Indeed, you're correct. But your comment is irrelevant—insofar as it is intended as a response to my post—because, while herkinorin behaves primarily as a mu-opioid receptor agonist, it is nonetheless a kappa-opioid receptor agonist. Thus: a.) my example of herkinorin is still valid, and b.) your comment is therein moot and supererogatory.
Herkinorin is the first mu-opioid receptor-selective ligand from the salvinorin A diterpenoid scaffold. Herkinorin has relative binding selectivity, and it can act as an agonist at both mu-and kappa-receptors, in vitro.
These studies were the first in vivo evaluation of the effects of herkinorin in nonhuman primates, using prolactin release, a neuroendocrine biomarker assay that is responsive to both mu-and kappa-agonists, as well as to compounds with limited ability to cross the blood-brain barrier. In cumulative dosing studies (0.01–0.32 mg/kg i.v.), herkinorin produced only small effects in gonadally intact males (n 4), but a more robust effect in females (n 4). Time course studies with herkinorin (0.32 mg/kg) confirmed this greater effectiveness in females and revealed a fast onset after i.v. administration (e.g., by 5–15 min).
Antagonism experiments with different doses of nalmefene (0.01 and 0.1 mg/kg) caused dose-dependent and complete prevention of the effect of herkinorin in females. This is consistent with a principal mu-agonist effect of herkinorin, with likely partial contribution by kappa-agonist effects. The peripherally selective antagonist quaternary naltrexone (1 mg/kg s.c.) caused approximately 70% reduction in the peak effect of herkinorin (0.32 mg/kg) in females, indicating that this effect of herkinorin is prominently mediated outside the blood-brain barrier.
[Source:
The Effects of Herkinorin, the First -Selective Ligand from a Salvinorin A-Derived Scaffold, in a Neuroendocrine Biomarker Assay in Nonhuman Primates]