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Zebrafish made the connection between a drug for weight loss and a treatment for epilepsy. This is the story of Fenfluramine, now marketed as Fintepla. Fenfluramine was commercialized for weight loss decades ago. But in a screening of a chemical library of ∼1000 compounds using a zebrafish epilepsy model, Dinday and Baraban identified 4 compounds that rescued the behavioral seizure component. Fenfluramine was one of them. There were prior clinical observations, but the zebrafish screen added a critical layer of in vivo evidence. Fenfluramine is now an FDA- and EMA-approved therapy for seizures associated with Dravet syndrome in patients aged 2 years and older. The scn1lab zebrafish model was part of the evidence chain that took fenfluramine all the way to the clinic. That's what a well-characterized in vivo model does. At ZeClinics, we have generated the scn1lab epilepsy models through CRISPR/Cas9‑mediated gene disruption. It displays spontaneous seizure-like behavior and heightened sensitivity to convulsive stimuli. It is useful for: → High‑throughput screening of antiseizure compounds. → Mechanistic studies of neuronal hyperexcitability driven by sodium‑channel or GABAergic dysfunction. → Genetic and variant-level target validation. Are you reassessing your preclinical strategy? Let's talk!

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