SummaryBenzodiazepines (BZDs), which enhance γ‐aminobutyric acid (GABAA) receptor–mediated inhibition, are the first‐line therapy for treatment of status epilepticus (SE). However, pharmacoresistance toBZDs develops rapidly afterSEinitiation. This is due to an activity‐dependent internalization ofBZD‐sensitiveGABAAreceptors duringSE. Stiripentol (STP) is a positive allosteric modulator ofGABAAreceptors with a unique subunit selectivity profile. We report that in a rodent model ofSE,STPterminates behavioral seizures and remains effective in establishedSEwhen seizures have becomeBZDresistant. The anticonvulsant effects ofSTPare age dependent, with greater potency in juvenile animals. Whole cell recordings from dentate granule cells in hippocampal slices reveal thatSTPpotentiatesGABAergic inhibitory postsynaptic currents (IPSCs) and tonicGABAergic currents by acting at a site on theGABAAreceptor that is separate from the benzodiazepine binding site. This potentiation persists in establishedSE, whereas potentiation ofGABAergic inhibition byBZDs is lost.STPpotentiatesIPSCs in juvenile animals with greater potency than in adult animals. We suggest thatSTP, either alone or as add‐on therapy, may prove useful in treating established andBZD‐resistant status epilepticus. Furthermore,STPmay be particularly effective in terminatingSEin children whenSEis most prevalent.