CID 16020046

CID 16020046 is a potent and selective GPR55 antagonist and inhibits GPR55 constitutive activity with an IC₅₀ of 0.15 μM. CID 16020046 inhibits GPR55-mediated Ca²⁺ signaling and GPR55-mediated ERK1/2 phosphorylation. CID 16020046 reduces wound healing in endothelial cells and is involved in the regulation of platelet function^[1]. In Vitro: CID 16020046 has weak activities close for inhibition of the acetylcholinesterase (pIC₅₀=4.4), antagonism of the m-opioid receptor (pIC₅₀=4.6), and blockade of KCNH2, the hERG channel (pIC₅₀=4.6) 6 in human embryonic kidney (HEK)-G protein–coupled receptor 55 (GPR55) cells^[1].
CID 16020046 (2.5 μM; for ≥25 minutes) significantly inhibits the lysophosphatidylinositol (LPI; 2.5 μM) induced ERK1/2 phosphorylation. CID 16020046 alone fails to induce intracellular Ca²⁺ release in HEK-GPR55, HEKCB1 cells and shows no ERK1/2 phosphorylation^[1].
Pretreatment with CID16020046 (0.01, 0.1, 1, 10 μM) leads to a concentration-dependent decrease in GPR55-mediated NFAT activation, NF-kB activation, and SRE induction in response to 1 μM LPI or GSK319197A in HEKGPR55 and HEK-CB1 cells^[1].
CID16020046 (2.5 μM) antagonizes GPR55-mediated activation and nuclear translocation of transcription factors but has no effect on CB1-mediated CREB activation^[1].
Pretreatment CID16020046 (1 μM) abolished the LPI-induced stimulation of wound healing in HMVEC-Ls^[1].