Fingolimod (FTY720 free base) is asphingosine 1-phosphate(S1P) antagonist with anIC₅₀of 0.033 nM in K562 and NK cells. Fingolimod also is apak1activator, a immunosuppressant^[1].

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 IC₅₀values 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 IC₅₀effect 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-treatedFoxn1^-/-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 of¹⁸F-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 of¹⁸F-GE180 (P<0.0001) after treatment with Fingolimod^[3].

307.47

Solid

C₁₉H₃₃NO₂

162359-55-9

芬戈莫德；芬戈利德

Room temperature in continental US; may vary elsewhere.

Ethanol : 7.69 mg/mL(25.01 mM;Need ultrasonic)

DMSO : 2 mg/mL(6.50 mM;ultrasonic and heat to 60℃)

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80℃, 6 months; -20℃, 1 month。-80℃ 储存时，请在 6 个月内使用，-20℃ 储存时，请在 1 个月内使用。

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照In Vitro方式配制澄清的储备液，再依次添加助溶剂：

——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

• 1.

  请依序添加每种溶剂： 10% EtOH    40%PEG300   5%Tween-80   45% saline

  Solubility: ≥ 1 mg/mL (3.25 mM); Clear solution

  此方案可获得 ≥ 1 mg/mL (3.25 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 10.0 mg/mL 的澄清 EtOH 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

  将 0.9 g 氯化钠，完全溶解于 100 mL ddH2O 中，得到澄清透明的生理盐水溶液
• 2.

  请依序添加每种溶剂： 10% EtOH    90% (20%SBE-β-CDin saline)

  Solubility: ≥ 1 mg/mL (3.25 mM); Clear solution

  此方案可获得 ≥ 1 mg/mL (3.25 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 10.0 mg/mL 的澄清 EtOH 储备液加到 900 μL20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

  将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
• 3.

  请依序添加每种溶剂： 10% EtOH    90%corn oil

  Solubility: ≥ 1 mg/mL (3.25 mM); Clear solution

  此方案可获得 ≥ 1 mg/mL (3.25 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

  以 1 mL 工作液为例，取 100 μL 10.0 mg/mL 的澄清 EtOH 储备液加到 900 μL玉米油中，混合均匀。