Fingolimod (FTY720) HCl

Catalog No.S5002

Fingolimod (FTY720) HCl Chemical Structure

Molecular Weight(MW): 343.9

Fingolimod (FTY720) HCl is a S1P antagonist with IC50 of 0.033 nM in K562, and NK cells.

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In DMSO USD 91 In stock
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USD 170 In stock
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Cited by 37 Publications

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Biological Activity

Description Fingolimod (FTY720) HCl is a S1P antagonist with IC50 of 0.033 nM in K562, and NK cells.
Targets
S1P receptor [1]
(K562, NK cells )
0.033 nM
In vitro

The inhibitory effect of S1P is revered by various concentrations of FTY720, with IC50 effect of 173 nM. In addition, FTY720 (10 nM) alone exerts no effect on the expression of co-stimulatory molecules. FTY720 reverses the increased expression of HLA-I induced by S1P for both the percentages of cells and the MFI, upon comparing the effect of S1P to the effect of combining S1P with FTY720. [1] Medium and high-dose FTY720-P also enhances the levels of TGF-β1. TGF-β1 and Foxp3 mRNA expression are upregulated in the high-dose FTY720-P group. The proliferation of effector T cells is suppressed significantly in the medium and high-dose FTY720-P group at a Treg/Teff cell ratio of 1:1. At a ratio of 1:1, the proliferation of effector T cells is also suppressed in the high-dose FTY720 group. [2]
Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
human U2OS cells NUXN[nhqTnWwY4Tpc44h[XO|YYm= MlzxRYdwdmm|dDDhZ5Rqfmm2eTDheEBpfW2jbjDTNXAyKHKnY3XweI9zKGW6cILld5Nm\CCrbjDoeY1idiCXMl;TJINmdGy|IHPvMYV5eHKnc4Ppcoch\UeIUDDhd5Nme3OnZDDhd{Bz\WOncITvdkBqdnSncn7hcIl7[XSrb36gbY51dyCleYTvdIxie21idYPpcochUG:nY3jzeEBlgWVic4ThbY5qdmduIFXDOVA:OC5yMEKg{txONg>? NIPCNIczOjFyNEG0OC=>
CHO cells M3Sxe2Z2dmO2aX;uJIF{e2G7 Mn:ySIl{eGyjY3Xt[Y51KG:oIGuzN3Bee3CqaX7nc5NqdmViMTDwbI9{eGijdHWg[pJwdSCqdX3hckBUOVBzIILlZ4VxfG:{IHX4dJJme3OnZDDpckBEUE9iY3XscJMtKEmFNUC9NE45PCEQvF2u NYPDSHZtOTV4MUW1NVM>
mouse bone marrow cells NHLqRWtEgXSxdH;4bYPDqGG|c3H5 NVi4U2kzPzJiaB?= MYHDfZRwfG:6aXPpeJkh[WejaX7zeEBDS1JvQVLMJIZ2e2mxbjDwdo91\WmwIEG5NEBmgHC{ZYPzbY5oKG2xdYPlJIJwdmVibXHydo94KGOnbHzzJIFnfGW{IEeyJIhzeyCkeTD2bZRidCCmeXWg[ZhkdHW|aX;uM4Ztd3diY4n0c41mfHKrYzDhcoFtgXOrczygTWM2OD1|LkOg{txONg>? MVmyOFI4OzZ|Mh?=
human MCF7 cells MXzQdo9tcW[ncnH0bY9vKGG|c3H5 NVf2S5k2PzhiaB?= NVfWNIhQSW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDNR2Y4KGOnbHzzJIF{e2W|c3XkJIF{KGe{b4f0bEBqdmirYnn0bY9vKGGodHXyJFc5KGi{czDifUBYW1RvMTDhd5NigSxiSVO1NF02KM7:TT6= MmjHNlE1PTZ3MkS=
MDA-MB-231 cells NFPNc2FRem:uaX\ldoF1cW:wIHHzd4F6 MX23PEBp NGrQeXRCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIF3ERU1OSi1{M{GgZ4VtdHNiYYPz[ZN{\WRiYYOg[5Jwf3SqIHnubIljcXSrb36gZYZ1\XJiN{igbJJ{KGK7IGfTWE0yKGG|c3H5MEBKSzVyPTC1JO69VS5? MWiyNVQ2PjV{NB?=
human SK-BR-3 cells NV7FWopGWHKxbHnm[ZJifGmxbjDhd5NigQ>? NELLPW44QCCq NFzFXGxCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIGPLMWJTNTNiY3XscJMh[XO|ZYPz[YQh[XNiZ4Lve5RpKGmwaHnibZRqd25iYX\0[ZIhPzhiaILzJIJ6KFeVVD2xJIF{e2G7LDDJR|UxRSB3IN88UU4> M{\CS|IyPDV4NUK0
human HCT116 cells MVzQdo9tcW[ncnH0bY9vKGG|c3H5 NEO3ZmE4QCCq M1uxTWFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iSFPUNVE3KGOnbHzzJIF{e2W|c3XkJIF{KGe{b4f0bEBqdmirYnn0bY9vKGGodHXyJFc5KGi{czDifUBYW1RvMTDhd5NigSxiSVO1NF02KM7:TT6= NHG3[2UzOTR3NkWyOC=>
human SW620 cells NHH1T3lRem:uaX\ldoF1cW:wIHHzd4F6 NVLhcolMPzhiaB?= MWXBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKFOZNkKwJINmdGy|IHHzd4V{e2WmIHHzJIdzd3e2aDDpcohq[mm2aX;uJIFnfGW{IEe4JIhzeyCkeTDXV3QuOSCjc4PhfUwhUUN3ME21JO69VS5? NFWzd3QzOTR3NkWyOC=>
human BLIN-1 cells MofqR5l1d3SxeHnjxsBie3OjeR?= Ml\oO|IhcA>? NWXCclVRS3m2b4TvfIlkcXS7IHHnZYlve3RiUHitcoVo[XSrdnWgbJVu[W5iQlzJUk0yKGOnbHzzJIFnfGW{IEeyJIhzeyCkeTD2bZRidCCmeXWg[ZhkdHW|aX;uM4Ztd3diY4n0c41mfHKrYzDhcoFtgXOrczygTWM2OD13LkWg{txONg>? M2ruZ|I1Ojd|NkOy
human BV173 cells M1nJTGN6fG:2b4jpZ:Kh[XO|YYm= Mnu0O|IhcA>? M13DdWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KFCqLYDvd4l1cX[nIHj1cYFvKEKYMUezJINmdGy|IHHmeIVzKDd{IHjyd{BjgSC4aYThcEBlgWViZYjjcJV{cW:wL3\sc5ch[3m2b33leJJq[yCjbnHsfZNqeyxiSVO1NF03NjNizszNMi=> M4Dw[|I1Ojd|NkOy
human DU145 cells MkD1R5l1d3SxeHnjxsBie3OjeR?= MnHWO|IhcA>? NYPqVIttS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hTFVzNEWgZ4VtdHNiYX\0[ZIhPzJiaILzJIJ6KH[rdHHsJIR6\SCneHPseZNqd25xZnzve{BkgXSxbXX0dolkKGGwYXz5d4l{NCCLQ{WwQVYvPSEQvF2u NGnQPIIzPDJ5M{[zNi=>
human SUP-B15 cells Mk\FR5l1d3SxeHnjxsBie3OjeR?= NHjOTWs4OiCq NYOwbnFlS3m2b4TvfIlkcXS7IHHnZYlve3RiUHitdI9{cXSrdnWgbJVu[W5iU2XQMWIyPSClZXzsd{Bi\nSncjC3NkBpenNiYomgeol1[WxiZInlJIV5[2y3c3nvck9ndG:5IHP5eI9u\XS{aXOgZY5idHm|aYOsJGlEPTB;Nj64JO69VS5? NGHM[2ozPDJ5M{[zNi=>
human CCRF-CEM cells MofIR5l1d3SxeHnjxsBie3OjeR?= NVTVNoF3PzJiaB?= MXTDfZRwfG:6aXPpeJkh[WejaX7zeEBRcC2wZXfheIl3\SCqdX3hckBES1KILVPFUUBk\WyuczDh[pRmeiB5MjDodpMh[nlidnn0ZYwh\HmnIHX4Z4x2e2mxbj;mcI94KGO7dH;t[ZRzcWNiYX7hcJl{cXNuIFnDOVA:Pi56IN88UU4> NWjhd49TOjR{N{O2N|I>
human NALM6 cells MkH6R5l1d3SxeHnjxsBie3OjeR?= MXO3NkBp MUfDfZRwfG:6aXPpeJkh[WejaX7zeEBRcC2wZXfheIl3\SCqdX3hckBPSUyPNjDj[YxteyCjZoTldkA4OiCqcoOgZpkhfmm2YXyg[JlmKGW6Y3z1d4lwdi:obH;3JIN6fG:vZYTybYMh[W6jbInzbZMtKEmFNUC9PU43KM7:TT6= M3KzVlI1Ojd|NkOy
human PC3 cells MV;DfZRwfG:6aXRCpIF{e2G7 Mk\kO|IhcA>? MWHDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDQR|Mh[2WubIOgZYZ1\XJiN{KgbJJ{KGK7II\peIFtKGS7ZTDlfINtfXOrb36v[oxwfyCleYTvcYV1emmlIHHuZYx6e2m|LDDJR|UxRTlwODFOwG0v MXmyOFI4OzZ|Mh?=
Sf9 insect cells M{XSR2Z2dmO2aX;uJIF{e2G7 M2jEfVEhcA>? NHX4So5KdmirYnn0bY9vKG:oIHj1cYFvKHKnY3;tZolv[W62IGOxVGwhMDZ{IITvJFU3QCliZYjwdoV{e2WmIHnuJHNnQSCrboPlZ5Qh[2WubIOgeZNqdmdiU{HQJIF{KHO3YoP0doF1\SCjZoTldkAyKGi{ MWKyOFgxQThzNB?=
human Jurkat cells MWHGeY5kfGmxbjDhd5NigQ>? NIWw[I8yQCCq MmHZVoV3\XK|YXygc4YhcW6qaXLpeIlwdiCxZjDtbZRw[2ixbnTybYFtKG[3bnP0bY9vKGmwIHj1cYFvKEq3cnvheEBk\WyuczDh[pRmeiBzODDodpMhcW5icILld4Vv[2Vib3[gXk1XSURvZn3r Mln6NVc1ODB3NUW=
mouse MN9D cells Mk\ZSpVv[3Srb36gZZN{[Xl? MlT1NE4yPiEQvF2= M2jNcFczKGh? MXnO[ZVzd3C{b4TlZ5RqfmViYXP0bZZqfHliaX6gcY92e2ViTV65SEBk\WyuczDhd5Nme3OnZDDhd{BjdG:la3nu[{Bw\iCWTl[tZYxxcGFiYYPzc4Nq[XSnZDD0c5hq[2m2eTDheEAxNjF4IIXNJIFnfGW{IEeyJIhzeyCkeTDUdplx[W5iYnz1[UB{fGGrbnnu[{4> Mn7ONlUxPTBzNkW=
mouse MN9D cells MYnGeY5kfGmxbjDhd5NigQ>? NETJbJcxNjF4IN88US=> NUT0ZpVDOjRiaB?= MmLqUoV2em:ycn;0[YN1cX[nIHHjeIl3cXS7IHnuJI1wfXOnIF3OPWQh[2WubIOgZZN{\XO|ZXSgZZMhe3SrbYXsZZRqd25ib3[gRmRPTiCneIDy[ZN{cW:wIHH0JFAvOTZidV2gZYZ1\XJiMkSgbJJ{ NXXlZ3NFOjVyNUCxOlU>
rat PC12 cells Mlq0SpVv[3Srb36gZZN{[Xl? NXn4S3BmPSEQvF2= NUG0S2JJOzBidH:gNVIxKG2rboO= MXPJcoR2[3Srb36gc4YhWFB{QTDjZZRidHm2aXOgd5VjfW6rdDDhZ5Rqfmm2eTDpckBz[XRiUFOxNkBk\WyuczDhd5Nme3OnZDDhd{BxcG:|cHjheIUhdGW4ZXygZZQhPSC3TTDt[YF{fXKnZDCzNEB1dyBzMkCgcYlvey5? M335RlI2ODVyMU[1
mouse MN9D cells Mki3SpVv[3Srb36gZZN{[Xl? NXjsPGpoPSEQvF2= MWDJcoR2[3Srb36gc4YhWFB{QTDjZZRidHm2aXOgd5VjfW6rdDDhZ5Rqfmm2eTDpckBud3W|ZTDNUllFKGOnbHzzJIF{e2W|c3XkJIF{KHCqb4PwbIF1\SCuZY\lcEBifCB3IIXN M3rmUFI2ODVyMU[1

... Click to View More Cell Line Experimental Data
Assay
Methods Test Index PMID
Western blot
p-AKT / AKT / p-mTOR / mTOR / p-GSK3β / GSK3β / p-IKKα/β / IKKα / NF-κB / Survivin; 

PubMed: 28717222     


Dose-dependent effects of FTY720 on the phosphorylation of Akt, mTOR, GSK3β, and IKKα/β, and the expression of NF-κB, and survivin in SCC2095 cells. Cells were treated with FTY720 in 5% FBS-supplemented DMEM/F12 medium for 24h, and cell lysates were immunoblotted as described in Material and Methods

p-STAT3 / STAT3 / Bcl-xl / Bcl-2 / Bax ; 

PubMed: 25344679     


CC cells were treated for 24 h with or without FTY720 and analyzed for the indicated protein by western blotting. 

Cyclin D1 / CDK4 / cyclin E / CDK2 / p27 / p16 ; 

PubMed: 25344679     


FTY720 induces expression of p16 and p27 and reduces expression of cyclin D1, CDK4, cyclin E and CDK2. CC cells were treated with FTY720 at the indicated concentrations for 24 h. Lysates were then prepared immediately and analyzed by western blotting for cyclin D1, CDK4, cyclin E, CDK2, p16 and p27. β-Actin was used as the internal control. All assays were done in triplicate. 

28717222 25344679
Immunofluorescence
NF-κB; 

PubMed: 28717222     


Effect of FTY720 on the nuclear translocation of NF-κB. SCC2095 cells were treated with 5μM FTY720 for 24h, stained with anti-NF-κB, and examined by confocal microscopy.

N-cadherin / Vimentin ; 

PubMed: 25344679     


Single and merged images show immunofluorescence staining of N-cadherin (green) and vimentin (red). The cell nucleus is stained blue by DAPI.

28717222 25344679
Growth inhibition assay
Cell viability; 

PubMed: 28717222     


Effect of FTY720 at the indicated concentrations on the viability of oral cancer cells. Cells were treated with FTY720 in 5% FBS-supplemented DMEM/F12 medium in 96- well plates at 24h, and cell viability was assessed by MTT assays. Points, means; bars, S.D. (n=6). *P<0.01 compared to the control group.

28717222
In vivo FTY720 is effective in Ph+ but not Ph- ALL xenografts using an early disease model. FTY720 produces a significant reduction in disease burden in the Ph+ ALL xenografts using an early disease model. Ph+ human ALL xenografts responds to FTY720 with an 80 % reduction in overall disease if treatment has been initiated early on. In contrast, treatment of mice with FTY720 does not result in reduced leukemia compared to controls using four separate human Ph- ALL xenografts. [3]

Protocol

Cell Research:[1]
+ Expand
  • Cell lines: Immature DCs
  • Concentrations: 10 nM
  • Incubation Time: 4 hours
  • Method: Immature DCs are left intact or are incubated with 2 μM S1P, 10 nM FTY720, 10 nM SEW2871 or the combinations of S1P with these drugs for 4 hours. As a control 1 μg/mL LPS is used. The cells are washed and incubated in a 96-well plate (v-bottom, 2 × 105 cells per well), washed again and resuspended in PBS buffer containing 0.1% sodium azide. They are labeled with 1 μg/mL FITC-conjugated mouse anti-human CD80, 1 μg/mL FITC-conjugated mouse anti-human CD83, 1 μg/mL FITC-conjugated mouse anti-human CD86, 1 μg/mL FITC-conjugated mouse anti-human HLA-class I, 1 μg/mL FITC-conjugated mouse anti-human HLA-DR, 1 μg/mL FITC-conjugated mouse anti-human HLA-E, or 1 μg/mL FITC-conjugated mouse IgG as a control. The cells are washed twice, and examined in the flow cytometer. Markers are set according to the isotype control FITC-conjugated mouse IgG. To stain NK cells with antibodies for various NK cell activating receptors, they are either left untreated or incubated with 2 μM S1P for 4 hours, washed and stained with 1 μg/mL PE-conjugated mouse anti-human NKp30 (CD337), 1 μg/mL PE-conjugated mouse anti-human NKp44 (CD336), 1 μg/mL PE-conjugated mouse anti-human NKG2D (CD314), or as a control 1 μg/mL PE-conjugated mouse IgG1, for 45 min at 4 °C. NK cells are also stained with 1 μg/mL FITC-conjugated anti-killer inhibitory receptor (KIR)/CD158 antibody which recognizes KIR2DL2, KIR2DL3, KIR2DS2 and KIR2DS4, and as a control with FITC-conjugated mouse IgG. The cells are washed twice, and examined in the flow cytometer. Markers are set according to the isotype control PE-conjugated or FITC-conjugated mouse IgG.
    (Only for Reference)
Animal Research:[3]
+ Expand
  • Animal Models: NOD/SCIDγc−/− mice bearing ALL cells.
  • Formulation: 2% ethanol or saline
  • Dosages: 5 mg/kg/day, 10 mg/kg/day
  • Administration: Administered via i.p.
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 69 mg/mL (200.63 mM)
Water 69 mg/mL (200.63 mM)
Ethanol 69 mg/mL (200.63 mM)
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
Saline
For best results, use promptly after mixing. 		20 mg/mL

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 343.9
Formula

C19H33NO2.HCl
CAS No. 162359-56-0
Storage powder
in solvent
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT03345940 Recruiting Drug: Fingolimod|Drug: Dimethyl Fumarate Relapsing Remitting Multiple Sclerosis Fondazione I.R.C.C.S. Istituto Neurologico Carlo Besta|Patient-Centered Outcomes Research Institute|Universita degli Studi di Genova April 30 2017 Phase 4
NCT02575365 Terminated Drug: 05 mg Fingolimod Cognition|Brain Volume Loss Novartis Pharmaceuticals|Novartis February 16 2016 Phase 4
NCT02490930 Completed Drug: Fingolimod Glioblastoma|Anaplastic Astrocytoma Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins July 2015 Early Phase 1
NCT01981161 Unknown status Procedure: biological samples and clinical data Multiple Sclerosis University Hospital Toulouse|European Commission November 2013 --
NCT01791192 Withdrawn Drug: FTY720|Drug: Oral Corticosteroid Acute Noninfectious Posterior Intermediate or Pan Uveitis Novartis Pharmaceuticals|Novartis November 2013 Phase 2
NCT01757691 Terminated Drug: Fingolimod 0.5mg/daily|Drug: Placebo Acute Demylelinating Optic Neuritis Novartis Pharmaceuticals|Novartis August 2013 Phase 2

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID