Orexin (OX) neurons originating in the lateral hypothalamus (LH) are ideally positioned to modulate reward processing as they form connections with several key brain regions known to be involved in the reward pathway. Consistent with these findings, a growing number of studies have implicated the OX system in modulating the rewarding properties of several drugs of abuse, including ethanol. However, the role of the OX system in excessive binge-like ethanol intake remains relatively unexplored. Here we assessed the participation of the OX-1 receptor (OX1R) in binge-like ethanol consumption using the drinking-in-the-dark (DID) paradigm to model binge-like ethanol drinking in male C57BL/6J mice. Binge-like ethanol and saccharin drinking following peripheral injections of 0.0, 5.0, or 10.0 mg/kg SB-334867 (SB), a selective OX1R antagonist was examined. Finally, mice were given peripheral injections of SB and open-field locomotor activity was measured. Results indicated that, inhibition of the OX1R via SB blunted ethanol and saccharin drinking, but did not alter open-field locomotor activity. Together, these data suggest that the OX system participates in the consumption of salient reinforcers regardless of calories without affecting general locomotor activity.