Electrochemical Strategies for the Screening of Synthetic Cannabinoid BB-22 (QUCHIC) within a Toxicological Specimen

Synthetic Cannabinoids (SC) are amongst the most prevalent class of novel psychoactive substances (NPS) which have emerged. The increase in hospitalisation and fatalities as a result of the prevalence of these SC and their abuse, highlights the necessity for the rapid and reliable screening for the substance within toxicological samples. Being able to rapidly screen for these substances would aim to improve overdose triage and ultimately improve treatment administration. Not only this but it would have further advantages for in-field applications such as the identification of drivers under the influence. To this avail we investigate the ability of a simple electrochemical screening strategy for the detection of SC, BB-22 and its primary metabolite BB-22-3-Carboxyindole. Assessment of the feasibility of the strategy for implementation into toxicological sample analysis was performed through detection not only under ideal electrolyte conditions (down to 5 µM for BB-22 and 2 µM for its metabolite) but also within the complex biological matrix of human pooled serum (between 200 and 700 µM), a relevant matrix it would likely encounter if employed within this field.

Synthetic Cannabinoid Agonist WIN 55212-2 Targets Proliferation, Angiogenesis, and Apoptosis via MAPK/AKT Signaling in Human Endometriotic Cell Lines and a Murine Model of Endometriosis

Endometriosis (EM) is characterized by the growth of endometrium-like tissue outside the uterus, leading to chronic inflammation and pelvic pain. Lesion proliferation, vascularization, and associated inflammation are the hallmark features of EM lesions. The legalization of recreational cannabinoids has garnered interest in the patient community and is contributing to a greater incidence of self medication; however, it remains unknown if cannabinoids possess marked disease-modifying properties. In this study, we assess the effects of synthetic cannabinoid, WIN 55212-2 (WIN 55), in EM-representative in vitro and in vivo syngeneic mouse models. WIN 55 reduced proliferation and angiogenesis in vitro, via MAPK/Akt-mediated apoptosis. These findings were corroborated in a mouse model of EM, where we found reduced TRPV1 expression in the dorsal root ganglia of the EM mouse model exposed to WIN 55, suggesting reduced signaling of pain stimuli. Ultimately, these pieces of evidence support the use of cannabinoid receptor agonists as a potential therapeutic intervention for EM associated pain and inflammation.