Endomorphin 1 acetate is a selective and highly effective μ-opioid receptor agonist with anti-nociceptive and analgesic effects. Endomorphin 1 acetate shows high affinity for kappa3 and can be used to study neurological diseases.

Caco-2 cells were treated with various concentrations of Endomorphin 1 acetate. When cells were incubated with Endomorphin 1 acetate alone, no changes in basal IL-8 production were detected. However, treatment of Caco-2 cells with Endomorphin 1 acetate in the presence of IL-1β significantly increased IL-8 compared with cells treated with IL-1β alone. [1]

Male Sprague Dawley rats (n=48) were randomly divided into four groups (n=12/group): i) Sham group, LAD ligation with no other intervention for 150 min; ii) IR group: LAD was ligated for 30 min (ischemia), and was reperfused for 120 min in vivo; iii) IPO group, after 30 min ischemia, three cycles of LAD clamping for 15 sec and declamping for 15 sec were performed before reperfusion; iv) EM50 group: Endomorphin 1 acetate (50 μg/kg) was administered intravenously following LAD ligation for 25 min, subsequently the LAD was reperfused for 120 min in vivo.
In the IR, IPO and Endomorphin 1 acetate groups, LDH and CK-MB activities were significantly higher compared with the sham group. Compared with the IR group, LDH and CK-MB activities were significantly decreased in the IPO and Endomorphin 1 acetate groups. In the IR group, IL-6 and TNF-α levels were significantly increased compared with the sham group. Compared with the IR group, IL-6, and TNF-α levels were significantly decreased in the IPO and Endomorphin 1 acetate groups. [2]