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. 2024 Apr 22;14:9181. doi: 10.1038/s41598-024-58845-7

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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GRK3-CB1R and β-arrestin2-CB1R interactions elicited by the tested cannabinoids. HEK293 cells were transiently transfected with CB1R-EYFP and β-arrestin2-Rluc or GRK3-Rluc8 (1:2 ratio). The cells were stimulated with increasing concentrations of compounds (9S)-HHC, (9R)-HHC, Δ⁹-THC, WIN, or their vehicles. BRET donor and acceptor emission was measured 12 min after the addition of the compounds. (A) Concentration–response relationship of GRK3-CB1R association mediated by CB1R stimulation. (B) Concentration–response relationship of β-arrestin2 recruitment to CB1R after CB1R stimulation. The data are presented as means ± SEM from three independent experiments. The data analysis is disclosed in Supplementary Tables 3 and 4.