Fingolimod

Manufactured by Cayman Chemical

Sourced in United States

Fingolimod is a laboratory compound that functions as a sphingosine 1-phosphate receptor modulator. It is commonly used in research settings to study cellular processes related to the sphingosine 1-phosphate signaling pathway.

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Lab products found in correlation

Penicillin streptomycin, by Thermo Fisher Scientific (2 mentions) Dulbecco modified eagle medium (dmem), by Thermo Fisher Scientific (2 mentions) Sphingosine 1 phosphate (s1p), by Avanti Polar Lipids (2 mentions) Dimethyl sulfoxide (dmso), by MP Biomedicals (2 mentions) Methyl thiazolyl tetrazolium (mtt), by MP Biomedicals (2 mentions) Phytohemagglutinin (pha), by Merck Group (1 mentions) Morphine sulfate, by Mallinckrodt (1 mentions) Cla31440, by Cedarlane (1 mentions) 10058 f4 c myc inhibitor, by Merck Group (1 mentions) Ac220, by Selleck Chemicals (1 mentions) Tc g 24, by Bio-Techne (1 mentions) Azd1208, by Bio-Techne (1 mentions) Mk 2206, by Selleck Chemicals (1 mentions) Ibrutinib, by Cayman Chemical (1 mentions) Ruxolitinib, by Cayman Chemical (1 mentions) Imatinib, by Cayman Chemical (1 mentions) Fty720, by Cayman Chemical (1 mentions) Sew2871, by Cayman Chemical (1 mentions) Eht1864, by Bio-Techne (1 mentions) Uc10 4f10 11, by BioXCell (1 mentions)

Spelling variants of this product

FTY720 (fingolimod, (10 citations) Fingolimod-P (2 citations)

15 protocols using fingolimod

Fingolimod and TGN-020 in Rat DBI Model

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The rats in the DBI + fingolimod group (n = 42) were intraperitoneally injected with 0.5 mg/kg body weight fingolimod (dissolved in 0.9% sodium chloride; Cayman Chemical, 10006292) daily for 3 consecutive days beginning 30 min after the DBI procedure according to prior research and our initial results.
³² (link) The rats in the sham (n = 42) and DBI groups (n = 42) were injected with equivalent amounts of 0.9% sodium chloride.
TGN‐020 is known to inhibit the expression of AQP4 M23, which leads to the disruption of astrocytic AQP4 polarization.
³³ (link) In the DBI + fingolimod + TGN‐020 group (n = 18), before fingolimod was administered, TGN‐020 was used to pharmacologically inhibit AQP4 polarity as previously described.
³⁴ (link)

Feng D., Liu T., Zhang X., Xiang T., Su W., Quan W, & Jiang R. (2024). Fingolimod improves diffuse brain injury by promoting AQP4 polarization and functional recovery of the glymphatic system. CNS Neuroscience & Therapeutics, 30(3), e14669.

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Fingolimod Modulates CD56 Expression in PBMC

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PBMC from healthy subjects and MS patients without DMD were cultured for 5 days at 1 × 10⁶ cells/ml in the presence of fingolimod (0.01, 0.1, 1, 5, 10 μM; Cayman Chemical, Ann Arbor, MI,USA) or fingolimod-phosPHAte (0.01 μM, 0.1 μM, 1 μM, 5 μM, 10 μM; Cayman Chemical) in AIM-V medium. On day 3 and day 5, CD56 expression was analyzed as described above.
To upregulate CD56 on T cells, PBMC from three HS and three MS without DMD were also cultured for 5 days at 1 × 10⁶ cells/ml in the presence of PHA (2 mg/ml; Sigma-Aldrich, St. Louis, MO, USA) in AMI-V supplemented with 10% FBS. fingolimod or fingolimod-phosPHAte was added to the cultured wells at the concentration of 0.1 μM and 1 μM, and compared to the culture with PHA alone.

Fujii C., Kondo T., Ochi H., Okada Y., Hashi Y., Adachi T., Shin-Ya M., Matsumoto S., Takahashi R., Nakagawa M, & Mizuno T. (2016). Altered T cell phenotypes associated with clinical relapse of multiple sclerosis patients receiving fingolimod therapy. Scientific Reports, 6, 35314.

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Comprehensive Analgesic Compound Preparation

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The functional S1PR1 antagonists FTY720 (Fingolimod, Cayman Chemical, Ann Arbor MI) and TASP0277308 (TASP, Shanghai Chempartner Co., Shanghai, China) were prepared according to a previously published protocol [18 ]. FTY720 and TASP0277308 were both prepared as stocks in DMSO, for oral administration drugs were diluted to the appropriate dose in 30% DMSO in 0.5% methylcellulose; for intraperitoneal (i.p.) injections FTY720 was diluted in saline. The selective A₃AR antagonist, MRS5698 ([1S,2R,3S,4R,5S)-4-(6-((3-chlorobenzyl)amino)-2-((3,4-difluorophenyl)ethynyl)-9H-purin-9-yl)-2,3-dihydroxy-N-methylbicyclo[3.1.0]hexane-1-carboxamide]) was synthesized as described previously [39 (link)] and dissolved in saline for i.p. injections. These compounds have been previously shown to be specific for their target receptors and efficacious in male rodent pain models at the doses used in this study [18 –20 (link); 38 (link); 40 (link)]. The antidepressant, duloxetine hydrochloride, was purchased from TCI America (Portland, OR) and dissolved in DMSO as a stock solution, for i.p. injections stock was diluted in saline. Morphine sulfate was a kind gift from Mallinckrodt Pharmaceuticals (St. Louis MO, USA) for i.p injections Morphine sulfate was diluted in saline. All therapeutic test compounds were given 20–30 min prior to chemotherapy, except where stated herein as a reversal paradigm.

Stockstill K., Wahlman C., Braden K., Chen Z., Yosten G.L., Tosh D.K., Jacobson K.A., Doyle T.M., Samson W.K, & Salvemini D. (2020). Sexually dimorphic therapeutic response in bortezomib-induced neuropathic pain reveals altered pain physiology in female rodents. Pain, 161(1), 177-184.

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Fingolimod Treatment for Ischemic Stroke

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Treatment was randomly allocated using a random list that assigned a given treatment (A/B) to each mouse, and treatment was administered in a blinded fashion. Fingolimod (1 mg/kg) (#10006292, Cayman Chemical, Ann Arbor, MI, USA) or the vehicle (saline containing 0.5% DMSO) was administered i.p. immediately after reperfusion following MCAo. For platelet depletion, mice received an i.p. injection of rabbit anti-mouse platelet serum (#CLA31440, Cedarlane, Burlington, NC, USA) (15 μl diluted in 200 μl of sterile saline) 10 min after reperfusion.

Salas-Perdomo A., Miró-Mur F., Gallizioli M., Brait V.H., Justicia C., Meissner A., Urra X., Chamorro A, & Planas A.M. (2019). Role of the S1P pathway and inhibition by fingolimod in preventing hemorrhagic transformation after stroke. Scientific Reports, 9, 8309.

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Inhibitors of FLT3, PP2A, and Signaling Pathways in AML

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Gilteritinib (4 (link)) (ASP2215; Active Biochem, Maplewood, NJ) and quizartinib (4 (link)) (AC220; Selleck Chemicals, Houston, TX), type I and II FLT3 inhibitors, respectively, clinically active in FLT3-ITD AML, were used at pharmacologically relevant concentrations (23 (link),24 (link)). The SET-sequestering PAD FTY720 (25 (link)) (Fingolimod; Cayman Chemical Company, Ann Arbor, MI) was also used at pharmacologically relevant concentrations. DT-061, an orally bioavailable small molecule activator of PP2A (SMAP) developed by reengineering tricyclic neuroleptics and proposed to directly bind the PP2A Aα subunit (26 (link)–29 (link)), was provided by Dr. Goutham Narla. The pan-Pim inhibitor AZD1208 and GSK-3β inhibitors TC-G 24 and TWS119 were from Tocris Bioscience, Minneapolis, MN, the c-Myc inhibitor 10058-F4 from Sigma-Aldrich, and the pan-AKT inhibitor MK-2206 from Selleck Chemicals, Houston, TX.

Scarpa M., Singh P., Bailey C.M., Lee J.K., Kapoor S., Lapidus R.G., Niyongere S., Sangodkar J., Wang Y., Perrotti D., Narla G, & Baer M.R. (2021). PP2A-activating drugs enhance FLT3 inhibitor efficacy through AKT inhibition-dependent GSK-3β-mediated c-Myc and Pim-1 proteasomal degradation. Molecular cancer therapeutics, 20(4), 676-690.

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Mast Cell Activation Assay with IgE and Inhibitors

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Mast cells were incubated overnight with 100 ng/ml murine monoclonal anti-DNP IgE, clone SPE-7 (D8406, RRID:AB_259249, Millipore-Sigma, St. Louis, MO) at 37 C. The next day, cells were centrifuged and washed twice with fresh media to remove unbound IgE and cells were replated in fresh media with 10 ng/ml IL-3. Stimulation was to the relevant wells added in the form of 10 ng/ml IL-33 and/or 100 ng/ml DNP-BSA for 24 h at 37 C, then cells were centrifuged and supernatant was collected. For the drug inhibition assays, ibrutinib, ruxolitinib, imatinib, and fingolimod were purchased from Cayman Chemical (936563-96-1, 941678-49-5, 220127-57-1, 162359-55-9, Ann Arbor, MI) and reconstituted per the manufacturer's instructions. Drug stocks were diluted in media and incubated with mast cells after the overnight IgE incubation step. Cells were treated for 1 h at 37 C, then washed out with fresh media twice. Cells were then stimulated as per above.

Strattan E., Palaniyandi S., Kumari R., Du J., Hakim N., Huang T., Kesler M.V., Jennings C.D., Sturgill J.L, & Hildebrandt G.C. (2019). Mast Cells Are Mediators of Fibrosis and Effector Cell Recruitment in Dermal Chronic Graft-vs.-Host Disease. Frontiers in Immunology, 10, 2470.

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Fingolimod and SEW2817 Treatment Protocol

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Fingolimod (also known as FTY720) or SEW2817 (both from Cayman Chemicals) were dissolved to 25 mg/ml in DMSO for storage at −80°C and diluted in sterile 2% hydroxypropyl-β-cyclodextrin (w/v) in PBS for injections. Mice were given 5 mg/kg of FTY720 or SEW2817 or an equivalent amount of vehicle i.p. starting 12 hr before infection and then every 24 hr after infection.

St. John A.L., Ang W.X., Huang M.N., Kunder C.A., Chan E.W., Gunn M.D, & Abraham S.N. (2014). S1P-Dependent Trafficking of Intracellular Yersinia pestis through Lymph Nodes Establishes Buboes and Systemic Infection. Immunity, 41(3), 440-450.

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Fingolimod and S1PR1 Agonist Interventions in GMH

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Fingolimod (2-amino-2-[4-octylphenyl)ethyl]-1,3-propanediol, hydrochloride) and the specific S1PR1 agonist (SEW2871) were purchased from Cayman Chemical Co. (Ann Arbor, MI). The S1PR1, S1PR3, S1PR4 antagonist (VPC20391) and the Rac1 inhibitor (EHT1864) were purchased from Tocris Bioscience (Minneapolis, MN). Low dose Fingolimod (0.25 mg/kg), high dose Fingolimod (1.0 mg/kg), SEW2871 (5 mg/kg), VPC23019 (0.5 mg/kg), and EHT1864 (40 mg/kg) were given by daily intraperitoneal injection (1, 24, and 48 hours after GMH). The dissolving manner and dosages were followed as previously described (Desire et al., 2005 (link), Awad et al., 2006 (link), Landeen et al., 2008 (link)). Sham and vehicle animals received the same volume of 5% DMSO in saline.

Rolland W.B., Krafft P.R., Lekic T., Klebe D., LeGrand J., Weldon A.J., Xu L, & Zhang J.H. (2017). Fingolimod Confers Neuroprotection through Activation of Rac1 after Experimental Germinal Matrix Hemorrhage in Rat Pups. Journal of neurochemistry, 140(5), 776-786.

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Immune Modulation in Radiation Therapy

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Mice received i.p. injections of depleting anti-CD8α mAbs (2.43, Bio X Cell) or anti-CD4 mAbs (GK1.5, Bio X Cell) at 200 μg per mouse in 100 μL PBS starting on day –1 prior to RT (day 0) and then on days 3, 6, and 9. For Treg depletion experiments, mice were injected i.p. with 250 μg depleting mouse IgG2a isotype CD25 mAbs (48 (link)) (modified clone of PC61, Evitria) in 100 μL PBS on day –1 prior to RT and on day 5. Blocking mAbs against CTLA-4 (UC10-4F10-11, Bio X Cell), PD-1 (RMP1-14, Bio X Cell), CD80 (1G10, Bio X Cell), and CD86 (GL-1, Bio X Cell) were injected i.p. at either 100 μg (anti–CTLA-4 and anti–PD-1) or 200 μg (anti-CD80 and anti-CD86) per mouse in 100 μL PBS on the day of RT (day 0) and on days 3 and 6 and, in the case of anti–CTLA-4, also on day 9. Control mice were injected with equal amounts of PBS (vehicle) according to the treatment schedule indicated. FTY720 (Fingolimod, Cayman Chemical) was dissolved in 0.9% NaCl solution (vehicle) and administered at 2 mg/kg by oral gavage. FTY720 treatment started 1 day prior to RT and was repeated 3 times per week throughout the duration of the experiment.

Frijlink E., Bosma D.M., Busselaar J., Battaglia T.W., Staal M.D., Verbrugge I, & Borst J. (2024). PD-1 or CTLA-4 blockade promotes CD86-driven Treg responses upon radiotherapy of lymphocyte-depleted cancer in mice. The Journal of Clinical Investigation, 134(6), e171154.

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Resveratrol's Effects on Sphingolipid Signaling

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Resveratrol was purchased from Sigma–Aldrich. DMEM and penicillin-streptomycin (10,000 U·mL⁻¹ penicillin and 10,000 mg·mL⁻¹ streptomycin) were from Invitrogen (Paisley, UK). DMSO and MTT were from MP Biomedicals, LLC. SPH and S1P were from Avanti Polar Lipids (Alabaster, AL, USA). D-erythro-N,N-Dimethylsphingosine (DMS) was purchased from Santa Cruz Biotechnology, USA. It was dissolved in DMSO and was stored at −20 °C until use. Fingolimod was from Cayman Chemicals (Ann Arbor, MI, USA Cat # 11975).

Momchilova A., Pankov R., Staneva G., Pankov S., Krastev P., Vassileva E., Hazarosova R., Krastev N., Robev B., Nikolova B, & Pinkas A. (2022). Resveratrol Affects Sphingolipid Metabolism in A549 Lung Adenocarcinoma Cells. International Journal of Molecular Sciences, 23(18), 10870.

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