Slow Dissociation of Nitazenes from the μ -Opioid Receptor Underlies the Challenge of Overdose Reversal

硝嗪类药物与μ-阿片受体的缓慢解离是过量用药逆转的根本挑战

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Abstract

Nitazenes are driving a wave of overdose deaths in the United States and Europe and often require additional doses of naloxone to reverse. To understand the molecular basis, we conducted a joint experimental and simulation study of three common nitazenes, eto-, etodes-, and protonitazene. Radioligand experiments demonstrated that all three nitazenes display higher receptor affinity and longer dissociation half-lives than fentanyl. Notably, protonitazene dissociates slower than carfentanil and its displacement requires fourfold higher antagonist concentrations. The observed trend in nitazene half-lives is recapitulated by molecular dynamics simulations, which suggest that kinetics is controlled by specific interactions with two receptor subpockets. A newly published cryo-EM structure of fluetonitazene- μ OR complex confirms the predicted interactions, including a π -hole bond between the nitro group and Tyr (1.39) , a residue recently shown to modulate μ OR signaling bias. Our findings suggest slow receptor dissociation as a key factor challenging overdose reversal. The mechanistic insights have implications for understanding opioid toxicity and designing more effective countermeasures.

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