“…Interestingly, in models of cardiac dysfunction, beta-1 adrenergic receptor stimulation by dobutamine ( 59 ) increases cell death and inflammation, but its blockade by the beta-1 selective antagonist metoprolol ( 60 ) enhances PGC-1α activation and improves cardiac metabolism and function. , Our laboratory has studied beta-2 adrenergic receptor selective agonists in renal MB. In particular, formoterol ( 61 ), fenoterol ( 62 ), and procaterol ( 63 ) induced MB in vitro at pharmacologically relevant doses. , Compound 61 has been confirmed to induce MB in vivo in naïve mice as well as in mice subjected to AKI, and this was associated with improvements in renal function, indicating that formoterol has therapeutic promise for treating AKI. However, other beta-2 adrenergic receptor agonists such as clenbuterol ( 64 ) and isoetharine ( 65 )did not induce MB in vitro , suggesting that biased agonism can be exploited to develop more effective mitochondrial biogenic beta-2 adrenergic receptor agonists.…”