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https://hdl.handle.net/2440/91883
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Type: | Journal article |
Title: | Molecular targets of FTY720 (Fingolimod) |
Author: | Pitman, M. Woodcock, J. Lopez, A. Pitson, S. |
Citation: | Current Molecular Medicine, 2012; 12(10):1207-1219 |
Publisher: | Bentham Science |
Issue Date: | 2012 |
ISSN: | 1566-5240 1875-5666 |
Statement of Responsibility: | M.R. Pitman, J.M. Woodcock, A.F. Lopez and S.M. Pitson |
Abstract: | FTY720 is a recently approved first line therapy for relapsing forms of multiple sclerosis. In this context, FTY720 is a pro-drug, with its anti-multiple sclerosis, immunosuppressive effects largely elicited following its phosphorylation by sphingosine kinase 2 and subsequent modulation of G protein-coupled sphingosine 1-phosphate (S1P) receptor 1 that induces lymphopenia by altering lymphocyte trafficking. A number of other biological effects of FTY720 have, however, been described, including considerable evidence that this drug also has anti-cancer properties. These other effects of FTY720 are independent of S1P receptors, and appear facilitated by modulation of a range of other recently described protein targets by nonphosphorylated FTY720. Here, we review the direct targets of FTY720 that contribute to its anti-cancer properties. We also discuss other recently described protein effectors that, in combination with S1P receptors, appear to contribute to its immunosuppressive effects. |
Keywords: | Apoptosis cancer FTY720 fingolimod lymphopenia lysophospholipid sphingosine sphingosine 1-phosphate therapeutic drug, Gilenya™ myriocin immunosuppressive activity immunosuppressants toxicity multiple sclerosis |
Rights: | Copyright status unknown |
DOI: | 10.2174/156652412803833599 |
Grant ID: | http://purl.org/au-research/grants/nhmrc/565217 |
Published version: | http://dx.doi.org/10.2174/156652412803833599 |
Appears in Collections: | Aurora harvest 2 Medicine publications |
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