Cyclin-dependent kinase-like 5 (CDKL5) deficiency disorder (CDD) is a developmental and epileptic encephalopathy (DEE) characterized by severe drug-resistant epileptic disorders beginning in early childhood, along with cognitive and social impairments in later childhood and adulthood. Existing pharmacological therapies for CDD primarily focus on anti-seizure medications, which often have associated sedative side effects. In addition, there are currently no effective treatments for cognitive or behavioral impairments associated with this disorder. Postnatal development expression of CDKL5 has a similar timeline as the developmental activity of the potassium chloride co-transporter (KCC2), the maturation of which is a prerequisite for the developmental switch to fast synaptic hyperpolarizing inhibition mediated by g-aminobutyric acid type A receptors (GABA