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Catalog No. T3068   CAS 896466-04-9
Synonyms: J-504568

AT9283 (J-504568) is an effective multi-targeted inhibitor of JAK2(IC50=1.2 nM) and JAK3(IC50=1.1 nM), Aurora A, Aurora B and Abl(T315I).

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AT9283 Chemical Structure
AT9283, CAS 896466-04-9
Pack Size Availability Price/USD Quantity
1 mg In stock $ 39.00
2 mg In stock $ 55.00
5 mg In stock $ 96.00
10 mg In stock $ 173.00
25 mg In stock $ 315.00
50 mg In stock $ 525.00
100 mg In stock $ 762.00
1 mL * 10 mM (in DMSO) In stock $ 98.00
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Purity: 99.98%
Purity: 99.87%
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Biological Description
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Description AT9283 (J-504568) is an effective multi-targeted inhibitor of JAK2(IC50=1.2 nM) and JAK3(IC50=1.1 nM), Aurora A, Aurora B and Abl(T315I).
Targets&IC50 JAK3:1.1 nM, JAK2:1.2 nM
In vitro In mice bearing HCT116 human colorectal carcinoma xenografts, AT9283 (15-20 mg/kg) was capable of inhibiting tumor growth.
In vivo In HCT116 cells, AT9283 inhibits Aurora B kinase activity with an IC50 value of 30 nM, leading to a polyploid phenotype and concurrently suppressing colony formation. Moreover, AT9283 significantly inhibits a range of kinases, including Aurora A (IC50=3 nM), Aurora B (IC50=3 nM), JAK3 (IC50=1.1 nM), JAK2 (IC50=1.2 nM), and Abl (IC50=4 nM).
Kinase Assay Aurora A and Aurora B Kinase Assays: Assays for Aurora A and B are performed in a DELFIA format. Aurora A enzyme is incubated with AT9283 and 3 μM cross-tide substrate (biotin-CGPKGPGRRGRRRTSSFAEG) in 10 mM MOPS, pH 7, 0.1 mg/mL BSA, 0.001% Brij-35, 0.5% glycerol, 0.2 mM EDTA, 10 mM MgCl2, 0.01% β-mercaptoethanol, 15 μM ATP, and 2.5% DMSO. Aurora B enzyme is incubated with AT9283, 3 μM of the above substrate in 25 mM Tris, pH 8.5, 5 mM MgCl2, 0.1 mg/mL BSA, 0.025% Tween-20, 1 mM DTT, 15 μM ATP, and 2.5% DMSO. Reactions are allowed to proceed for 60 minutes and 45-90 minutes for Aurora A and Aurora B, respectively, before quenching with EDTA. The reaction mixtures are then transferred to a neutravidin-coated plate, and phosphorylated peptide is quantified by means of a phospho-specific antibody and a europium labeled secondary antibody using time-resolved fluorescence (excitation, 337 nm; emission, 620 nm). IC50 values for the control compounds are 92 nM (Aurora A assay) and 17 nM (Aurora B).
Cell Research HCT 116 cells are cultured in DMEM + 10% FBS + GLUTAMAX I. Black 96-well flat-bottomed (clear) tissue culture treated plates are seeded in 200 μL of medium and incubated for approximately 16 hours at 37°C in a humidified atmosphere of 5% CO2 in air. Cells are treated with test compound at nine different concentrations (spanning 1 nM to 10 μM, plus DMSO vehicle control) and then incubated for 72 hours. Polyploidy morphological observations of the cells are then noted. The concentration of AT9283 required to produce a distinct polyploid phenotype is reported. Cells are seeded at a concentration of 75−100 cells/mL relevant culture media onto 6- or 24-well tissue culture plates and allowed to recover for 16 hours. Test compound (11 concentrations spanning 0.1 nM to 10 μM) or vehicle control (DMSO) is added to duplicate wells to give a final DMSO concentration of 0.1%. Following compound addition, colonies are allowed to grow between 10 and 14 days for optimum discrete colony counting. Colonies are fixed in 2 mL of Carnoys fixative (25% acetic acid, 75% MeOH) and stained in 2 mL of 0.4% w/v crystal violet. The numbers of colonies in each well is counted. IC50 values are calculated by sigmoidal dose-response (variable slope) IC50 curves using Prism Graphpad software. (Only for Reference)
Synonyms J-504568
Molecular Weight 381.43
Formula C19H23N7O2
CAS No. 896466-04-9


Powder: -20°C for 3 years | In solvent: -80°C for 1 year

Solubility Information

DMSO: 71 mg/mL (186.1 mM)

Ethanol: 22 mg/mL(57.7 mM)

H2O: < 1 mg/mL (insoluble or slightly soluble)

TargetMolReferences and Literature

1. Howard S, et al. J Med Chem, 2009, 52(2), 379-388. 2. Qi W, et al. Int J Cancer. 2012, 130(12), 21997-32005. 3. Santo L, et al. Clin Cancer Res. 2011, 17(10), 3259-3271. 4. Hou W, Wang Z Y, Lin J, et al. Induction of differentiation of the acute myeloid leukemia cell line (HL-60) by a securinine dimer[J]. Cell Death Discovery. 2020, 6(1): 1-11.


1. Cheng S, Jin P, Li H, et al. Evaluation of CML TKI Induced Cardiovascular Toxicity and Development of Potential Rescue Strategies in a Zebrafish Model. Frontiers in Pharmacology. 2021: 2866. 2. Hou W, Wang Z Y, Lin J, et al. Induction of differentiation of the acute myeloid leukemia cell line (HL-60) by a securinine dimer. Cell Death Discovery. 2020, 6(1): 1-11

Related compound libraries

This product is contained In the following compound libraries:
Drug Repurposing Compound Library Anti-Cancer Active Compound Library Tyrosine Kinase Inhibitor Library Anti-Neurodegenerative Disease Compound Library Anti-Cancer Clinical Compound Library Anti-Cancer Drug Library Kinase Inhibitor Library Inhibitor Library Anti-Aging Compound Library Clinical Compound Library

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AT9283 896466-04-9 Angiogenesis Apoptosis Autophagy Cell Cycle/Checkpoint Chromatin/Epigenetic Cytoskeletal Signaling JAK/STAT signaling Stem Cells Tyrosine Kinase/Adaptors Aurora Kinase Bcr-Abl JAK FLT AT-9283 Cluster of differentiation antigen 135 J-504568 Janus kinase inhibit Fms like tyrosine kinase 3 FLT3 J504568 AT 9283 Inhibitor J 504568 CD135 inhibitor