ArticleCell & bioscience2026
Anti-seizure potential of J4, an equilibrative nucleoside transporter 1 inhibitor, in a mouse model of tuberous sclerosis complex in response to pentylenetetrazol.
Article in Cell & bioscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Tuberous sclerosis complex (TSC) is a neurodevelopmental disorder with epileptic seizures caused by genetic mutations in either TSC1 or TSC2 gene. Multiple genetic, epigenetic, and environmental factors can affect the phenotypical outcomes of TSC individuals. Accumulating evidence has shown that the seizures occurred in early life may contribute to the epileptogenesis and aggravate the neurological setting and neuropsychiatric symptoms of TSC. Therefore, treatments targeting seizures and/or epileptogenesis have always been the main focus on TSC therapies. Current anti-epileptic drugs and mTOR inhibitors show some efficacy, yet up to one-third of TSC-epileptic individuals are classified as refractory epilepsy. Vigabatrin, which has been used as the first-line therapy for infantile spasms in TSC, has demonstrated to delay the onset and lower the overall incidence of seizures in infants with TSC when it was used as a preventive treatment. Recently, because of its efficacy, cannabidiol, which targets adenosine signaling pathway, has been approved by the U.S. FDA for the treatment of TSC-associated epilepsy, suggesting an anti-epilepsy strategy other than mTOR inhibition is also plausible for TSC. To this end, we sought for a preventative treatment of an adenosine pathway-targeted therapeutic strategy. In this study, we pretreated Tsc2
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