Fructose-1,6-bisphosphate (F1,6BP) has actions that suggest it may be an effective anticonvulsant (see Fig. 1). First, F1,6BP has been shown to increase flux of glucose into the pentose phosphate pathway (Kelleher et al., 1995; Espanol et al., 1998) and preserve cellular GSH levels (Vexler et al., 2003). Second, F1,6BP modulates the activity of phosphofructokinase-1 (PFK-1), which is the enzyme that controls the rate-limiting step in glycolysis. F1,6BP is a weak stimulator of PFK-1, but becomes inhibitory in the presence of fructose-2,6-bisphosphate (F2,6BP), a potent activator of PFK-1 (Heylen et al., 1982; Van Schaftingen, 1987). These data suggest that F1,6BP will slightly enhance basal glucose metabolism, but will prevent stimulation of glycolysis by F2,6BP. Diverting glucose from glycolysis toward the pentose phosphate pathway, thus increasing GSH levels while maintaining an energy source for the brain, should provide significant anticonvulsant efficacy.