Sunitinib

Sunitinib (SU 11248) 是一种多靶点受体酪氨酸激酶抑制剂，对 VEGFR2 和 PDGFRβ 的 IC50 分别为 80 nM 和 2 nM。 Sunitinib 是一种 ATP 竞争性抑制剂，通过抑制自身磷酸化和随后的 RNase 激活，有效抑制 Ire1α 的自身磷酸化。

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库存: 现货

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100mg

￥437.00

350.00

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500mg

￥875.00

700.00

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1g

￥1387.00

1110.00

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2g

￥1900.00

1520.00

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货号: ajci19544
CAS: 557795-19-4
别名: 舒尼替尼; SU 11248
分子式: C22H27FN4O2
分子量: 398.47
纯度: >98%
溶解度: ≥ 19.9mg/mL in DMSO with gentle warming
储存: Store at -20°C
库存: 现货

Background

Sunitinib is an oral, multi-targeted and small-molecule inhibitor of receptor tyrosine kinase (RTK) [1].

Sunitinib is a RTK inhibitor against vascular endothelial growth factor receptors (VEGFR1-3), platelet-derived growth factor receptors (PDGFRα and PDGFRβ ), stem cell factor receptor (c-kit), glial cell-line derived neurotrophic factor receptor(RET). Sunitinib has been reported to inhibit the growth in five NPC cell lines (HK1, CNE-2, HON E-1, CNE-1 and C666-1) with the IC50 values of 2.06 ± 0.29μM, 3.45 ± 0.11μM, 4.07 ± 1.07μM, 2.60 ± 0.38 and 7.57 ± 1.74μM, respectively. Apart from these, Sunitinib has been observed to induce apoptosis in NPC cells as well as induce cell cycle arrest at the G0 /G1 phase in HONE-1 and CNE-2 cells. In vivo, Sunitinib treatment could induce a significant reduction in MVD in CNE2 NPC xenograft [1].

参考文献:
[1]Hui EP1, Lui VW, Wong CS, Ma BB, Lau CP, Cheung CS, Ho K, Cheng SH, Ng MH, Chan AT. Preclinical evaluation of sunitinib as single agent or in combination with chemotherapy in nasopharyngeal carcinoma. Invest New Drugs. 2011 Dec;29(6):1123-31.

Protocol

Cell experiment: [1]
Cell lines	Human 786-O and RCC4 cells, murine Renca cells
Preparation method	The solubility of this compound in DMSO is >10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 °C for 10 minutes and/or shake it in the ultrasonic bath for a while.Stock solution can be stored below -20°C for several months.
Reaction Conditions	10 μM, 24 hours
Applications	Sunitinib induced RCC tumor cell apoptosis in all three tumor cell lines. It also inhibited cell proliferation in a dose-dependent manner. For concentrations at which sunitinib caused effective tumor cell death; there were corresponding increases in cleaved PARP. Sunitinib treatment (24 h) of 786-O, RCC4 and Renca tumor cells reduced expression of several key anti-apoptotic and pro-proliferation genes, including Cyclin E, Cyclin D1 and Survivin.
Animal experiment: [1]
Animal models	Female BALB/c mice injected with Renca cells
Dosage form	Oral administration, 40, 20, 10 mg/kg body weight, daily
Applications	Sunitinib induced tumor cell apoptosis in vivo as early as 1 day post treatment, which occurred in the presence of apparently intact tumor vessels. There appeared to be more apoptosis in the tumor on days 3 and 11 post treatment, with greater disruption of the tumor vasculature. Sunitinib treatment reduced Stat3 activity and induced tumor cell death as early as one day post treatment.
Other notes	Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.
参考文献: [1] Xin H, Zhang C, Herrmann A, et al. Sunitinib inhibition of Stat3 induces renal cell carcinoma tumor cell apoptosis and reduces immunosuppressive cells. Cancer research, 2009, 69(6): 2506-2513.