Background and Purpose Opioids remain the most efficient medications against severe pain; they act on receptors that couple to heterotrimeric G‐proteins in the G αi/o family. Opioids exert many of their acute effects through modulating ion channels via G βγ subunits. Many of their side effects are attributed to β‐arrestin recruitment. Several biased agonists that do not recruit β‐arrestins, but activate G‐protein‐dependent pathways, have recently been developed. While these compounds have been proposed to be full agonists of G‐protein signalling in several high throughput pharmacological assays, their effects were not studied on ion channel targets. Experimental Approach Here, we used patch‐clamp electrophysiology and Ca 2+ imaging to test the effects of TRV130, PZM21, and herkinorin, three G‐protein‐biased agonists of μ‐opioid receptors, on ion channel targets of G αi/o /G βγ signalling. We also studied G‐protein dissociation using a FRET‐based assay. Key Results All three biased agonists induced smaller activation of G‐protein‐coupled inwardly rectifying K + channels (K ir 3.2) and smaller inhibition of transient receptor potential melastatin (TRPM3) channels than the full μ receptor agonist DAMGO. Co‐application of TRV130 or PZM21, but not herkinorin, alleviated the effects of DAMGO on both channels. PZM21 and TRV130 also decreased the effect of morphine on K ir 3.2 channels. The Ca V 2.2 channel was also inhibited less by PZM21 and TRV130 than by DAMGO. We also found that TRV130, PZM21, and herkinorin were less effective than DAMGO at inducing dissociation of the G αi /G βγ complex. Conclusion and Implications TRV130, PZM21, and potentially herkinorin are partial agonists of μ receptors.