Free shipping on all orders over $ 500


Cat. No. M1641
AC220 Structure


Size Price Availability Quantity
10mg USD 80 In stock
50mg USD 150 In stock
200mg USD 400 In stock
Free Delivery on orders over USD 500 Bulk Inquiry?

Quality Control
  • Current batch:
  • Purity >98%
  • COA
  • MSDS
Biological Activity

AC220 (Quizartinib) is a orally-administered, potent and selective inhibitor of two receptor tyrosine kinases, FLT3 and KIT. AC220 is currently in a Phase 2 clinical study in the relapsed/refractory AML patient population with internal tandem duplication (ITD positive) activating mutations of the FLT3 kinase (FLT3-ITD positive). AC220 (Quizartinib) exhibits low nanomolar potency in biochemical and cellular assays and exceptional kinase selectivity, and in animal models is efficacious at doses as low as 1 mg/kg given orally once daily. While other agents showed some ability to clear leukemia from the circulating blood, AC220 has shown significant ability to clear leukemic cells from the bone marrow, where the disease originates. AC220-resistant FLT3 kinase domain mutants represent high-value targets for future FLT3 inhibitor development efforts.

Product Citations
Customer Product Validations & Biological Datas
Source Mol Cancer (2013). Figure 3. AC220
Method PCR
Cell Lines Ba/F3 cells
Concentrations 0 – 5000 nM
Incubation Time 48 h
Results Comparison of inhibition of cellular proliferation after quizartinib treatment revealed strong correlation between naturally occurring and engineered cell lines expressing identical mutant kinases
Source Mol Cancer (2013). Figure 2. AC220
Method cell apoptosis assay
Cell Lines leukemia cell line
Concentrations 0 – 5000 nM
Incubation Time 48 h
Results This finding suggests that the distinct mutant-KIT isoform directly orchestrates sensitivity towards quizartinib.
Cell Experiment
Cell lines MV4-11 and RS4;11 cells
Preparation method Cellular assays. MV4-11 and RS4;11 cells were cultured in Iscove media with 10% fetal bovine serum (FBS) and RPMI complete with 10% FBS, respectively. For proliferation assays, cells were cultured overnight in low serum media (0.5% FBS), then seeded in a 96-well plate at 40 000 cells per well. Inhibitors were added to the cells and incubated at 37°C for 72 hours. Cell viability was measured using the Cell Titer-Blue Cell Viability Assay from Promega. To measure inhibition of FLT3 autophosphorylation, cells were 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 were incubated with inhibitors for 2 hours at 37°C. To induce FLT3 autophosphorylation in RS4;11 cells, 100 ng/mL FLT3 ligand (R&D Systems) was added for 15 minutes after the 2-hour compound incubation. Cell lysates were prepared and incubated in 96-well plates precoated with a total FLT3 capture antibody (R&D Systems). The coated plates were incubated with either a biotinylated antibody against FLT3 (R&D Systems) to detect total FLT3 or an antibody against phosphotyrosines (Millipore) to detect FLT3 autophosphorylation. In both cases, a SULFO-tagged streptavidin secondary antibody was used for electrochemiluminescence detection on the Meso Scale Discovery platform.
Concentrations 0~10 µM
Incubation time 72 h
Animal Experiment
Animal models subcutaneous tumor model
Formulation 22% hydroxypropyl-β-cyclodextrin
Dosages 10 mg/kg
Administration orally
Conversion of different model animals based on BSA (Value based on data from FDA Draft Guidelines)
Species Mouse Rat Rabbit Guinea pig Hamster Dog
Weight (kg) 0.02 0.15 1.8 0.4 0.08 10
Body Surface Area (m2) 0.007 0.025 0.15 0.05 0.02 0.5
Km factor 3 6 12 8 5 20
Animal A (mg/kg) = Animal B (mg/kg) multiplied by  Animal B Km
Animal A Km

For example, to modify the dose of resveratrol used for a mouse (22.4 mg/kg) to a dose based on the BSA for a rat, multiply 22.4 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for resveratrol of 11.2 mg/kg.

Chemical Information
Molecular Weight 560.67
Formula C29H32N6O4S
CAS Number 950769-58-1
Purity >98%
Solubility DMSO ≥100 mg/mL
Storage at -20°C

Validation of ITD mutations in FLT3 as a therapeutic target in human acute myeloid leukaemia.
Smith et al. Nature. 2012 Apr 15;485(7397):260-3. PMID: 22504184.

AC220 is a uniquely potent and selective inhibitor of FLT3 for the treatment of acute myeloid leukemia (AML).
Zarrinkar et al. Blood. 2009 Oct 1;114(14):2984-92. PMID: 19654408.

Related FLT3 Products

Gilteritinib is a potent FLT3/AXL inhibitor with IC50 of 0.29 nM/0.73 nM, respectively.

AMG 925

AMG 925 is a potent and orally bioavailable dual FLT3/CDK4 inhibitor with IC50 of 1 nM and 3 nM, respectively.


G-749 is a novel and potent FLT3 inhibitor with IC50 of 0.4 nM, 0.6 nM and 1 nM for FLT3 (WT), FLT3 (D835Y), and Mer, respectively, showing lower potency against other tyrosine kinases.


UNC-2025 is a potent and orally bioavailable dual MER/FLT3 inhibitor with IC50 of 0.74 nM and 0.8 nM, respectively, about 20-fold selectivity over Axl and Tyro3.


CGP52421 is a FLT3 inhibitor, which is also an metabolite of midostaurin (PKC412).

Abmole Inhibitor Catalog 2017

Keywords: AC220, Quizartinib supplier, FLT3, inhibitors

Contact Us

Products are for research use only. Not for human use. We do not sell to patients.
© Copyright 2010-2017 AbMole BioScience. All Rights Reserved.