Reducing the chances of relapsing-remitting multiple sclerosis (RRMS) relapse is an important part of the treatment of RRMS, which will greatly reduce the rate of death and disability due to recurrent multiple exacerbations.Disease-Modifying Drugs such as β-Interferon, Gramoxone, Mitoxantrone Hydrochloride, and Natalizumab are the drugs that have been proven to be effective and have been applied in the clinic, however these However, most of these drugs are administered parenterally over a long period of time, which often increases the burden on patients and decreases compliance with drug application. With the recent FDA approval process for Fingolimod and Cladribine, two oral medications for the treatment of multiple sclerosis, we can look forward to the application of these medications to the clinical management of relapsing-remitting multiple sclerosis, not only in the mode of administration, but also in the reduction of the annual relapse rate, which is becoming more and more significant. In fact the results of multicenter randomized controlled double-blind trials of Fingolimod and cladribine were published in the New England Journal of Medicine earlier this year. These studies compared the efficacy of Fingolimod versus placebo, Fingolimod versus intramuscular beta-interferon 1a, and oral cladribine tablets versus placebo, respectively, in relapsing-remitting multiple sclerosis. Fingolimod exerts its therapeutic effect by decreasing the number of self-invasive lymphocytes entering the central nervous system.Fingolimod (FTY720) is a sphingosine 1-phosphate receptor modulator that prevents the release of lymphocytes from lymph nodes.Fingolimod phosphorylates to become a sphingosine 1-phosphate type 1 receptor antagonist, resulting in the internalization of the receptor molecule. Fingolimod is a lipophilic drug that stably crosses the blood-brain barrier and is phosphorylated in the central nervous system. Fingolimod may also have neuroprotective and neuroregenerative properties by interacting with sphingosine 1-phosphate receptors on nerve cells. Cladribine has immunomodulatory effects due to its selective action on lymphocyte subtypes. The active metabolite of Cladribine, 2-chlorodeoxyadenosine phosphate, accumulates intracellularly, leading to disruption of cellular metabolism (inhibition of DNA synthesis and repair), resulting in apoptosis. Cladribine acts primarily on lymphocytes because lymphocytes have a relatively large number of deoxycytidine kinases at the 5′ end of the nucleotidase and because lymphocytes are dependent on adenosine deaminase activity to maintain a stable intracellular concentration of nucleotide triphosphate. Aggregation of cladribine nucleotides produces a rapid and long-lasting decrease in CD4+ and CD8+ cells. Cladribine also reduced levels of inflammatory cytokines, decreased expression of adhesion molecules and decreased monocyte migration. All three published studies used annual relapse rate as the primary endpoint and showed that cladribine was more effective in relapsing-remitting multiple sclerosis than the placebo group and Fingolimod was more effective than placebo and interferon. Both drugs were also more effective than the control group on secondary endpoints, including active or new lesions on MRI, time to progression to stable disability, rate of patients without relapses, and time to first relapse. Also, the convenience of short-term administration (8-20 days/year) of cladribine in the study, among other things, makes it quite enticing for relapsing-remitting multiple sclerosis treatment applications. Studies have demonstrated the side effects of Cladribine and Fingolimod. Among the common side effects of Cladribine include 1. Lymphopenia 2. Infections (herpes zoster infections are common), mostly skin-limited herpes infections. Correlation studies have shown a negative correlation between the lowest absolute lymphocyte values and the incidence of infections in the group treated with Cladribine.3. Tumors, such as benign uterine fibroids, melanoma, pancreatic cancer, and ovarian cancer. However, studies have shown that the relationship between the development of tumors and the administration of cladribine is unclear. Common side effects of Fingolimod include herpes virus infection, slowed heart rate, atrioventricular block, mildly increased blood pressure, macular edema, skin cancer, and elevated liver enzymes. Heart rate slowing and atrioventricular (AV) block occur after the first dose of Fingolimod and are mostly asymptomatic, with only a small percentage of patients experiencing dizziness, chest discomfort, and palpitations, and continuing to take Fingolimod has not resulted in heart rate slowing or AV block. Fingolimod and cladribine represent a significant change in the current treatment of multiple sclerosis, and these studies offer new hope and more options for the treatment of multiple sclerosis, although long-term follow-up is needed to further assess the risks of these new treatments. Results from three additional Phase III trials of oral MS therapies are expected to be published in 2011-2012.