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AMB-FUBINACA is a synthetic cannabinoid receptor agonist (SCRA) and is primarily metabolized by liver enzymes to generate AMB-FUBINACA carboxylic acid. The metabolic enzymes involved in this biotransformation are not yet known. The aim of this study was to determine whether AMB-FUBINACA metabolism is decreased in the presence of carboxylesterase (CES) inhibitors and recreational drugs commonly consumed together. To determine metabolite activity, we examined the affinity and activity of the acidic metabolite AMB-FUBINACA at the cannabinoid type 1 receptor (CB1). Buy Amb Fubinaca Online, amb-fubinaca for sale, amb fubinaca drug, amb-fubinaca zombie

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method
The effects of CES1 and CES2 inhibitors and delta-9-tetrahydrocannabinol (Δ9-THC) on AMB-FUBINACA metabolism were determined using both human liver microsomes (HLM) and recombinant carboxylesterase. Radioligand binding and cAMP assays comparing AMB-FUBINACA and AMB-FUBINACA acid were performed in HEK293 cells expressing human CB1.

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result
AMB-FUBINACA was rapidly metabolized by HLM in the presence and absence of NADPH. Moreover, both CES1 and CES2 inhibitors significantly reduced AMB-FUBINACA metabolism. Furthermore, digitonin (100 μM) significantly inhibited CES1-mediated metabolism of AMB-FUBINACA by approximately 56%, whereas the effect induced by Δ9-THC was not statistically significant. AMB-FUBINACA acid produced only 26% radioligand displacement consistent with low affinity binding. In the cAMP assay, the potency of AMB-FUBINACA was approximately 3000-fold higher with CB1 than with the acid metabolite.

Conclusion
CES1A1 has been identified as the key hepatic enzyme involved in the metabolism of AMB-FUBINACA to its less potent carboxylic acid metabolites. This biotransformation was significantly inhibited by digitonin. Other xenobiotics can inhibit her SCRA pathway as well, so understanding these interactions may explain why some users experience severe injury after using her SCRA. may become apparent.

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