The G protein-coupled receptor 55 (GPR55), a lysophosphatidylinositol (LPI) receptor that is responsive to certain cannabinoids, has been implicated in several (patho)physiologic functions. CID-16020046 (40 nM – 10 μM) acts as an inverse agonist, inhibiting GPR55 constitutive activity with an IC50 of 0.15 μM. In HEK-GPR55 cells, pretreatment with increasing concentrations of CID-16020046 inhibited GPR55 agonist-induced intracellular Ca2+ release. Further, 2.5 μM CID-16020046 significantly inhibited the LPI (a GPR55 agonist)-induced ERK1/2 phosphorylation, GPR55 internalization and GPR55-mediated transcription factor activation in HEK-GPR55 cells[3]. In the DSS (dextran sulfate sodium) and TNBS (trinitrobenzene sulfonic acid) colitis models, treatment with CID-16020046 at a dosage of 20 mg/kg significantly reduced macroscopic scores and MPO (myeloperoxidase) activity as compared to vehicle-treated animals[4].
CID 16020046 细胞实验
Cell Line
Concentration
Treated Time
Description
References
MDA-MB-231 cells
1μM
24 h
Enhanced cytotoxicity of doxorubicin
Pharmacol Res. 2016 Sep;111:757-766
U87MG cells
1μM
24 h
Enhanced cytotoxicity of doxorubicin
Pharmacol Res. 2016 Sep;111:757-766
rat mesenteric artery endothelial cells
2.5 µM
To investigate the effect of CID 16020046 on LPI-induced vasorelaxation. The results showed that CID 16020046 significantly reduced LPI-induced vasorelaxation
Br J Pharmacol. 2015 Jun;172(12):3043-57
PANC-1 cells
1μM
24 h
Reduced MDR protein expression and enhanced cytotoxicity of chemotherapeutic drugs
Pharmacol Res. 2016 Sep;111:757-766
CID 16020046 动物实验
Species
Animal Model
Administration
Dosage
Frequency
Description
References
BALB/c mice
Antiretroviral-induced neuropathic pain model
Intraperitoneal injection
10 mg/kg
Single administration, experiment lasted up to 70 minutes post-administration
To evaluate the effect of GPR55 antagonist CID 16020046 on the antihyperalgesic activity of 2-AG. Results showed that CID 16020046 significantly antagonized the antihyperalgesic effect of 2-AG.
搜索
