Distress intolerance (DI), a trait-like individual difference reflective of the inability to endure aversive affective states, is relevant to multiple forms of psychopathology, but its relations to theoretically relevant neurobiological systems have received little attention. Altered cognitive control-related neurobiology has been theorized to underlie individual differences in DI, but little empirical work has been conducted. To test this hypothesis, baseline data from a large community sample with elevated high levels of emotional psychopathology and comorbidity was utilized (N = 256). Participants completed a complex go/no-go task while EEG was recorded, and P2, N2, and P3 amplitudes were measured. Based upon prior findings on the relations between these components and response inhibition, a core cognitive control function, we hypothesized that DI would predict reduced no-go N2 and P3 amplitude while controlling for current anxious/depressive symptom severity (i.e., negative affect). Peak amplitudes from the raw data and principal components analysis were used to quantify amplitude of ERP components. Partially consistent with predictions, high DI was independently associated with reduced no-go N2 peak amplitude in the raw ERP data, and was significantly related to a frontal positivity factor in the N2 time window across no-go and go trials. Contrary to predictions, no relations between DI and the P3 were found. Overall, results support the theorized relevance of cognitive control-linked neurobiology to individual differences in tolerance of distress over and above distress severity itself, and suggest specific relations between DI and alterations in early controlled attention/conflict-monitoring but not response inhibition or response inhibition-related sequelae.