An oral sphingosine-1-phosphate-receptor modulator.

Following phosphorylation, fingolimod acts as a functional antagonist of the sphingosine-1-phosphate type 1 receptor, and causes T and B cells to be insensitive to signals needed for egress from lymphoid tissues.

Acts by preventing lymphocyte egress from lymph nodes (Mandala S).

May reduce infiltration into the central nervous system of potentially aggressive lymphocytes (Compsyon A).

In MS associated with a decrease in the total mean lymphocyte count and blocks the exit of naïve and central memory lymphocytes, but not effector memory T cells from the lymph node.

Naïve T cells and central memory cells, but not effector memory cells, express the chemokine receptor CCR7, which induces homing to the lymph nodes.

Part of this agent’s therapeutic action may be independent of its effect on peripheral lymphocytes.

This agent is lipophilic and readily crosses the blood brain barrier, where it is phosphorylated in the CNS (Foster CA).

Laboratory testing indicates that this agent may protect neurologic tissue and promote repair processes within the CNS via modulation of sphingosine-1-phosphate-receptors expressed on neurons.

Cardiovascular effects of felt to be due to binding of the drug to sphingosine-1-phosphate receptors in cardiac muscle.

Can cross the blood brain barrier and bindss to S1P1,S3, and S1P5 receptors on neural cells.

S1P1 and S1P3 receptors are strongly expressed in multiple sclerosis lesions, and expression of these receptors is associated with astrogliosis, a main pathological feature of multiple sclerosis lesions.

Treatment can reduce neuroinflammatory disease and improve CNS tissue integrity.

The anti-inflammatory effects of this drug does not slow disease progression in primary progressive multiple sclerosis (Lubli )

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