R-PSOP is a potent and selective nonpeptidic NMUR2 antagonist, exhibiting binding affinity to human and rat NMUR2 with Ki values of 52 nM and 32 nM, respectively. This compound demonstrates moderate central nervous system (CNS) penetration and is valuable in the study of eating disorders, obesity, pain, and stress-related disorders [1].

From Schild analyses, the functional K b values for R-PSOP are 92 and 155 nM at human and rat NMUR2, respectively (the effects of R-PSOP on the intracellular calcium mobilization response induced by NMU-25 in HEK293 cells expressing human or rat NMUR2) [1]. R-PSOP strongly inhibits the responses stimulated by peptide agonists NMU-25, NMU-23, and NMU-8 in human embryonic kidney 293 cells expressing NMUR2 [1]. In functional assays measuring phosphoinositide turnover or intracellular calcium mobilization, R-PSOP strongly inhibits the responses stimulated by peptide agonists NMU-25, NMU-23, and NMU-8 in human embryonic kidney 293 cells expressing NMUR2 [1]. R-PSOP concentration-dependently inhibits the phosphoinositide (PI) turnover turnover response in human NMUR2-expressing cells stimulated by 10 nM NMU-25 (EC 50 of 5 nM). The IC 50 value is determined to be 86 nM [1].

R-PSOP (10 μL 50 nmol; intrathecal injection; male Sprague-Dawley rats) attenuates NMU-23-evoked nociceptive responses in a rat spinal reflex preparation [1].