Current findings indicate that the symptom clusters of inattention and hyperactivity-impulsivity, the primary behavioral characteristics of Attention-Deficit/Hyperactivity Disorder (ADHD), serve as risk factors for reduced academic performance in postsecondary educational settings. The proposed investigation is designed to clarify the extent and mechanisms through which these associated symptoms clusters predict reduced academic performance in an undergraduate sample. This investigation tests four hypotheses: (a) ADHD symptoms predict inversely undergraduates' academic performance; (b) deficiencies in academic coping partially mediate the relationship between undergraduates' ADHD symptoms and academic performance; (c) deficiencies in undergraduates' executive functioning partially mediate the association between students' ADHD symptoms and their academic coping; and (d) the predictive association between students' ADHD symptoms and academic performance is more fully explained by their level of academic coping and executive functioning. To achieve these goals, 111 undergraduates from The University of Texas with variable levels of ADHD symptoms were recruited for participation in this study. Participants' academic performance (i.e., concurrent and cumulative semester grade point average, number of problem credit hours, and number of completed credit hours) will be compared to their level of self-reported ADHD symptoms (i.e., current and childhood ADHD symptoms). The hypothesized mediating effect of academic coping on this relationship was evaluated using two questionnaires of academic coping that separately assess students' general academic coping strategies and more specific academic coping behaviors. Further, the anticipated mediating effect of executive functioning on the relation between ADHD symptoms and academic coping was investigated using two neuropsychological tests of attentional control and planful problem solving. Results did not support the proposed model although several study hypotheses received partial support. A data-derived alternative explanatory model is presented and clinical implications are discussed.