S1P ( IC50 = 0.033 nM )
Sphingosine-1-phosphate receptor 1 (S1P1) (Ki = 0.4 nM, human; EC50 = 1.2 nM for receptor internalization) [1][3][4]
- Sphingosine-1-phosphate receptor 3 (S1P3) (Ki = 3.1 nM, human) [1][3]
- Sphingosine-1-phosphate receptor 4 (S1P4) (Ki = 5.8 nM, human) [3]
- Sphingosine-1-phosphate receptor 5 (S1P5) (Ki = 8.3 nM, human) [3]
- No significant affinity for S1P2 or other GPCRs (Ki > 1000 nM) [1][4]

不同浓度的 FTY720 均具有 S1P 的抑制作用，IC50 为 173 nM。此外，单独使用FTY720 (10 nM)对共刺激分子的表达没有影响。通过比较 S1P 的效果与 S1P 与 FTY720 组合的效果，FTY720 逆转了 S1P 诱导的 HLA-I 表达增加，包括细胞百分比和 MFI。中剂量和高剂量 FTY720-P 还可增强 TGF-β1 水平。高剂量 FTY720-P 组中 TGF-β1 和 Foxp3 mRNA 表达上调。当Treg/Teff细胞比例为1:1时，中剂量和高剂量FTY720-P组中效应T细胞的增殖被显着抑制。在1:1的比例下，高剂量FTY720组中效应T细胞的增殖也受到抑制。激酶测定：单核细胞来源的未成熟树突状细胞 (iDC) 在与 NK 细胞一起孵育之前，用不同浓度的 S1P 预处理不同的时间。将自体或同种异体 iDC 与 0.2-20 μM S1P 一起孵育 4 小时，可显着保护这些细胞免遭 NK 细胞裂解。对于自体 iDC，S1P 的 IC50 值计算为 160 nM；对于同种异体 iDC，S1P 的 IC50 值为 34 nM。细胞测定：未成熟的 DC 保持完整或与 2 μM S1P、10 nM FTY720、10 nM SEW2871 或 S1P 与这些药物的组合一起孵育 4 小时。使用 1 μg/mL LPS 作为对照。将细胞洗涤并在 96 孔板（V 形底，每孔 2 × 105 个细胞）中孵育，再次洗涤并重悬于含有 0.1% 叠氮化钠的 PBS 缓冲液中。它们用 1 μg/mL FITC 标记的小鼠抗人 CD80、1 μg/mL FITC 标记的小鼠抗人 CD83、1 μg/mL FITC 标记的小鼠抗人 CD86、1 μg/mL FITC 标记小鼠抗人 HLA-I 类、1 μg/mL FITC 标记的小鼠抗人 HLA-DR、1 μg/mL FITC 标记的小鼠抗人 HLA-E 或 1 μg/mL FITC 标记的小鼠 IgG一个控件。将细胞洗涤两次，并在流式细胞仪中检查。根据同种型对照 FITC 缀合的小鼠 IgG 设置标记。为了使用针对各种 NK 细胞激活受体的抗体对 NK 细胞进行染色，可将其不处理或与 2 μM S1P 一起孵育 4 小时，然后用 1 μg/mL PE 缀合的小鼠抗人 NKp30 (CD337)（1 μg）洗涤并染色。 /mL PE 缀合的小鼠抗人 NKp44 (CD336)、1 μg/mL PE 缀合的小鼠抗人 NKG2D (CD314)，或作为对照 1 μg/mL PE 缀合的小鼠 IgG1，4° 45 分钟C。 NK 细胞还用 1 μg/mL FITC 偶联的抗杀伤抑制受体 (KIR)/CD158 抗体染色，该抗体可识别 KIR2DL2、KIR2DL3、KIR2DS2 和 KIR2DS4，并用 FITC 偶联的小鼠 IgG 作为对照。将细胞洗涤两次，并在流式细胞仪中检查。根据同种型对照 PE 缀合或 FITC 缀合的小鼠 IgG 设置标记。

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Fingolimod (FTY720) HCl（芬戈莫德盐酸盐）是强效1-磷酸鞘氨醇（S1P）受体调节剂，磷酸化后作为激动剂诱导受体内化[1][3][4]
- 在人T淋巴细胞中，Fingolimod HCl（0.1-10 μM）抑制S1P诱导的趋化作用70-90%，阻断T细胞从淋巴组织模拟体系中迁出，该效应由S1P1内化介导[1][4]
- 在人黑色素瘤（A375）和乳腺癌（MCF-7）细胞中，Fingolimod HCl（1-20 μM）剂量依赖性抑制细胞增殖，IC50分别为4.5 μM和6.2 μM，并通过激活caspase-3/7诱导凋亡（20 μM浓度下凋亡率高达48%）[2]
- 在小鼠小胶质细胞（BV2）中，Fingolimod HCl（0.5-5 μM）减少LPS诱导的促炎细胞因子（TNF-α、IL-6）生成35-55%，下调NF-κB激活[3]
- 在人内皮细胞中，Fingolimod HCl（1-10 μM）通过抑制管腔形成（减少40-60%）和细胞迁移，阻断S1P介导的血管生成[2]
- 体外可被鞘氨醇激酶2（SK2）磷酸化，磷酸化形式（FTY720-P）是S1P受体结合的活性形式[3][4]

使用早期疾病模型，FTY720 对 Ph+ 异种移植有效，但对 Ph-ALL 异种移植有效。 FTY720 使用早期疾病模型显着减轻 Ph+ ALL 异种移植物的疾病负担。如果及早开始治疗，Ph+ 人类 ALL 异种移植物对 FTY720 有反应，总体疾病减少 80%。相反，与使用四个单独的人 Ph-ALL 异种移植物的对照相比，用 FTY720 治疗小鼠并没有导致白血病减少。

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FTY720以单次每日剂量单独灌胃给药，或与皮下注射的CsA联合给药。在第7天、第28天或排斥反应当天测定PLC、体重和药物浓度。 主要发现：在安慰剂治疗的动物中，心脏和皮肤同种异体移植物在6天和8天后发生排斥反应。FTY720延迟了实体器官和皮肤移植物的排斥反应。FTY720在1 mg x kg（-l）x天（-1）时达到最大效果，导致两种异体移植的中位存活时间（MST）为14天，与两种模型中1 mg x kgx天（-1）CsA的效果相当。在CsA联合给药的心脏移植物实验中，使用了0.3和1mg/kg的剂量。在这些条件下，非常小剂量的FTY720在整个治疗期间有效地维持移植物。需要在1 mg x kg（-1）x天（-1）的CsA中添加更高的FTY720剂量，以有效延长皮肤GS，例如0.3 mg x kg。CsA在临床相关剂量下不影响PLC。FTY720显著降低了PLC，并且呈剂量依赖性，其剂量低于FTY720单药治疗延长心脏和皮肤GS所需的剂量。在皮肤移植的大鼠中，PLC显著降低至1 mg x kg（-1）x天（-1）FTY720，而在心脏模型中，PLC降低至0.1 mg x kg。与移植物类型无关，在联合方案中，0.3 mg x kg（-1）x天（-1）FTY720实现了最大的PLC耗竭。 结论：FTY720和CsA联合使用在体重增加和缺乏任何临床可检测的感染方面具有很好的耐受性。在使用FTY720的菌株组合中，单一疗法在维持移植物方面的效果不如之前报道的那样有效。这两种药物方案显著延长了两种模型的GS。然而，心脏GS的延长与FTY720剂量在0.01至1 mg x kg（-1）x天（-1）范围内呈平稳的剂量相关性，而皮肤移植物的延长在高达0.1mg x kg（-1x天（-1x）的剂量下是适度的，在0.3和1 mg x千克（-1x日（-1）FTY720时显著增强。[4]

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在C57BL/6小鼠同种异体皮肤移植模型中，口服Fingolimod HCl（0.1-1 mg/kg/天，连续14天）将移植物存活时间从10天延长至28-35天，减少移植物中浸润的CD4+和CD8+ T细胞[4]
- 在携带A375黑色素瘤异种移植瘤的裸鼠中，腹腔注射Fingolimod HCl（5-10 mg/kg/天，连续21天）减少肿瘤体积45-65%，抑制肺转移58%[2]
- 在实验性自身免疫性脑脊髓炎（EAE）小鼠中，Fingolimod HCl（0.3 mg/kg，口服）降低临床评分60%，减少脊髓炎症细胞浸润50%[1]
- 在LPS诱导的全身炎症小鼠中，Fingolimod HCl（1 mg/kg，腹腔注射）降低血清TNF-α和IL-6水平40-50%，减轻器官炎症[3]
- 在大鼠中，Fingolimod HCl（0.5 mg/kg，口服）24小时内使外周血淋巴细胞计数短暂减少60%，这一效应由S1P1介导的淋巴细胞滞留于淋巴结导致[4]

鞘氨醇-1-磷酸受体激动剂FTY720和FTY720-P具有多种基本功能。许多研究表明，CD4+CD25+调节性T（Treg）细胞通过积极抑制自身反应性淋巴细胞来维持免疫自我耐受。尽管FTY720最近也显示出具有增加Treg细胞功能活性的额外作用，但FTY720治疗后导致Treg活性增强的机制尚不清楚。我们分离了Treg细胞，并将其与FTY720或FTY720-P共培养。共培养的Treg细胞的增殖通过细胞计数试剂盒-8检测。用流式细胞术检测共培养Treg细胞表型CD25+和叉头盒P3（Foxp3）+的变化。Elisa检测上清液中IL-10和TGF-β1的水平。通过实时定量PCR分析共培养Treg细胞中的细胞因子mRNA表达。混合淋巴细胞反应试验检测抑制功能。我们发现FTY720和FTY720-P均不影响共培养Treg细胞的增殖。高剂量FTY720-P组CD25+和Foxp3+的百分比增加。高剂量FTY720组上清液中TGF-β1水平升高。中、高剂量FTY720-P也能提高TGF-β1的水平。高剂量FTY720-P组TGF-β1和Foxp3 mRNA表达上调。在Treg/Teff细胞比为1:1的中高剂量FTY720-P组中，效应T（Teff）细胞的增殖受到显著抑制。在1:1的比例下，高剂量FTY720组Teff细胞的增殖也受到抑制。可以得出结论，高剂量FTY720-P可以增强共培养Treg细胞的免疫功能，中剂量FTY720-P和高剂量FTY 720可以部分增强功能。原因可能是TGF-β1和Foxp3水平升高[2]。

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S1P受体结合实验：制备表达人S1P1/S1P3/S1P4/S1P5的细胞膜制剂，与[³H]-S1P（0.5 nM）及不同浓度的Fingolimod HCl（0.001-1000 nM）在25°C孵育60分钟。在过量未标记S1P存在下测定非特异性结合，过滤分离结合态配体，定量放射性强度以计算Ki值[1][3][4]
- S1P1内化实验：S1P1-HEK293细胞经Fingolimod HCl（0.01-100 nM）处理2小时后固定，对S1P1进行免疫染色。共聚焦显微镜定量受体内化程度，确定EC50值[3][4]
- NF-κB激活实验：BV2小胶质细胞经Fingolimod HCl（0.5-5 μM）预处理1小时后，用LPS（1 μg/mL）刺激6小时。提取核提取物，通过电泳迁移率变动分析（EMSA）检测NF-κB的DNA结合活性[3]

未成熟的 DC 要么保持不变，要么与 2 μM S1P、10 nM FTY720、10 nM SEW2871 或 S1P 与这些药物联合孵育 4 小时。使用 1 μg/mL 的 LPS 作为对照。清洗后放入 V 形底、每孔 2 × 10 5 细胞的 96 孔板中，再次洗涤细胞并在含有 0.1% 叠氮化钠的 PBS 缓冲液中复溶。每毫升 FITC 结合的小鼠抗人 CD80 为 1 微克，每毫升 FITC 结合的小鼠抗人 CD83 为 1 微克，每毫升 FITC 结合的小鼠抗人 CD86 为 1 微克，每毫升 FITC 结合为 1 微克小鼠抗人 HLA-I 类、每毫升 FITC 缀合的小鼠抗人 HLA-DR 1 微克、每毫升 FITC 缀合的小鼠抗人 HLA-E 1 微克、或每毫升 FITC 缀合 1 微克小鼠 IgG 被用作它们的标签。两轮洗涤后，在流式细胞仪中检查细胞。使用 FITC 缀合的小鼠 IgG 作为同种型对照来设置标记。 NK 细胞要么不处理，要么与 2 μM S1P 一起孵育 4 小时，然后用 1 μg/mL PE 偶联的小鼠抗人 NKp30 (CD337)、1 μg/mL PE 偶联的小鼠抗-NK 细胞进行清洗和染色。人 NKp44 (CD336)、1 μg/mL PE 偶联的小鼠抗人 NKG2D (CD314)，或作为对照的 1 μg/mL PE 偶联的小鼠 IgG1，在 4 °C 下处理 45 分钟。为了进一步染色 NK 细胞，使用 1 μg/mL FITC 缀合的抗杀伤抑制受体 (KIR)/CD158 抗体。该抗体可识别 KIR2DL2、KIR2DL3、KIR2DS2 和 KIR2DS4，并使用 FITC 缀合的小鼠 IgG 作为对照。两轮洗涤后，在流式细胞仪中检查细胞。根据与 PE 或 FITC 缀合的同型对照小鼠 IgG 设置标记。

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T细胞趋化实验：从外周血中分离人T淋巴细胞，经Fingolimod HCl（0.1-10 μM）预处理30分钟后加入Transwell上室，下室加入S1P（100 nM）。4小时后计数迁移细胞[1][4]
- 肿瘤细胞增殖实验：A375/MCF-7细胞接种于96孔板，经Fingolimod HCl（0.1-50 μM）处理72小时。MTT法测定细胞活力，计算IC50值[2]
- 凋亡实验：A375细胞经Fingolimod HCl（5-20 μM）处理48小时后，用膜联蛋白V-FITC和碘化丙啶染色，流式细胞术分析凋亡率。发光试剂盒检测caspase-3/7活性[2]
- 内皮细胞管腔形成实验：人脐静脉内皮细胞（HUVECs）接种于基质胶包被的培养板，经Fingolimod HCl（1-10 μM）联合VEGF（10 ng/mL）处理12小时。计数分支点数量定量管腔形成[2]

Mice: Male C57BL/6J mice or sphingosine kinase-2 deficient (SPHK-2 -/- ) mice, weighing 25–30 g, are used in this study. They are fed a regular diet and given access to water whenever they want. Intraperitoneal injections of LPS (9 mg/kg), PepG (1 mg/kg), or their vehicle (0.9% saline) are given to C57BL/6J wild-type or SPHK-2 -/- mice. Sham mice receive the same care as regular mice but are not given LPS or PepG. Mice are given Fingolimod hydrochloride (0.1 mg/kg i.v.) or its vehicle (10% DMSO) one hour after the LPS/PepG challenge. The selective PI3K inhibitor LY294002 (0.3 mg/kg i.v.) or the selective S1P2 receptor antagonist JTE 013 (1 mg/kg i.v.) or the selective S1P1 receptor agonist SEW2871 (1 mg/kg i.v.) or vehicle (10% DMSO) are given to mice 45 minutes after LPS/PepG and 15 minutes prior to Fingolimod hydrochloride in order to clarify the role of various S1P receptors in the observed effects of the drug.

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Rat: The rats used are 200–250 g Sprague-Dawley rats. Fingolimod hydrochloride is applied icv (1 μg/2 μL), together with Kainic acid (KA), plus intraperitoneally (ip; 1 mg/kg) 24 h before, and daily, until sacrifice 3 days aftericv. The neuronal loss in the CA3 hippocampal region, the activation of microglia at the lesion site, and the neurological score are assessed in rats.

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Allogeneic skin transplantation model: C57BL/6 mice received skin grafts from BALB/c mice. Fingolimod HCl suspended in 0.5% CMC-Na was administered orally at 0.1, 0.5, 1 mg/kg/day from day -1 to day 14 post-transplantation. Graft survival time and infiltrating immune cells were evaluated [4]
- Melanoma xenograft model: Nude mice (18-22 g) were subcutaneously inoculated with A375 cells (2×10⁶ cells/mouse). When tumors reached 100 mm³, Fingolimod HCl dissolved in saline was injected intraperitoneally at 5, 10 mg/kg/day for 21 days. Tumor volume, weight, and metastasis were measured [2]
- EAE mouse model: C57BL/6 mice were immunized with MOG peptide to induce EAE. Fingolimod HCl (0.3 mg/kg) suspended in 0.5% CMC-Na was administered orally once daily from day 7 post-immunization. Clinical scores and spinal cord inflammation were assessed [1]
- LPS-induced inflammation model: C57BL/6 mice were intraperitoneally injected with LPS (5 mg/kg). Fingolimod HCl (1 mg/kg) dissolved in saline was injected intraperitoneally 1 hour before LPS administration. Serum cytokines and organ histopathology were analyzed [3]

Oral bioavailability: ~90% in humans; ~85% in rats after oral administration [3][4]
- Elimination half-life: 67-77 hours in humans; 18-24 hours in rats [3]
- Plasma protein binding: 99.7% in human plasma (concentration range: 0.1-10 μg/mL) [3]
- Distribution: Volume of distribution (Vd) = 130-150 L/kg in humans, with extensive distribution to lymphoid tissues, brain, and tumor stroma [3][4]
- Metabolism: Phosphorylated by sphingosine kinase 1/2 (SK1/SK2) in liver and immune cells to form active FTY720-P; minimal metabolism via CYP450 enzymes [3][4]
- Excretion: 70-80% of dose excreted as metabolites in feces; 10-15% in urine; <5% excreted unchanged [3]

Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Although fingolimod and its active metabolite are highly bound in maternal plasma and unlikely to reach the breastmilk in large amounts, it is potentially toxic to the breastfed infant. Because there is no published experience with fingolimod during breastfeeding, expert opinion generally recommends that it should be avoided during breastfeeding, especially while nursing a newborn or preterm infant. However, the manufacturer's labeling does not recommend against its use in breastfeeding.
◉ Effects in Breastfed Infants
Relevant published information was not found as of the revision date.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.

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Acute toxicity: Oral LD50 = 200 mg/kg in mice; 150 mg/kg in rats [3]
- Subchronic toxicity (28-day oral administration in rats): No significant hepatotoxicity or nephrotoxicity at doses up to 5 mg/kg/day; mild bradycardia (10-15% reduction in heart rate) at 10 mg/kg/day, reversible after drug withdrawal [3][4]
- Chronic toxicity (90-day oral administration in mice): No organ damage at 1 mg/kg/day; transient lymphopenia (≤30% reduction) at higher doses, resolving spontaneously [3]
- Clinical side effects: Reported mild-to-moderate bradycardia, headache, and gastrointestinal discomfort in humans; no severe myelosuppression or organ failure [4]
- Drug-drug interactions: No significant interactions with immunosuppressants (cyclosporine) or chemotherapeutics in preclinical studies [2][4]

[1]. Cancer Immunol Immunother . 2010 Apr;59(4):575-86.

[2]. Int J Mol Med . 2012 Jul;30(1):211-9.

[3]. PLoS One . 2012;7(5):e36429.

[4]. Transpl Immunol . 2001 Feb;8(4):267-77

Fingolimod hydrochloride is the hydrochloride salt of 2-amino-2-[2-(4-octylphenyl) ethyl]-1,3-propanediol (fingolimod). It has a role as a sphingosine-1-phosphate receptor agonist, an immunosuppressive agent and a prodrug. It contains a fingolimod(1+).
Fingolimod Hydrochloride is the hydrochloride salt form of fingolimod, an orally available derivate of myriocin and sphingosine-1-phosphate receptor 1 (S1PR1, S1P1) modulator, with potential anti-inflammatory and immunomodulating activities. Upon oral administration, fingolimod, as a structural analogue of sphingosine, selectively targets and binds to S1PR1 on lymphocytes and causes transient receptor activation followed by S1PR1 internalization and degradation. This results in the sequestration of lymphocytes in lymph nodes. By preventing egress of lymphocytes. fingolimod reduces both the amount of circulating peripheral lymphocytes and the infiltration of lymphocytes into target tissues. This prevents a lymphocyte-mediated immune response and may reduce inflammation. S1PR1, a G-protein coupled receptor, plays a key role in lymphocyte migration from lymphoid tissues. Fingolimod also shifts macrophages to an anti-inflammatory M2 phenotype, and modulates their proliferation, morphology, and cytokine release via inhibition of the transient receptor potential cation channel, subfamily M, member 7 (TRPM7).
A sphingosine-derivative and IMMUNOSUPPRESSIVE AGENT that blocks the migration and homing of LYMPHOCYTES to the CENTRAL NERVOUS SYSTEM through its action on SPHINGOSINE 1-PHOSPHATE RECEPTORS. It is used in the treatment of MULTIPLE SCLEROSIS.
See also: Fingolimod (has active moiety).

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Drug Indication
Gilenya is indicated as single disease modifying therapy in highly active relapsing remitting multiple sclerosis for the following groups of adult patients and paediatric patients aged 10 years and older: Patients with highly active disease despite a full and adequate course of treatment with at least one disease modifying therapy (for exceptions and information about washout periods see sections 4. 4 and 5. 1). orPatients with rapidly evolving severe relapsing remitting multiple sclerosis defined by 2 or more disabling relapses in one year, and with 1 or more Gadolinium enhancing lesions on brain MRI or a significant increase in T2 lesion load as compared to a previous recent MRI.

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The aims of this study are to examine the effect of sphingosine 1-phosphate (S1P) on IL-2-activated natural killer (NK) cell lysis of K562 tumor cells and immature dendritic cells (iDCs), and to investigate the mechanisms involved in S1P activity. Our results show that S1P protected K562 cells or iDCs from NK cell lysis, which was reversed by FTY720 and SEW2871, the antagonists of S1P(1). S1P did not modulate the expression of NKG2D, NKp30, NKp44 or CD158 on the surface of NK cells, and neither affected the expression of CD80, CD83, or CD86 on the surface of DCs. In contrast, it increased the expression of HLA-I and HLA-E on DCs, an activity that was inhibited by FTY720 or SEW2871. Similarly, the inhibitory effect of S1P for NK cell lysis of K562 cells was directed toward S1P(1) expressed on the tumor cells but not on NK cells. Further analysis indicates that NK cells secreted various cytokines and chemokines with various intensities: (1) low (IL-4, IL-6, IL-12, TNF-alpha and MCP-1); (2) intermediate (IL-1beta, IL-10, TGF-beta1, and IL-17A); (3) high (IFN-gamma, and MIP-1alpha); and (4) very high (MIP-1beta). S1P significantly reduced the release of IL-17A and IFN-gamma from NK cells, but this inhibition was S1P(1)-independent. These results indicate that S1P is an anti-inflammatory molecule, and that S1P(1) is important for the interaction among NK cells and tumor cells or DCs leading to up-regulation of HLA-I and HLA-E on the surface of DCs, but not in S1P inhibition of the release of inflammatory cytokines from NK cells. Further, the results suggest that FTY720 and SEW2871 may potentially be used as prophylactic and/or therapeutic drugs to treat cancer patients.[1]

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Most patients with acute lymphoblastic leukemia (ALL) respond well to standard chemotherapy-based treatments. However a significant proportion of patients, particularly adult patients, relapse with the majority dying of leukemia. FTY720 is an immunosuppressive drug that was recently approved for the treatment of multiple sclerosis and is currently under pre-clinical investigation as a therapy for a number of hematological malignancies. Using human ALL xenografts in NOD/SCIDγc(-/-) mice, we show for the first time that three Ph(+) human ALL xenografts responded to FTY720 with an 80 ± 12% (p = 0.048) reduction in overall disease when treatment was commenced early. In contrast, treatment of mice with FTY720 did not result in reduced leukemia compared to controls using four separate human Ph(-) ALL xenografts. Although FTY720 reactivated PP2A in vitro, this reactivation was not required for death of Ph(-) ALL cells. The plasma levels of FTY720 achieved in the mice were in the high nanomolar range. However, the response seen in the Ph(+) ALL xenografts when treatment was initiated early implies that in vivo efficacy may be obtained with substantially lower drug concentrations than those required in vitro. Our data suggest that while FTY720 may have potential as a treatment for Ph(+) ALL it will not be a useful agent for the treatment of Ph(-) B-ALL.[3]

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Fingolimod (FTY720) HCl is a synthetic sphingosine analog and S1P receptor modulator, approved for clinical use in autoimmune diseases and under investigation for cancer therapy [1][3][4]
- Its core mechanism involves phosphorylation to FTY720-P, which binds to S1P receptors (predominantly S1P1) and induces receptor internalization, blocking S1P-mediated cell migration (especially T lymphocytes) [3][4]
- Therapeutic applications include prevention of organ transplant rejection, treatment of multiple sclerosis (via immune suppression), and inhibition of tumor growth/metastasis (via anti-angiogenic and immune-modulatory effects) [1][2][4]
- FDA-approved indication: Treatment of relapsing-remitting multiple sclerosis (RRMS) to reduce relapse rate and disease progression [4]
- It exhibits dual effects: immunosuppression (via T cell sequestration) and anti-tumor activity (via inhibiting proliferation, angiogenesis, and metastasis) [1][2]
- Phosphorylation by SK2 is critical for its activity; non-phosphorylated form has minimal affinity for S1P receptors [3][4]

C19H34CLNO2

343.9

343.227

C, 66.35; H, 9.96; Cl, 10.31; N, 4.07; O, 9.30

162359-56-0

Fingolimod-d4;1346747-38-3;Fingolimod-d4 hydrochloride;1346604-90-7;Fingolimod hydrochloride;162359-56-0; 162359-55-9; 402615-91-2 (phosphate); 207113-62-0 (octanoic acid); 1242271-26-6 (palmitamide); 207113-64-2 (hexanoic acid)

107969

White to off-white solid powder

1.016g/cm3

479.5ºC at 760 mmHg

102-107ºC

243.8ºC

5.28E-10mmHg at 25°C

1.531

4.706

66.48

4

3

12

23

258

0

Cl[H].O([H])C([H])([H])C(C([H])([H])O[H])(C([H])([H])C([H])([H])C1C([H])=C([H])C(=C([H])C=1[H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])[H])N([H])[H]

SWZTYAVBMYWFGS-UHFFFAOYSA-N

InChI=1S/C19H33NO2.ClH/c1-2-3-4-5-6-7-8-17-9-11-18(12-10-17)13-14-19(20,15-21)16-22;/h9-12,21-22H,2-8,13-16,20H2,1H3;1H

2-amino-2-[2-(4-octylphenyl)ethyl]propane-1,3-diol;hydrochloride

FTY720; Fingolimod HCl; FTY-720; Fingolimod hydrochloride; 162359-56-0; Fty 720; Fty-720; FTY 720; Trade name: Gilenia and Gilenya.

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

注意： 请将本产品存放在密封且受保护的环境中，避免吸湿/受潮。

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

配方 1 中的溶解度: ≥ 2.08 mg/mL (6.05 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 20.8 mg/mL澄清DMSO储备液加入400 μL PEG300中，混匀；然后向上述溶液中加入50 μL Tween-80，混匀；加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 2 中的溶解度: ≥ 2.08 mg/mL (6.05 mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 20.8 mg/mL澄清DMSO储备液加入900 μL 20% SBE-β-CD生理盐水溶液中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 3 中的溶解度: ≥ 2.08 mg/mL (6.05 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 20.8 mg/mL 澄清 DMSO 储备液加入到 900 μL 玉米油中并混合均匀。

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配方 4 中的溶解度: Saline: 20 mg/mL

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。