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G protein-coupled receptors, such as the cannabinoid type 1 receptor (CB1R), have been shown to interact with multiple binding partners to transmit signals. In both transfected cell systems and in endogenously expressing cell lines, CB1R signaling has been described as multifaceted. The question remains as to how this highly widely expressed receptor signals in a given cell at a given time in vivo. The concept of functional selectivity, or biased agonism, describes the ability of an agonist to engage the receptor in a manner that preferentially engages certain signaling interactions (e.g., G proteins) over others (e.g., β-arrestins), presumably by stabilizing certain receptor conformations. There is growing interest in using such properties of ligands to direct signaling downstream of CB1R toward desirable therapeutic outcomes and to avoid adverse side effects. While it is not currently clear what pathways should be engaged and which should be avoided, the development of biased agonist tool compounds will aid in answering these questions. In this chapter, we discuss the approaches and caveats to assessing biased agonism at the CB1R.

Approaches to Assess Biased Signaling at the CB1R Receptor