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Axitinib

产品编号 T1452 CAS 319460-85-0

别名: AG-013736, 阿昔替尼, 阿西替尼

Axitinib 是一种多靶点酪氨酸激酶抑制剂，能够抑制 VEGFR1 (IC50:4 nM)，VEGFR2 (IC50:20 nM)，VEGFR3 (IC50:0.4 nM)，PDGFRβ (IC50:2 nM)。

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Axitinib, CAS 319460-85-0

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生物活性

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产品描述	Axitinib 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, 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

存储

store at low temperture,keep away from moisture,keep away from direct sunlight　|　Powder: -20°C for 3 years | In solvent: -80°C for 2 years

溶解度

DMSO: 9.7 mg/mL (25 mM)

( < 1 mg/mL refers to the product slightly soluble or insoluble )

参考文献

1. Hu-Lowe DD, et al. Nonclinical antiangiogenesis and antitumor activities of axitinib (AG-013736), an oral, potent, and selective inhibitor of vascular endothelial growth factor receptor tyrosine kinases 1, 2, 3. Clin Cancer Res. 2008 Nov 15;14(22):7272-83. 2. Rössler J, et al. The selective VEGFR1-3 inhibitor axitinib (AG-013736) shows antitumor activity in human neuroblastoma xenografts. Int J Cancer. 2011 Jun 1;128(11):2748-58. 3. Fenton BM, et al. The addition of AG-013736 to rractionated radiation improves tumor response without functionally normalizing the tumor vasculature. Cancer Res. 2007 Oct 15;67(20):9921-8. 4. Huang M, Chen M, Qi M, et al. Perivascular cell‐derived extracellular vesicles stimulate colorectal cancer revascularization after withdrawal of antiangiogenic drugs[J]. Journal of Extracellular Vesicles. 2021, 10(7): e12096. 5. Wei N, Liang J, Peng S, et al. Design, synthesis, and biological evaluation of axitinib derivatives[J]. Molecules. 2018 Mar 23;23(4). 6. Wei R, Ma Q, Li T, et al. Carbazole alkaloids with antiangiogenic activities from Clausena sanki[J]. Bioorganic chemistry. 2018 Apr;77:387-392.

文献引用

1. Huang M, Chen M, Qi M, et al. Perivascular cell‐derived extracellular vesicles stimulate colorectal cancer revascularization after withdrawal of antiangiogenic drugs. Journal of Extracellular Vesicles. 2021, 10(7): e12096. 2. Wei R, Ma Q, Li T, et al. Carbazole alkaloids with antiangiogenic activities from Clausena sanki. Bioorganic Chemistry. 2018 Apr;77:387-392 3. Wei N, Liang J, Peng S, et al. Design, synthesis, and biological evaluation of axitinib derivatives. Molecules. 2018 Mar 23;23(4) 4. Li H, Zhang R, Hu Y, et al.Axitinib attenuates the progression of liver fibrosis by restoring mitochondrial function.International Immunopharmacology.2023, 122: 110555.

剂量换算

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请在以下方框中输入您的动物实验信息后点击计算，可以得到母液配置方法和体内配方的制备方法：比如您的给药剂量是10 mg/kg，每只动物体重20 g，给药体积100 μL，一共给药动物10 只，您使用的配方为5% DMSO+30% PEG300+5% Tween 80+60% ddH2O。那么您的工作液浓度为2 mg/mL。

母液配置方法：2 mg 药物溶于 50 μL DMSO (母液浓度为 40 mg/mL)，如您需要配置的浓度超过该产品的溶解度，请先与我们联系。

体内配方的制备方法：取 50 μL DMSO 主液，加入 300 μL PEG300，混匀澄清，再加 50 μL Tween 80，混匀澄清，再加 600 μL ddH2O, 混匀澄清。

第一步：请输入动物实验的基本信息

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% DMSO+

% +

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计算结果如下:

工作液浓度: mg/ml;

母液配置方法: mg 药物溶于 μL DMSO (母液浓度为 mg/mL)，如您需要配置的浓度超过该产品的溶解度，请先与我们联系。

体内配方的制备方法：取 μL DMSO 主液，加入 μL PEG300，混匀澄清，再加 μL Tween 80，混匀澄清，再加 μL ddH₂O, 混匀澄清。

备注:

要按顺序从左向右依次添加助溶剂。可配合物理方法，如涡流、超声波或热水浴使之帮助溶解。

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您可能有的问题的答案可以在抑制剂处理说明中找到，包括如何准备库存溶液，如何存储产品，以及基于细胞的分析和动物实验需要特别注意的问题。

Keywords

Axitinib 319460-85-0 Angiogenesis Tyrosine Kinase/Adaptors c-Kit PDGFR VEGFR inhibit AG013736 Platelet-derived growth factor receptor Inhibitor Vascular endothelial growth factor receptor AG-013736 阿昔替尼 AG 013736 阿西替尼 inhibitor

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Axitinib

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