CID 16020046 是一种有效的，选择性 GPR55 拮抗剂，抑制 GPR55 的组成型活性，IC₅₀ 为 0.15 μM。CID 16020046 抑制 GPR55 介导的 Ca²⁺ 信号传导和 GPR55 介导的 ERK1/2 磷酸化。CID 16020046 降低了内皮细胞的伤口愈合，并参与了血小板功能的调节。

CID 16020046 is a potent and selective GPR55 antagonist and inhibits GPR55 constitutive activity with an IC 50 of 0.15 μM. CID 16020046 inhibits GPR55-mediated Ca signaling and GPR55-mediated ERK1/2 phosphorylation. CID 16020046 reduces wound healing in endothelial cells and is involved in the regulation of platelet function.

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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.
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 Ca release in HEK-GPR55, HEKCB1 cells and shows no ERK1/2 phosphorylation.
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.
CID16020046 (2.5 μM) antagonizes GPR55-mediated activation and nuclea

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[1]. Kargl J, et al. A selective antagonist reveals a potential role of G protein-coupled receptor 55 in platelet and endothelial cell function. J Pharmacol Exp Ther. 2013 Jul;346(1):54-66.

In Vitro: DMSO : 100 mg/mL (235.05 mM; Need ultrasonic)配制储备液