13585831301
021-59541103 021-60443211
3004967995
13585831301021-59541103 021-604432113004967995
在線訂購 免費訂購熱線：021-59541103 021-60443211
標簽:Fingolimod
聯系人:高小姐
電話:021-59541103 021-60443211
手機:13585831301
Q Q： 3004967995
Email:3004967995@qq.com
詳細地址：上海嘉定區嘉羅公路1661
化學性質：
| 規格 | 5mg 10mg 25mg 50mg |
| CAS | 162359-55-9 |
| 別名 | N/A |
| 化學名 | N/A |
| 分子式 | C19H33NO2 |
| 分子量 | 307.5 |
| 溶解度 | DMF: 20 mg/ml,DMSO: 10 mg/ml,Ethanol: 5 mg/ml |
| 儲存條件 | Store at -20°C |
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while. |
| Shipping Condition | Evaluation sample solution : ship with blue ice |
產品描述：
Fingolimod is a sphingosine 1-phosphate (S1P) antagonist with IC50 of 0.033 nM in K562 and NK cells. Fingolimod also is a pak1 activator, a immunosuppressant.
The monocyte-derived immature dendritic cells (iDCs) are pretreated with various concentrations of S1P for various periods of time prior to their incubation with NK cells. Four hours incubation of autologous or allogeneic iDCs with 0.2-20 μM of S1P significantly protectes these cells from NK cell lysis. The IC50 values of S1P are calculated at 160 nM for autologous iDCs, and 34 nM for allogeneic iDCs. Next, the inhibitory effect of S1P is revered by various concentrations of Fingolimod or SEW2871, with an IC50 effect of 173 or 15 nM, respectively[1]. Fingolimod has been reported to reduce LPA synthesis via inhibition of the lysophospholipase autotaxin. Fingolimod treatment correlates with a significant elevation of axonal cAMP, a crucial factor for axonal outgrowth. Additionally, Fingolimod significantly reduces LPA levels in the injured nerve. PF-8380 treatment correlates with improved myelin thickness[2].
Fingolimod treatment results in significantly increased nerve conduction at 14 days post-crush in wildtype C57BL/6 mice. However, Foxn1-/- mice, which are devoid of T- but not B-lymphocytes, show an improvement of nerve regeneration under fingolimod treatment. Although the mean increase in nerve conduction velocity in both fingolimod-treated and controlFoxn1-/- mice implies a potentially positive role of T-lymphocyte deficiency on nerve regeneration, only fingolimod-treated Foxn1-/- mice show a significant improvement compared to C57BL/6 controls and performed better in the functional analysis[2]. Treatment of the animals with Fingolimod for 28 d results in a clear reduction in the binding of 18F-GE180 when compare with vehicle-treated animals and evaluated by ex vivo autoradiography. Quantification of the binding of the radiotracer revealed a significant reduction in the binding potential of 18F-GE180 (P<0.0001) after treatment with Fingolimod[3].
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原創作者：上海莼試生物技術有限公司
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普票匯款信息
賬 戶 名：上海生物
開 戶 行：中國銀行山東省分行營業部
賬 號：2169 2341 6278
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