Table of Contents  
Year : 2011  |  Volume : 2  |  Issue : 3  |  Page : 207-208  

Author's reply

Department of Pharmacology, Army College of Medical Sciences, Delhi Cantt, New Delhi, India

Date of Web Publication29-Jul-2011

Correspondence Address:
Sushil Sharma
Department of Pharmacology, Army College of Medical Sciences, Delhi Cantt, New Delhi - 110 010
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Source of Support: None, Conflict of Interest: None

PMID: 21897725

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How to cite this article:
Sharma S. Author's reply. J Pharmacol Pharmacother 2011;2:207-8

How to cite this URL:
Sharma S. Author's reply. J Pharmacol Pharmacother [serial online] 2011 [cited 2021 Apr 20];2:207-8. Available from:


We thank the respondents for expressing an interest in the article. Our comments are as follows:

Fingolimod (FTY 720) is a modulator of the sphingosine 1-phosphate receptor (S1P-R) on the surface of the lymphocytes and inhibits their ability to travel from the lymph nodes to the peripheral circulation and thereby ensuring the decreased entry of potentially encephalitogenic T cells to the CNS in multiple sclerosis. [1] The substantial decrease in blood lymphocyte counts that occurs in a Fingolimod-treated patient reflects their sequestration in the lymph nodes rather than a destruction of lymphocytes. Thus Fingolimod-treated patients may have preservation of many aspects of the immune system, including the capacity for lymphocyte activation in lymph nodes and tissues, the capacity to generate antibodies, and other innate immune responses. [2] This retaining of the functional capacity of the lymphocytes is very important and explains why Fingolimod-treated patients do not develop the frank clinical features of immune suppression.

The reference cited by the respondents mentioning that 2000 patients were taken as part of the FREEDOMS trial is a website of a commercial firm which deals in outsourcing of the drug development technology. However, we draw your attention to the original FREEDOMS trial published in NEJM which clearly mentions that 1272 patients were studied as part of this placebo-controlled trial. [3]

The TRANSFORMS trial witnessed two deaths; one patient died because of primary Varicella zoster infection and the other succumbed to herpes simplex encephalitis. Both the fatalities were seen in patients receiving 1.25 mg/day of Fingolimod. [4] It is too premature to directly implicate Fingolimod to these deaths at present. However, Fingolimod therapy has shown an association with an increased risk of certain viral infections particularly herpes infections [4] and further studies are likely to throw more light on this adverse event.

   References Top

1.Matloubian M, Lo CG, Cinamon G, Lesneski MJ, Xu Y, Brinkmann V, et al. Lymphocyte egress from thymus and peripheral lymphoid organs is dependent on S1P receptor. Nature 2004; 427:355-60.  Back to cited text no. 1
2.Mehling M, Brinkmann V, Antel J, Bar-Or A, Goebels N, Vedrine C et al.FTY 720 therapy exerts differential effects on T cell subsets in multiple sclerosis. Neurology 2008; 71:1261-7.  Back to cited text no. 2
3.Kappos L, Radue EW, O' Connor P, Polman C, Hohlfeld R, Calabresi P, et al. A placebo controlled trial of oral Fingolimod in relapsing multiple sclerosis. N Engl J Med 2010; 362:387-401.  Back to cited text no. 3
4.Cohen JA, Barkhof F, Comi G, Hartung HP, Khatri BO, Montalban X, et al. Oral Fingolimod or intramuscular interferon for relapsing multiple sclerosis. N Engl J Med 2010; 362:402-15.  Back to cited text no. 4


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