Table 1.
Drug | MOA | MRI Outcome | Clinical outcome |
---|---|---|---|
Laquinimod | – Induction of type ii myeloid cells. – Induction of Th2 cytokine balance. – Increase of BDNF and suppression of TH17 responses. – Attenuation of astrocytic NF-κB activation. |
– Reduction of enlarging or new T2 hyperintense lesions. – Reduction of gadolinium enhancing lesions. – Reduction in the loss of brain volume. |
– Reduction of ARR. – Modest reduction in the risk of confirmed disability progression. |
Fingolimod | – Modulation of S1PR 1, 3–5. – Inhibits egress of lymphocytes. from lymph nodes towards CNS. – Retains Th17 cells. – May reduce astrogliosis and favor remyelination. |
– Reduction of enlarging or new T2 hyperintense lesions. – Reduction of gadolinium enhancing lesions. – Reduction of brain atrophy. |
– Reduction of ARR. – Reduces the risk of disability progression. – Superior efficacy with respect to ARR compared to IFN-β-1a. |
Teriflunomide | – Downregulation of T- and B-cell proliferation by suppression of pyrimidine synthesis. | – Reduction of enlarging or new T2 hyperintense lesions. – Reduction of gadolinium enhancing lesions. |
– Reduction of ARR. – Reduces the risk of disability progression. |
Cladribine | – Induction of DNA damage via accumulation in monocytes and lymphocytes. | – Reduction of active T2 lesions. – Reduction of gadolinium enhancing lesions. |
– Reduction of ARR. – Reduces the risk for disability progression. |
BG-12 | – Induction of Th2-like cytokines and apoptosis in activated T cell. – Activation of Nrf2 pathway and antioxidant response elements. – Decrease of vascular and intracellular adhesion molecules. |
– Reduction of enlarging or new T2 hyperintense lesions. – Reduction of gadolinium enhancing lesions. – Reduction of brain atrophy. – Reduces the number of newhypointense T1-lesions. |
– Reduction of ARR and the proportion of patients relapsing. – Reduces the risk of disability progression. – Superior efficacy with respect to ARR compared to GA. |
Abbreviations: ARR, annual relapse rate; GA, glatiramer acetate; Ian; interferon, MOA; mechanisms of action, MRI; magnetic resonance imaging.