Cannabinoid receptors, CB1 and CB2 are two extensively studied targets of the GPCR family for the treatment of numerous​ conditions, including inflammatory diseases, autoimmune disorders, pain, and cancer.​

Cannabis sativa L. has gained interest because, apart from Δ9-THC and CBD, as there are other compounds that are bioactive, by interacting with cannabinoid receptors and/or interacting with a variety of other GPCRs, e.g. GPR18, GPR55.

Pharmacology of cannabinoids acting on cannabinoid receptors is complex. Recent data that have elucidated the structure of the cannabinoid receptors show that the site of agonist binding is not readily available to extracellular molecules, but the active compounds must enter through the lipid bilayer (1,2). Also, it has been described the existence of exosites to which agonists of GPCRs may interact and regulate receptor functionality (3). Moreover GPCRs may interact to form heteromers whose functional properties are different from those of individually expressed receptors (4,5). 

Despite the significance of these receptors, researchers lack reliable analytical tools, in particular to assess their tissue and cellular distribution and understand complex signalling mechanisms.​

Thanks to the use of innovative receptor binding technologies  designed by Celtarys, CELT-335 and CELT-331, it was possible to characterize through whole cell direct signaling pathways studies, new   pharmacological properties derived from the action of Δ9-tetrahydrocannabinolic acid (Δ9-THCA) and Δ9- tetrahydrocannabivarin (Δ9-THCV) on CB1R, CB2R and CB1-CB2Hets.