October 2022 "Cannabinoid Receptor 2 (CB2) is a G protein-coupled receptor (GPCR) with considerable, Promising preclinical data supports the applicability of CB2 activation in autoimmune and inflammatory cannabinoid ligands is available, which has led to considerable advancements in the understanding of CB2 However, until recently, most CB2 ligands were highly lipophilic and as such not optimal for clinical A number of strategies have been applied to develop CB2 ligands to achieve closer to 'drug-like' properties

August 2022 "Cannabinoid Receptor 2 (CB2) is a G protein-coupled receptor (GPCR) with considerable, though Promising preclinical data support the applicability of CB2 activation in autoimmune and inflammatory cannabinoid ligands is available, which has led to considerable advancements in the understanding of CB2 However, until recently, most CB2 ligands were highly lipophilic and as such, not optimal for clinical A number of strategies have been applied to develop CB2 ligands to achieve closer to 'drug-like' properties

target for regulating schizophrenia-relevant brain circuits "Although the cannabinoid type-2 receptor (CB2 ) is highly expressed in the immune system, emerging evidence points to CB2 playing a key role in regulating Recent anatomical studies, combined with electrophysiological studies, indicate that CB2 receptors are effects of CB2 receptor activation, make this receptor an intriguing target for treating schizophrenia The development of new CB2-related pharmacological and genetic tools, including the first small molecule

< GPCR News < GPCRs in Oncology and Immunology CB2 stimulation of adipose resident ILC2s orchestrates Here, we demonstrate that CB2, a G-protein-coupled receptor (GPCR) and member of the endocannabinoid combination of ex vivo and in vivo approaches to explore the functional and therapeutic impacts of CB2 Our results show that CB2 stimulation of ILC2s protects against insulin-resistance onset, ameliorates Our mechanistic studies reveal that the therapeutic effects of CB2 are mediated through activation of

GPR35, muscarinic acetylcholine receptor M3, alpha-1A adrenergic receptor α1A and cannabinoid receptor CB2