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Significance An enhanced Kv2.1–syntaxin interaction precedes the neuronal cell death-promoting loss of cytosolic K+ in many neurodegenerative conditions. The work presented here characterizes the interaction of the disordered C terminus of Kv2.1 to syntaxin at a molecular level and further translates these findings to discover a first-in-class small molecule with neuroprotective properties. In doing so, we demonstrate a rational drug discovery workflow that can elucidate protein–protein interactions involving highly unstructured domains.

Defining the Kv2.1–syntaxin molecular interaction identifies a first-in-class small molecule neuroprotectant