTcW6mdXPld{B{cWewaX\pZ4FvfCCjbnSg[I9{\S2mZYDlcoRmdnRiUFHSVEBkdGWjdnHn[UBidmRiYXPjeY12dGG2aX;uJI9nKHO3Yj2yUkBFVkF? Mki0NlM1OTJ7M{G=
SEM-K2 M3v6dWFxd3C2b4Ppd{BCe3OjeR?= MoL4PE8zPCCq MmS5bY5lfWOnczDzbYdvcW[rY3HueEBidmRiZH;z[U1l\XCnbnTlcpQhWEGUUDDjcIVifmGpZTDhcoQh[WOldX31cIF1cW:wIH;mJJN2[i1{TjDEUmE> MmHmNlM1OTJ7M{G=
MV4-11 NHTlcXBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWrMc2dpPzJiaB?= M4HQ[WlEPTB;MD61OkDDuSByLkOgcm0> M3\TUlE6PjV2NEC4
A375 M1\zc2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVS3NkBp MYPJR|UxRiBzMDCwNFAhdk1? NWjyXGFSOTl4NUS0NFg>

... 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