S-MTC is a selective inhibitor of type I nitric oxide synthase.

S-MTC (100?μM) is able to obviously reduce nitrite production (25.2±1.1?μM) as compared to Aβ1-42 treatment alone (38.3±2.7?μM) when administered after Aβ1-42 at the 1?h time point. S-MTC (10 or 100?μM) reduces cellular NO release in the absence of Aβ1-42. S-MTC (100?μM) reduces cell viability. Nitrite productions after Aβ1-42 and L-NOARG (100?μM) or Aβ1-42 and S-MTC (100?μM) treatments are significantly lower than Aβ1-42 alone (33.5±2.0 and 34.5±1.6?μM, respectively). S-MTC (100?μM) concentration decreases both MTT (87±1% of control) and NR (80±1% of control, respectively) levels [1].

S-MTC is a selective neuronal NOS-inhibitor. The HBO2-induced antinociception is significantly antagonized following pretreatment with S-MTC (i.c.v.). At a dose of 0.3 mg/kg, S-MTC (SMTC) induces a rise in mean blood pressure (BP). At doses of 1.0, 3.0, and 10 mg/kg, S-MTC causes a fall in heart rate, rises in BP, and vasoconstriction in all three vascular beds [2][3].