CCR2 receptor antagonist (CCR2 RA-[R]) administration reversed existing nociceptive behavior. Animals were subjected to a nerve demyelination injury on day 0 and nociceptive behavior was assessed for 28 days. On days 14 and 28 post-surgery, animals received 5 mg/kg CCR2 RA-[R] or 5 mg/kg of its inactive enantiomer, (CCR2 RA-[S], or saline by intraperitoneal injection, and behavioral responses were tested 1 h later. Administration of the CCR2 RA-[R] to focal nerve demyelination injured rats resulted in a significant bilateral increase of mN force required to elicit a paw withdrawal compared with vehicle-treated controls and animals subjected to CCR2 RA-[S]. Nociceptive behavior in vehicle-treated controls and animals subjected to CCR2 RA-[S] differed significantly from day 0 pre-injury baseline responses (*p < 0.01). Data represent means ± SE.