Axitinib

规格	价格/CNY		数量
25 mg	￥ 328	现货
50 mg	￥ 465	现货
100 mg	￥ 751	现货
200 mg	￥ 1,180	现货
500 mg	￥ 2,090	现货
1 g	￥ 3,330	现货
1 mL * 10 mM (in DMSO)	￥ 511	现货

规格

价格/CNY

货期

数量

25 mg

￥ 328

现货

50 mg

￥ 465

现货

100 mg

￥ 751

现货

200 mg

￥ 1,180

现货

500 mg

￥ 2,090

现货

1 g

￥ 3,330

现货

1 mL * 10 mM (in DMSO)

￥ 511

现货

存储

store at low temperature,keep away from moisture,keep away from direct sunlight　|　Powder: -20°C for 3 years | In solvent: -80°C for 1 year

溶解度

DMSO: 9.7 mg/mL (25 mM)

溶液配制表

可选溶剂	浓度体积质量	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	2.5875 mL	12.9376 mL	25.8752 mL	64.6881 mL
	5 mM	0.5175 mL	2.5875 mL	5.175 mL	12.9376 mL
	10 mM	0.2588 mL	1.2938 mL	2.5875 mL	6.4688 mL
	20 mM	0.1294 mL	0.6469 mL	1.2938 mL	3.2344 mL

产品描述	Axitinib (AG-013736) is an orally bioavailable tyrosine kinase inhibitor with IC50s of 0.1, 0.2, 0.1-0.3, 1.7, 1.6 nM for VEGFR1, VEGFR2, VEGFR3, c-kit, and PDGFRβ, respectively.
靶点活性	PDGFRβ:1.6 nM, c-Kit:1.7 nM, VEGFR1/FLT1:0.1 nM, VEGFR2/KDR: 0.2 nM, VEGFR2/Flk1:0.18 nM, VEGFR3: 0.1-0.3 nM
体外活性	In transfected or endogenous RTK-expressing cells, axitinib potently blocked growth factor-stimulated phosphorylation of VEGFR-2 and VEGFR-3 (IC50s: 0.2 and 0.1 to 0.3 nmol/L, respectively). Cellular activity against VEGFR-1 was 1.2 nmol/L. Axitinib rapidly and dose-dependently reduced the phosphorylation of Akt, endothelial nitric oxide synthase (eNOS), and extracellular signal-regulated kinase 1/2 (ERK1/2), key downstream signaling molecules of VEGF [1]. Axitinib reduced cell viability in a dose-dependent manner with IC50 doses of >10,000, 849 and 274 nmol/l for IGR-N91, IGR-NB8, and SH-SY5Y, respectively. the sensitivity to axitinib of neuroblastoma cell lines appeared to be in a similar range as non-VEGF stimulated HUVEC (IC50: 573 nmol/l) [2].
体内活性	Acute axitinib treatment rapidly and significantly reduced retinal vascular VEGFR-2 phosphorylation. One hour after the second dose, retinal VEGFR-2 phosphorylation was reduced by 80% to 90% compared with that of the control tissues. Six and 24 to 32 h post-dose, the phospho-VEGFR-2 levels returned to ～50% and 100% of the control, respectively. The EC50 value for the inhibition of VEGFR-2 phosphorylation was 0.49 nmol/L [1]. Mice were next treated for a period of 2 weeks with either fractionated radiation (5 × 2 Gy/wk) or AG-013736 (25 mg/kg/d) and 1 to 3 weeks for the combination. Tumor volume at the end of 2 weeks was significantly reduced for either single or combination treatments. Percentage increases in tumor volume were similar between radiotherapy (40 ± 9.8%) and AG-013736 (48 ± 9.2%), and the combination was markedly reduced versus controls (12 ± 5.7% versus 77 ± 11%) [3].
激酶实验	Porcine aorta endothelial (PAE) cells overexpressing full-length VEGFR-2, PDGFR-β, KIT, and NIH-3T3 overexpressing murine VEGFR-2 (Flk-1) or PDGFR-α were generated as described previously. The ELISA capture plates were prepared by coating 96-well ReactiBind plates with 100 μL/well of 2.5 μg/mL anti-VEGFR-2 antibody, 0.75 μg/mL anti-PDGFR-β antibody, 0.25 μg/mL anti-PDGFR-α antibody, 0.5 μg/mL anti-KIT antibody, or 1.20 μg/mL anti-Flk-1 antibody. Measurement of RTK phosphorylation by ELISA was done as described previously [1].
细胞实验	Endothelial or tumor cells were starved for 18 h in the presence of either 1% FBS (HUVEC) or 0.1% FBS (tumor cells). Axitinib was added and cells were incubated for 45 min at 37°C in the presence of 1 mmol/L Na3VO4. The appropriate growth factor was added to the cells, and after 5 min, cells were rinsed with cold PBS and lysed in the lysis buffer and a protease inhibitor cocktail. The lysates were incubated with immunoprecipitation antibodies for the intended proteins overnight at 4°C. Antibody complexes were conjugated to protein A beads and supernatants were separated by SDS-PAGE. The Super Signal West Dura kit was used to detect the chemiluminescent signal [1].
动物实验	AG-013736, a receptor kinase inhibitor of VEGFRs and, at higher doses, PDGFRs (IC50 = 0.1 nmol/L for VEGFR-1, 0.2 nmol/L for VEGFR-2, 0.1–0.3 nmol/L for VEGFR-3, and 1.6 nmol/L for PDGFRβ; ref. 18), was provided by Pfizer Global Research and given once daily by gavage in a volume of 0.13 mL. Control animals received 0.5% carboxymethylcellulose drug carrier. Irradiations were done on nonanesthetized mice using a 137Cs source operating at 2.4 Gy/min. Mice were confined to plastic jigs with tumor-bearing legs extended through an opening in the side, allowing local irradiations. Fractionated doses were given in five daily 2 Gy fractions per week (omitting weekends). For combination treatments, radiotherapy was delivered first, and AG-013736 was given within ～4 h. Mice were sacrificed, and tumors were excised and then quick frozen (using liquid nitrogen) following 1, 2, or 3 weeks of treatment [3].

别名	AG-013736, 阿昔替尼, 阿西替尼
分子量	386.47
分子式	C22H18N4OS
CAS No.	319460-85-0

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