[4] The most common side effects of fingolimod have been head colds,[vague] headache,[6] increased gamma-glutamyl transfer (≤15%), diarrhea (13%), nausea (13%), abdominal pain (11%)[6] and fatigue.

[7] Fingolimod has also been associated with potentially fatal infections, bradycardia and, in 2009, a case of hemorrhaging focal encephalitis, an inflammation of the brain with bleeding.

[13] A rare brain infection that usually leads to death or severe disability, called progressive multifocal leukoencephalopathy (PML) has been reported in patients being treated with the drug.

It modulates their proliferation, morphology, and cytokine release via inhibition of the transient receptor potential cation channel, subfamily M, member 7.

[25] First synthesized in 1992 by Yoshitomi Pharmaceuticals, fingolimod was derived from an immunosuppressive natural product, myriocin (ISP-I) through chemical modification.

Myriocin was isolated from the culture broth a type of entomopathogenic fungus (Isaria sinclairii) that was an eternal youth nostrum in traditional Chinese medicine.

[26] Elimination of side chain functionalities and removal of chiral centers was part of the simplification process and an intermediate compound (ISP-I-28) with the carboxylic acid of myriocin transformed to a hydroxymethyl group was generated.

[34] In December 2019, generic fingolimod was approved in the United States for the treatment of relapsing forms of multiple sclerosis in adults.

Novartis appealed and the federal circuit upheld the patent office decision in April 2017, leaving a high likelihood of generics coming to market by 2019.

[36] In January 2020, a panel of judges at the Court of Appeal for the Federal Circuit called into question the validity of the last remaining orange book patent protecting Gilenya.

[37] In October 2022, the Supreme Court turned down a request by Novartis to block the launch of generic versions of Gilenya in the United States.

[41] Recently, the fingolimod molecule has been incorporated in mRNA delivery vehicles to increase targeting of lymphocytes expressing the S1P1 receptor in pre-clinical models.