Development of Novel Inhibitors of α-2 adrenergic receptors: Therapeutic Leads for Safer Reversal of α-2 adulterated opioid overdoses

Advisor(s)

Edward Ofori M.S, Ph.D., RPh(Gh)

Confirmation

1

Document Type

Poster

Location

ONU McIntosh Center; Activities Room

Start Date

11-4-2025 10:00 AM

End Date

11-4-2025 10:50 AM

Abstract

The increasing prevalence of opioid adulteration with alpha-2 adrenergic receptor (α2AR) agonists, such as xylazine and medetomidine, has introduced new challenges in overdose management. These α2AR agonists exacerbate opioid-induced respiratory depression and complicate emergency medical interventions due to the absence of clinically approved reversing agents. Our current research sought to identify and characterize potential α2AR antagonists or modulators for human use, addressing this critical gap in medical research. Particularly, our work focused on finding ligands that display selectivity for the α2AAR and α2CAR, the α2AR subtypes found predominantly in the brain and implicated in the sedative effects.

We identified lead compounds through structure-activity relationship (SAR) studies, with 2- methoxyphenyl-piperazine derivatives showing high to moderate binding affinity for α2AR subtypes. Iterative synthesis and optimization were conducted using multiparametric drug design strategies, followed by receptor binding and functional assays to a panel of α2ARs.

The identified ligands demonstrate competitive binding to the α 2A AR and α 2C AR subtypes, with 1-(4-methoxy-3-(4-(4-(2-methoxyphenyl) piperazin-1-yl) butoxy) phenyl) ethan-1-one displaying the best affinity (Ki < 100 nM at all α2AR subtypes) among the compounds synthesized.

This research identifies promising α2AR-modulating compounds with potential as reversing agents for xylazine and related sedatives in opioid-polysubstance overdoses. The findings provide a foundation for further preclinical development and could inform future clinical strategies for overdose treatment representing a significant advancement in addressing the emerging public health crisis of opioid-adulterant toxicity.

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Apr 11th, 10:00 AM Apr 11th, 10:50 AM

Development of Novel Inhibitors of α-2 adrenergic receptors: Therapeutic Leads for Safer Reversal of α-2 adulterated opioid overdoses

ONU McIntosh Center; Activities Room

The increasing prevalence of opioid adulteration with alpha-2 adrenergic receptor (α2AR) agonists, such as xylazine and medetomidine, has introduced new challenges in overdose management. These α2AR agonists exacerbate opioid-induced respiratory depression and complicate emergency medical interventions due to the absence of clinically approved reversing agents. Our current research sought to identify and characterize potential α2AR antagonists or modulators for human use, addressing this critical gap in medical research. Particularly, our work focused on finding ligands that display selectivity for the α2AAR and α2CAR, the α2AR subtypes found predominantly in the brain and implicated in the sedative effects.

We identified lead compounds through structure-activity relationship (SAR) studies, with 2- methoxyphenyl-piperazine derivatives showing high to moderate binding affinity for α2AR subtypes. Iterative synthesis and optimization were conducted using multiparametric drug design strategies, followed by receptor binding and functional assays to a panel of α2ARs.

The identified ligands demonstrate competitive binding to the α 2A AR and α 2C AR subtypes, with 1-(4-methoxy-3-(4-(4-(2-methoxyphenyl) piperazin-1-yl) butoxy) phenyl) ethan-1-one displaying the best affinity (Ki < 100 nM at all α2AR subtypes) among the compounds synthesized.

This research identifies promising α2AR-modulating compounds with potential as reversing agents for xylazine and related sedatives in opioid-polysubstance overdoses. The findings provide a foundation for further preclinical development and could inform future clinical strategies for overdose treatment representing a significant advancement in addressing the emerging public health crisis of opioid-adulterant toxicity.