[5] Common side effects include loss of appetite, abdominal pain, diarrhea, and feeling tired.

[4] Serious side effects include suicidal thoughts, low blood cell levels, and lupus erythematosus.

Its mechanism of action is thought to be due to antagonism of the postsynaptic T-type voltage-gated calcium channel.

[9][10][11] Ethosuximide is approved for absence seizures,[12] and is considered the first choice medication for treating them, in part because it lacks the idiosyncratic hepatotoxicity of the alternative anti-absence drug, valproic acid.

In March 1989, Coulter, Huguenard and Prince showed that ethosuximide and dimethadione, both effective anti-absence agents, reduced low-threshold Ca2+ currents in T-type calcium channels in freshly removed thalamic neurons.

[15] In June of that same year, they also found the mechanism of this reduction to be voltage-dependent, using acutely dissociated neurons of rats and guinea pigs; it was also noted that valproic acid, which is also used in absence seizures, did not do that.

[17] The first part was supported by Kostyuk et al. in 1992, who reported a substantial reduction in current in dorsal root ganglia at concentrations ranging from 7 μmol/L to 1 mmol/L.

[22] In the introduction of a paper published in 2001, Dr. Juan Carlos Gomora and colleagues at the University of Virginia in Charlottesville pointed out that past studies were often done in isolated neurons that had lost most of their T-type channels.