Fingolimod fty720

Manufactured by Merck Group

Sourced in United States, Germany

Fingolimod/FTY720 is a laboratory product developed by Merck Group. It is a synthetic analog of the natural product myriocin. The core function of Fingolimod/FTY720 is to act as a modulator of sphingosine-1-phosphate receptor.

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Lab products found in correlation

6 protocols using fingolimod fty720

Immunosuppression Enhances Helminth Infection

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Anti-MHC-II (400 μg/injection, produced inhouse by L. Boon) was injected intravenously and Fingolimod/FTY720 (3 mg/kg, Sigma Aldrich) intraperitoneally the day before and just before SWAg footpad injection. In some experiments, FTY720 was injected from 1 day prior to H. polygyrus infection and then daily for 14 days.

Classon C.H., Li M., Clavero A.L., Ma J., Feng X., Tibbitt C.A., Stark J.M., Cardoso R., Ringqvist E., Boon L., Villablanca E.J., Rothfuchs A.G., Eidsmo L., Coquet J.M, & Nylén S. (2021). Intestinal helminth infection transforms the CD4+ T cell composition of the skin. Mucosal Immunology, 15(2), 257-267.

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Molecular Mechanism of Programmed Cell Death

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MMF was purchased from Selleckchem (Houston, TX). Neratinib was kindly supplied by Puma Biotechnology Inc. (Los Angeles, CA). Fingolimod (FTY720) was purchased from Sigma-Aldrich (St. Louis MO). Trypsin-EDTA, DMEM, RPMI, penicillin-streptomycin were purchased from GIBCOBRL (GIBCOBRL Life Technologies, Grand Island, NY). Other reagents and performance of experimental procedures were as described (15 (link), 20 (link)–24 (link)). Antibodies used: AIF (5318), BAX (5023), BAK (12105), BAD (9239), BIM (2933), BAK1 (12105), Beclin1 (3495), cathepsin B (31718), CD95 (8023), FADD (2782), eIF2α (5324), P-eIF2α S51 (3398), ULK-1 (8054), P-ULK-1 S757 (14202), P-AMPK S51 (2535), AMPKα (2532), P-ATM S1981 (13050), ATM (2873), ATG5 (12994), mTOR (2983), P-mTOR S2448 (5536), P-mTOR S2481 (2974), ATG13 (13468), MCL-1 (94296), BCL-XL (2764), P-AKT T308 (13038), P-ERK1/2 (5726), P-STAT3 Y705 (9145), P-p65 S536 (3033), p62 (23214), LAMP2 (49067) all from Cell Signaling Technology; P-ULK-1 S317 (3803a) from Abgent; P-ATG13 S318 (19127) from Novus Biologicals.

Dent P., Booth L., Roberts J.L., Poklepovic A, & Hancock J.F. (2020). Fingolimod Augments Monomethylfumarate Killing of GBM Cells. Frontiers in Oncology, 10, 22.

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Synthesis and Purification of Azido-PEG3-Val-Cit-PAB-PNP-Fingolimod Conjugate

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To the solution of azido-PEG3-Val-Cit-PAB-PNP (compound 9, BroadPharm, San Diego, CA, USA) (9.2 mg, 0.01 mmol) in 3 mL of tetrahydrofuran (THF) and 1.5 mL of dimethylformamide (DMF) was added N,N-diisopropylethylamine (DIPEA) (38.7 mg, 0.3 mmol) at 0 °C. The reaction mixture was stirred for 15 min. Next, fingolimod, FTY720 (19.3 mg, 0.063 mmol) (Sigma Aldrich, Saint-Louis, MO, USA), which was previously dissolved in a mixed solution of 3 mL of THF and 1.5 mL of DMF, was added at 0 °C and stirred for 5 min under a nitrogen atmosphere. The reaction mixture was stirred at room temperature (r.t.) overnight. After solvent removal under reduced pressure, the crude mixture was purified by preparative HPLC (0 min: 10% CH₃CN, 90% H₂O; 20 min: 90% CH₃CN; flow of 20 mL/min; all solvents contained 0.1% TFA). The pure fractions were evaporated and lyophilized to afford compound 10 (5 mg, 45%) as a tacky solid. MS (ESI) m/z calcd: 941.5586; found: 942.7114 ([M + H]⁺) (Figures S6 and S7).

Gonzalez P., Debnath S., Chen Y.A., Hernandez E., Jha P., Dakanali M., Hsieh J.T, & Sun X. (2023). A Theranostic Small-Molecule Prodrug Conjugate for Neuroendocrine Prostate Cancer. Pharmaceutics, 15(2), 481.

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Pharmacological Modulation of SphK1 and S1P Receptors

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All drugs were administered by intraperitoneal injection (I.P.). FG-7142 (Sigma-Aldrich, #E006-100MG) was used as an anxiolytic drug, and administered as described previously (Evans and Lowry, 2007 (link)) at a final concentration of 5 mg/kg body weight 30 min before behavioral testing. The SphK1 antagonist PF-543 (Cayman Chemicals, #17034) was dissolved in 2% DMSO/PBS 0.01M and administered at a final dosage of 10mg/kg. Fingolimod (FTY-720, Sigma-Aldrich, #SML0700-5MG) was used as an S1P receptor agonist, dissolved in saline solution and administered at a final dosage of 0.1 mg/kg, as described (Deogracias et al., 2012 (link)).

Panayotis N., Sheinin A., Dagan S.Y., Tsoory M.M., Rother F., Vadhvani M., Meshcheriakova A., Koley S., Marvaldi L., Song D.A., Reuveny E., Eickholt B.J., Hartmann E., Bader M., Michaelevski I, & Fainzilber M. (2018). Importin α5 Regulates Anxiety through MeCP2 and Sphingosine Kinase 1. Cell Reports, 25(11), 3169-3179.e7.

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Blocking Lymphocyte Egress with Fingolimod

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Blocking the egress of activated lymphocytes from the LNs to the peripheral tissues was achieved through treatment of transplanted animals with the sphingosine-1-phosphate antagonist, fingolimod (FTY720; Sigma-Aldrich), as previously described (64 (link)). Briefly, BMT recipients were injected intraperitoneally with 1.0 mg/kg FTY720 daily, from D+3 to D+7 (experiment terminus); control subjects received an equivalent volume of saline.

Santos e Sousa P., Ciré S., Conlan T., Jardine L., Tkacz C., Ferrer I.R., Lomas C., Ward S., West H., Dertschnig S., Blobner S., Means T.K., Henderson S., Kaplan D.H., Collin M., Plagnol V., Bennett C.L, & Chakraverty R. (2018). Peripheral tissues reprogram CD8+ T cells for pathogenicity during graft-versus-host disease. JCI Insight, 3(5), e97011.

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Fingolimod Treatment in Animal Study

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Animals were distributed into eight experimental groups (see also Table A1):

(a)

Early vehicle-treated males;

(b)

Early FTY-treated males;

(c)

Early vehicle-treated females;

(d)

Early FTY-treated females;

(e)

Late vehicle-treated males;

(f)

Late FTY-treated males;

(g)

Late vehicle-treated females;

(h)

Late FTY-treated females.

Fingolimod (FTY720, Sigma-Aldrich, Darmstadt, Germany) was given dissolved in drinking water at a dose of 1 mg/kg bodyweight per day. The animals had a mean uptake between 2.8 mL (late treated males) and 3.5 mL (early treated males) per day from the drinking water. The FTY720 dose in water was corrected according to water consumption in each group. The treatment was administered for 50 days starting at 50 or 125 days of age, respectively, depending on the experimental group (Figure 7). The body weight and water consumption rate of the animals was controlled weekly to monitor potential side effects and to adjust the dose.

Bascuñana P., Brackhan M., Möhle L., Wu J., Brüning T., Eiriz I., Jansone B, & Pahnke J. (2023). Time- and Sex-Dependent Effects of Fingolimod Treatment in a Mouse Model of Alzheimer’s Disease. Biomolecules, 13(2), 331.

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