nancy145
Bluelighter
I looked online and couldn't find what it's classified as, like phycadellic, disassociative, etc.
It's technically an atypical dissociative drug I believe.
It has a number of unique features... salvinorin A acts as a kappa agonist and has a structure without any nitrogen, making it something other than an alkaloid. Something otherwise mostly unheard of.
Considering how immersive the state is, and the detachment from your normal sense of surroundings do you really need that analysis to call it dissociative? Cause it feels like a dissociative to me..
Even though herkinorin is a structural analogue of salvinorin A, it is primarily an agonist on the mu opioid receptor.Practically every drug that behaves as a kOR agonist (bremazocine, herkinorin, (−)-pentazocine, 8-Carboxamidocyclazocine, LPK-26, Oxilorphan, etc.) possesses dissociative effects at sufficient doses.
Even though herkinorin is a structural analogue of salvinorin A, it is primarily an agonist on the mu opioid receptor.
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]