It is well known that ACTH/MSH-like peptides (melanocortins) apart from their classical endocrine effects exert pleiotropic non-endocrine actions. Melanocortins affect nociception and inflammatory process, also ACTH-like peptides have antagonistic effect on opioids induced analgesia. Heptapeptide SEMAX (MEHFPGP) is the analogue of ACTH(4–10). In the present study we investigate Semax influence on stress-induced analgesia and antinociception produced by morphine in white rats. It is well known that exposure of animals to any of a wide range of stressful situation can induce an analgetic reaction – stress-induced analgesia (SIA). Different stressors induce either naloxone reversible (opioid form of SIA) or naloxone nonreversible (nonopioid form of SIA) analgesia. As a stressful agent we used a force swimming at 10 min (water t=28°). Semax was administrated intraperitonealy at dose 0,5 mg/kg 15 min before swimming. Pain sensitivity was measured by using Randall-Selitto paw-withdrawal test. The stressogenic action produced an elevation in the paw withdrawal latency. In control group the decrease of pain sensitivity was observed at 60 min after swimming. Semax administration significantly reduced the SIA – in experimental group pain threshold was different from baseline only at 5 min after swimming. Pre-treatment with naloxone (1 mg/kg) attenuated the swim stress-induced analgesia that indicated of the opioid form of SIA observed. Study of Semax influence on analgesia produced by exogenous opioid showed that peptide (0,5 mg/kg) attenuated antinociception produced by morphine (5 mg/kg). The data obtained allow to suggest that Semax can attenuate analgesia induced by exogenous and endogenous opioids. We can propose that the peptide has antiopioid properties.