Fingolimod is a well-tolerated, highly effective disease-modifying therapy successfully utilized in the management of multiple sclerosis. The active metabolite, fingolimod-phosphate, acts on sphingosine-1-phosphate receptors (S1PRs) to bring about an array of pharmacological effects. While being initially recognized as a novel agent that can profoundly reduce T-cell numbers in circulation and the CNS, thereby suppressing inflammation and MS, there is now rapidly increasing knowledge on its previously unrecognized molecular and potential therapeutic effects in diverse pathological conditions. In addition to exerting inhibitory effects on sphingolipid pathway enzymes, fingolimod also inhibits histone deacetylases, transient receptor potential cation channel subfamily M member 7 (TRMP7), cytosolic phospholipase A2α (cPLA2α), reduces lysophosphatidic acid (LPA) plasma levels, and activates protein phosphatase 2A (PP2A). Furthermore, fingolimod induces apoptosis, autophagy, cell cycle arrest, epigenetic regulations, macrophages M1/M2 shift and enhances BDNF expression. According to recent evidence, fingolimod modulates a range of other molecular pathways deeply rooted in disease initiation or progression. Experimental reports have firmly associated the drug with potentially beneficial therapeutic effects in immunomodulatory diseases, CNS injuries, and diseases including Alzheimer’s disease (AD), Parkinson’s disease (PD), epilepsy, and even cancer. Attractive pharmacological effects, relative safety, favorable pharmacokinetics, and positive experimental data have collectively led to its testing in clinical trials. Based on the recent reports, fingolimod may soon find its way as an adjunct therapy in various disparate pathological conditions. This review summarizes the up-to-date knowledge about molecular pharmacology and potential therapeutic uses of fingolimod.

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Background: Psychological problems, such as post-traumatic stress symptoms (PTSS), are among the most important complications associated with the COVID-19 pandemic in people. Studying the social determinants of health (SDH) and its impact on the populations during the crisis will help governments deal better with health emergencies so that every person can have an equal opportunity to stay healthy. Objective: To determine what factors affect PTSS, we conducted a study to investigate the association between structural determinants of health and PTSS during the COVID-19 pandemic. Methods: We conducted a cross-sectional study on 370 people referred to a selected laboratory between June and July 2020 in Karaj province, Iran. Post-traumatic stress disorder (PTSD) 8-item inventory was used to evaluate the PTSS and its subscales, including intrusion, avoidance, and hypervigilance in the participants. Results: Overall, 51.2% of participants were male, and 17.3% were positive for the IgM or IgG COVID-19 test. The most common symptoms in these patients were weakness, myalgia, cough, anosmia, and fever. The prevalence of total PTSS, intrusion, avoidance, and hypervigilance symptoms were 7.1%, 25.7%, 41.6%, and 16.2%, respectively. In univariable regression analysis, female gender (p-value=0.01, 95%CI (2.25-0.31)), un-employment (p-value=0.011, 95%CI (0.37-2.81)), having symptoms of COVID-19 disease (p-value=0.000, 95%CI (.82-2.75)), underlying chronic disease, were directly associated with PTSS. Conclusion: Results showed that sex and occupation as structural determinants of health could affect PTSS in the COVID-19 pandemic. However, in the multivariable model, having symptoms of the COVID-19 disease and underlying disease affected PTSS.