O-1602 is an agonist of GPR55 (EC50 = 13 nM in a GTPγS binding assay) and a derivative of the GPR55 agonist abnormal cannabidiol.[1] It is selective for GPR55 over cannabinoid (CB) receptor 1 (CB1) and CB2 (EC50s = >30 μM for both in GTPγS binding assays). O-1602 (50 μM) reduces growth of Mz-ChA-1, HuCCT-1, CC-LP-1, and SG231 cholangiocarcinoma cells and reduces tumor growth in a Mz-ChA-1 mouse xenograft model when administered at a dose of 10 mg/kg per day.[2] O-1602 increases calcium mobilization and lipogenesis in 3T3-L1 adipocytes in a concentration-dependent manner and increases food intake and fat mass in rats; however, this effect was also observed in mice lacking GPR55.[3] O-1602 reduces movement-induced firing of nociceptive C fibers in a rat model of inflammatory joint pain.[4] It also decreases IL-6 and TNF-α levels and myeloperoxidase activities in the plasma, lungs, and pancreas in a mouse model of acute pancreatitis.[5]

Reference:
[1]. Ryberg, E., Larsson, N., Sjogren, S., et al. The orphan receptor GPR55 is a novel cannabinoid receptor. Br. J. Pharmacol. 152(7), 1092-1101 (2007).
[2]. Huang, L., Ramirez, J.C., Frampton, G.A., et al. Anandamide exerts its antiproliferative actions on cholangiocarcinoma by activation of the GPR55 receptor. Lab Invest. 91(7), 1007-1017 (2011).
[3]. Díaz-Arteaga, A., Vázquez, M.J., Vazquez-Martínez, R., et al. The atypical cannabinoid O-1602 stimulates food intake and adiposity in rats. Diabetes Obes. Metab. 14(3), 234-243 (2012).
[4]. Schuelert, N., and Mcdougall, J.J. The abnormal cannabidiol analogue O-1602 reduces nociception in a rat model of acute arthritis via the putative cannabinoid receptor GPR55. Nuerosci. Lett. 500(1), 72-76 (2011).
[5]. Li, K., Feng, J.-Y., Li, Y.-Y., et al. Anti-inflammatory role of cannabidiol and O-1602 in cerulein-induced acute pancreatitis in mice. Pancreas 42(1), 123-129 (2013).