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In vitro transcription of capped mRNA with modified nucleotides and Poly(A) tail
TSA (Tyramide Signal Amplification), used for signal amplification of ISH, IHC and IC etc.
Separation of phosphorylated and non-phosphorylated proteins without phospho-specific antibody
A convenient and sensitive way for cell proliferation assay and cytotoxicity assay
Protect the integrity of proteins from multiple proteases and phosphatases for different applications.
Fingolimod is a mechanistically novel, orally bioavailable therapy for multiple sclerosis (MS) [1].
Fingolimod is a FDA approved drug for Multiple sclerosis treatment. It is a folk medicine emerged from Fungi. Fingolimod was firstly found to be a therapeutic agent in organ transplantation. Then Fingolimod was found to have similar structure with natural sphingosine and interact with S1P1, S1P4, S1P5 and S1P3 receptors as high affinity agonist with EC50 values of 0.3-3.1 nM. It plays the role in MS treatment through receptor-mediated actions both on the immune system and in the CNS. Fingolimod can prevent normal lymphocyte egress and reduce the infiltration of autoaggressive lymphocytes into the CNS [1, 2].
References:[1] Chun J, Brinkmann V. A mechanistically novel, first oral therapy for multiple sclerosis: the development of fingolimod (FTY720, Gilenya). Discovery medicine, 2011, 12 (64): 213.[2] Chun J, Hartung H P. Mechanism of action of oral fingolimod (FTY720) in multiple sclerosis. Clinical neuropharmacology, 2010, 33 (2): 91.
Cell lines
MCF-7, MDA-MB-231, Sk-Br-3, HCT-116 and SW620 cells
Preparation method
The solubility of this compound in DMSO is >10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37°C for 10 minutes and/or shake it in the ultrasonic bath for a while.Stock solution can be stored below -20°C for several months.
Reaction Conditions
IC50: 79.1 μM (MCF-7), 59.9 μM (MDA-MB-231), 72.9 μM (Sk-Br-3), >100 μM (HCT-116) and 40.0 μM (SW620); 48 hours
Applications
The IC50 values of fingolimod were determined by a WST-1 assay. The results demonstrated that treatment of the compound caused cell death in a dose-dependent manner. Fingolimod exhibited comparatively low IC50 values within the concentration range of 5-7 μM for all of the cells tested in this study.
Animal models
C57BL/6J mice
Dosage form
Intraperitoneal injection, 0.1 mg per kg of body weight
As early as 30 min after injection of fingolimod (0.1 mg per kg of body weight), the levels of phosphorylated ERK1/2 (pERK1/2) were significantly increased in hippocampal neurons. After an additional 30 min, BDNF mRNA levels were elevated, and protein levels were significantly increased in the hippocampus, the cortex, and the striatum after 48 h.
Other notes
Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.
References:
[1] Nagaoka Y, Otsuki K, Fujita T, et al. Effects of phosphorylation of immunomodulatory agent FTY720 (fingolimod) on antiproliferative activity against breast and colon cancer cells. Biological and Pharmaceutical Bulletin, 2008, 31 (6): 1177-1181.
[2] Deogracias R, Yazdani M, Dekkers M P J, et al. Fingolimod, a sphingosine-1 phosphate receptor modulator, increases BDNF levels and improves symptoms of a mouse model of Rett syndrome. Proceedings of the National Academy of Sciences, 2012, 109 (35): 14230-14235.
