Drug Database
FE

fentanyl

✓ Approved

Luye Pharma Group Ltd. · OPRD1 · Small Molecule

What is fentanyl?

fentanyl is a small molecule developed by Luye Pharma Group Ltd.. It is approved for therapeutic indications via transdermal.

Drug Profile

CompanyLuye Pharma Group Ltd.
Drug ClassSmall Molecule
Molecular TargetOPRD1, OPRK1, OPRM1
RouteTransdermal
StatusApproved
Sources: ClinicalTrials.gov, Luye Pharma Group Ltd.

Mechanism of Action

Molecular Targets

fentanyl acts on 3 molecular targets:

OPRD1opioid receptor delta 1 (DOR, OPRD)
OPRK1opioid receptor kappa 1 (KOR1, OPRK)
OPRM1opioid receptor mu 1 (MOR1, LMOR)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

fentanyl is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Gastrointestinal disordersAbdominal pain✓ Approved

Related Research Articles

PubMedAnalytical chemistry2026-11-11

96-Sample Parallel BioSPME-DART-MS Platform for Rapid Screening of Fentanyl and its Analogues in Biofluids.

Zhou Wei W, Driezen Marc M, Pawliszyn Janusz J

Solid-phase microextraction (SPME) with biocompatible coating material is highly compatible with ambient mass spectrometry (AMS), such as direct analysis in real time (DART), for improving sensitivity and reducing matrix effects. However, the practical throughput of SPME-DART-MS remains limited by the mismatch between parallel sample preparation and device-to-source transfer. Here, we introduce a 96-sample parallel BioSPME-DART-MS platform that integrates automated SPME extraction, 96-channel liquid transfer, and a matched 96-position DART mesh interface. This design enables 96 biological samples to be processed in a plate-based format, greatly improves workflow transferability. Thin HLB/PAN-coated SPME blades were used to provide bio-compatible extraction and cleanup from whole blood, plasma, and urine. After desorption in 200 μL of solvent, only 5 μL of the extract was transferred to the DART mesh for rapid MS/MS screening, while the remaining solution was retained for sequential LC-MS/MS confirmation without additional sample preparation. The system enabling an average analysis time of approximately 40 s per sample. Using six fentanyl and its analogues as model analytes, the BioSPME-DART-MS method achieved good sensitivity across the three biofluids, with limits of detection of 0.10-0.50 ng mL-1 in whole blood, 0.03-0.20 ng mL-1 in plasma, and 0.01-0.20 ng mL-1 in urine. In addition, a comparative study of absolute matrix effects revealed that chromatography-free DART-MS and blade spray-MS remained susceptible to ion suppression, whereas LC-ESI-MS showed negligible matrix effects. This platform establishes a high-throughput, two-tier SPME-MS workflow that combines rapid ambient MS screening with chromatography-based confirmation.

PMID 43010421
Read full article →
PubMedDrug and alcohol dependence2026-11-10

Fentanyl and xylazine precipitated withdrawal in Swiss Webster mice.

Shepherd Brandon B, Cakir Kerim K, Walker Ellen A EA

In recent years, α2-adrenoreceptor (α2AR) agonists have become common adulterants of illicit fentanyl supplies. One such drug is xylazine, a veterinary anesthetic not approved for human use. There is little known about effects of xylazine upon repeated administration, interactions between fentanyl and xylazine, and how xylazine may alter withdrawal from fentanyl. In this work, we established a precipitated withdrawal procedure with the goal of understanding withdrawal from xylazine and how it may impact withdrawal from fentanyl. Mice received fentanyl, xylazine, or both, followed by antagonists naloxone, idazoxan, or both 2h later. Mice were then placed into a large glass beaker and observed for two 60s intervals at 9- and 17-min post injection, and presence of withdrawal signs was recorded in each interval. Injections of fentanyl or xylazine followed by antagonists naloxone or idazoxan, respectively, each produced a unique set of precipitated withdrawal signs. Both produced significant grimace and wet dog shakes; however, precipitated fentanyl withdrawal also produced paw tremors and jumps whereas xylazine withdrawal produced scratching. Xylazine coadministration with fentanyl increased the frequency of some signs of fentanyl precipitated withdrawal while decreasing others. This work suggests that the addition of xylazine to illicit fentanyl supplies is changing the somatic state of fentanyl withdrawal, which may impact patients in clinical settings.

PMID 43008358
Read full article →
PubMedBehavioural pharmacology2026-11-10

Fentanyl-induced postural changes across species: behaviors, mechanisms, and translational implications.

Raffa Robert B RB, Phay Monichan H MH, Kwee Lia L, Miller Thomas L TL et al.

This narrative review summarizes fentanyl-induced postural effects across species, focusing on a postulated cerulospinal noradrenergic connection linking rodent catalepsy models to human wooden-chest syndrome (WCS). This could have possible translational relevance for fentanyl overdose and its clinical management. A review of English-language literature was conducted using PubMed and EMBASE. Reference lists of retrieved articles and prior reviews on the topic were searched for additional sources. The evidence supports that fentanyl-induced postural effects are centrally mediated to a significant extent through µ-opioid receptor (MOR) activation in the locus cœruleus, with downstream engagement of cerulospinal noradrenergic projections onto spinal α1-adrenoceptors. Further, this integrated pathway is subject to modulation by nitric oxide and glutamatergic signaling, striatal dopaminergic-medium spiny neuron circuitry, and pontine respiratory nuclei. Phenomenology differs substantially across species, dose, and route of administration, but a phylogenetically conserved MOR-cerulospinal-noradrenergic pathway, modulated by nitric oxide and dopaminergic circuitry, appears to underlie fentanyl-induced postural disturbances across species, from cataleptic immobility in rodents to WCS in humans. The conserved mechanism is expressed as species-specific chest-wall mechanics that are a determinant of clinical severity, and helps to understand the potential role of α2-adrenoceptor agonists as being mechanistically rational for overdose management.

PMID 43006687
Read full article →
PubMedRSC medicinal chemistry2026-11-10

Development of novel Mu opioid receptor antagonists based on a 6,4-spiro bicyclic fentanyl-derived scaffold.

Li Ennian E, Neel Logan T LT, Upadhyay Neha N, Reda Ahmed A et al.

Scaffold reorganization represents a strategy for modulating Mu opioid receptor (MOR) signaling within flexible opioid scaffolds. Herein, a 6,4-spiro bicyclic core derived from the fentanyl framework was adopted to reduce conformational flexibility while preserving key pharmacophoric features of the parent 8-membered scaffold. Biological evaluations identified compound 3, bearing 2-furanyl and cyclobutylmethyl substituents, as the most potent analogue in this series. Compound 3 exhibited MOR binding affinity (K i = 25 nM), and antagonist-like activity in vivo against morphine- and fentanyl-induced antinociception while displaying minimal intrinsic efficacy (E max = 3% of DAMGO) in functional assays. Compound 3 also showed excellent metabolic stability in human liver S9 fractions, reduced CNS exposure relative to naltrexone, and no measurable respiratory depression at the tested dose. Conformational analysis and molecular docking suggest that the 6,4-spiro scaffold preserves MOR binding while limiting accessible ligand conformations, supporting scaffold reorganization as a strategy to finetune MOR efficacy through fentanyl-derived scaffolds.

PMID 43005752
Read full article →
PubMedAlcohol, clinical & experimental research2026-11-10

Alcohol and Opioids Modulate Excitatory Inputs to the SCN.

Vierkant Valerie V, Purvines William W, Li Ziyi Z, Qi Ling L et al.

Disturbance of circadian rhythms is a hallmark of substance use disorders, with depressant drugs often causing soporific effects such as reduced sleep latency. The suprachiasmatic nucleus (SCN) of the hypothalamus is the central circadian pacemaker in mammals, regulating daily rhythms in physiology and behavior. However, the cellular mechanisms through which depressants alter SCN function remain poorly defined. We used whole-cell patch clamp electrophysiology in coronal brain slices to examine how alcohol and opioids modulate excitatory glutamatergic transmission onto SCN neurons. Ethanol effects were examined acutely and following chronic exposure paradigms. Optogenetic stimulation was used to activate either retinohypothalamic tract (RHT) input or μ-opioid receptor-expressing (MOR+) terminals, and MOR agonists were used to assess opioid-mediated effects on synaptic transmission. We show that acute application of ethanol enhances SCN firing rates during the inactive locomotor stage of circadian rhythms (daytime for rodents). In contrast, chronic alcohol exposure reduces glutamatergic drive. We also found that activating MOR+ terminals via an excitatory channelrhodopsin transgenically expressed in MOR+ neurons produced bidirectional modulation of SCN firing and that MOR+ inputs formed functional glutamatergic synapses onto SCN neurons. We also found that chronic alcohol consumption significantly altered MOR-dependent modulation of SCN neuronal activity, demonstrating an interaction between ethanol exposure and opioidergic signaling. Notably, MOR-mediated transmission could be suppressed by the MOR agonists DAMGO and fentanyl. Together, these findings reveal that both alcohol and opioids modulate glutamatergic input to the SCN. This work establishes the SCN as a novel target of depressant substances and highlights glutamatergic transmission as a key point of vulnerability in circadian dysregulation associated with substance use.

PMID 43009453
Read full article →
PubMedInternational journal of legal medicine2026-11-10

Fatal polysubstance intoxications involving inhalation of nitazene analogues: identification of fluetonitazepyne and 5-methyl etodesnitazene.

Leclerc Maurine M, Widmer Christèle C, Sporkert Frank F, Magliocco Gaëlle G et al.

The illicit opioid market has undergone notable diversification, with 2-benzylbenzimidazoles (nitazenes) representing an increasingly prevalent class of non-fentanyl synthetic opioids. These compounds challenge forensic toxicology through marked µ-opioid receptor potency and rapid structural evolution, often undetected by routine immunoassay screening. We report two fatal polysubstance intoxications involving inhalation of nitazene analogues via vaping devices, identified in biological matrices. GC-MS-based identification was corroborated by untargeted LC-HRMS screening with in silico data mining and confirmed against certified reference standards.Case 1 involved a 40-year-old male found deceased after an estimated 2-3 days without contact. Fluetonitazepyne was quantified at 0.58 ng/mL in peripheral blood alongside ethanol (0.55 g/kg), supra-therapeutic citalopram (340 ng/mL), sub-therapeutic lithium, and cannabinoid metabolites, concordant with a recovered vaping vial containing the same nitazene. Death could not be established with certainty; based on toxicological findings, it was most likely acute fluetonitazepyne intoxication in the presence of central nervous system (CNS) depressants. Case 2 concerned a 22-year-old male with a witnessed cardiorespiratory arrest following inhalation from a vaping device confirmed to contain 5-methyl etodesnitazene. Despite bystander cardiopulmonary resuscitation (CPR), naloxone administration (1.6 mg), and intensive care, he died from acute anoxic encephalopathy approximately 24 h later. Ante mortem peripheral blood confirmed 5-methyl etodesnitazene at 3.3 ng/mL alongside barbital at toxic concentrations (39 mg/L).Concurrent CNS depressant exposure potentiated fatal respiratory depression, more clearly established in Case 2. These cases document the lethal potential of emerging nitazene analogues and the value of untargeted HRMS-based screening in the absence of certified reference standards.

PMID 43003943
Read full article →

+9996 more articles available with a free account

Sign up free to view all articles →

Ask about fentanyl