| Chemical Properties | Back Directory | [Boiling point ]
710.2±70.0 °C(Predicted) | [density ]
1.407±0.06 g/cm3(Predicted) | [storage temp. ]
Store at -20°C | [solubility ]
DMSO : 125 mg/mL (305.29 mM; Need ultrasonic) | [form ]
Solid | [pka]
14.19±0.10(Predicted) | [color ]
White to yellow |
| Hazard Information | Back Directory | [Uses]
AKI603 is an inhibitor of Aurora kinase A (AurA), with an IC50 of 12.3 nM. AKI603 is developed to overcome resistance mediated by BCR-ABL-T315I mutation. AKI603 exhibits strong anti-proliferative activity in leukemic cells[1][2]. | [Biological Activity]
AKI603 is an inhibitor of Aurora kinase A (AurA), with an IC50 of 12.3 nM. AKI603 is developed to overcome resistance mediated by BCR-ABL-T315I mutation. AKI603 exhibits strong anti-proliferative activity in leukemic cells[1][2].
AKI603 (0.039-0.6 μM; 48 hours) extensively inhibits proliferation of leukemia cells[1].AKI603 (0.039-0.6 μM; 48 hours) significantly inhibits the phosphorylation of AurA in NB4, K562, and Jurkat cell lines in a dose-dependent manner while the level of total AurA protein is not changed[1].AKI603 inhibits the proliferation and colony formation of imatinib resistant CML cells[1].AKI603 (0.3-0.6 μM; 48 hours) inhibits cell proliferation and colony formation capacities in imatinib-resistant CML cells by inducing cell cycle arrest with polyploidy accumulation[1].Inhibition of AurA by AKI603 induces leukemia cell senescence in both BCR-ABL wild type and T315I mutation cells[1].AKI603 exhibits inhibitory activities on breast cancer cell proliferation, such as SUM149 (IC50=2.04), BT549 (IC50=0.86), MCF-7 (IC50=0.97), MCF-7-Epi (IC50=21.01), Sk-br-3 (IC50=0.73), MDA-MB-231 (IC50=3.49), MDA-MB-453 (MTT, IC50=0.18; Cell counting, IC50=0.19), MDA-MB-468 (MTT, IC50=0.15; Cell counting, IC50=0.17)[2].
AKI603 (12.5-25 mg/kg; i.p.; every 2 days; for 14 days) abrogates the growth of xenografted KBM5-T315I cells in nude mice[1].AKI603 exhibits moderate oral bioavailability (rat 28.7%) and Cmax (rat 202.4 μg/L) following oral administration (rat 25 mg/kg)[3].AKI603 exhibits terminal elimination half-life (rat 8.9 h) following intravenous administration (rat 2.5 mg/kg)[3]. | [in vivo]
AKI603 (12.5-25 mg/kg; i.p.; every 2 days; for 14 days) abrogates the growth of xenografted KBM5-T315I cells in nude mice[1].
AKI603 exhibits moderate oral bioavailability (rat 28.7%) and Cmax (rat 202.4 μg/L) following oral administration (rat 25 mg/kg)[3].
AKI603 exhibits terminal elimination half-life (rat 8.9 h) following intravenous administration (rat 2.5 mg/kg)[3].
| Animal Model: | Female BALB/c nude mice, with KBM5-T315I cells xenografted[1] | | Dosage: | 12.5?mg/kg, 25?mg/kg | | Administration: | Intraperitoneal injection, every 2 days, for 14 days | | Result: | Significantly inhibited the growth of tumors. |
| Animal Model: | SD rats (220-280 g)[3] | | Dosage: | 2.5 mg/kg for i.v.; 25 mg/kg for p.o. (Pharmacokinetic Analysis) | | Administration: | Intravenous injection, oral administration | | Result: | Oral bioavailability (28.7%), Cmax (202.4 μg/L), T1/2 (8.9 h) |
| [IC 50]
Aurora A: 12.3 nM (IC50) | [storage]
Store at -20°C | [References]
[1]. Le-Xun Wang, et al. Aurora A Kinase Inhibitor AKI603 Induces Cellular Senescence in Chronic Myeloid Leukemia Cells Harboring T315I Mutation. Sci Rep. 2016 Nov 8;6:35533. [2]. Fei-Meng Zheng, et al. A novel small molecule aurora kinase inhibitor attenuates breast tumor-initiating cells and overcomes drug resistance. Mol Cancer Ther. 2014 Aug;13(8):1991-2003. [3]. Zhenzhen Zhao, et al. Determination of a novel Aurora-A (AurA) kinase AKI603 by UPLC-MS/MS and its application to a bioavailability study in rat. J Pharm Biomed Anal. 2016 Jun 5;125:303-9. |
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BOC Sciences
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DC Chemicals
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nanjing
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www.linye-e.com/ |
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