Methoxyflurane 99.9% inhalation vapour liquid 3ml bottles with device
Requires a prescription from a doctor or prescriber
An inhalation anesthetic.
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Suspected adverse reactions reported for Methoxyflurane
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Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
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Suspected adverse reactions reported for Methoxyflurane
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Penthrox inhalation vapour liquid 3ml bottles with device
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
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Codes for healthcare professionals and prescribing systems
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NHS UK identifiers
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF code shown is the factual mapping value distributed by NHS Business Services Authority (NHSBSA) in the dm+d supplementary file under OGL v3.0; it is not affiliated with, nor licensed from, the publishers of the British National Formulary. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 20 · Randomised trials: 22 · 1966–2026
Showing the 50 most relevant studies, sorted by most relevant.
Keith Porter, Mohd Kashif Siddiqui, Ikksheta Sharma, et al.
Journal of Pain Research, 2017
Louisa Lam, H. J. Brouwer, M. Gupta, et al.
The American journal of emergency medicine, 2025
- Methoxyflurane
- Anesthetics, Inhalation
- Acute Pain
INTRODUCTION Inhaled Methoxyflurane has emerged as a popular analgesic agent for the management of acute traumatic pain in emergency settings. The aim of this review was to assess the analgesic efficacy of methoxyflurane compared to placebo and standard analgesics. METHODS We performed a systematic review of the literature with searches of seven databases (Medline Complete, CINAHL Complete, OVID Emcare, Embase Classic + Embase, Cochrane Library, Scopus and Web of Science Core Collection) for randomized controlled trials where patients presented to the emergency department with acute traumatic pain and were administered inhaled methoxyflurane compared to placebo or standard analgesics. The primary outcome was the effectiveness of analgesia. Secondary outcomes were adverse events and patient and clinician satisfaction. RESULTS The literature search produced 250 results, of which six met the eligibility criteria. All six studies reported improved pain scores with pain reduction of up to -30.392 mm on a 100 mm VAS scale and - 5.75 on an NRS 0-10 point scale for the methoxyflurane groups. All six studies concluded a shorter time to obtain pain relief for patients in the methoxyflurane groups. Patients and clinicians reported higher satisfaction in the methoxyflurane groups and there was a low incidence of adverse events. CONCLUSION Inhaled methoxyflurane provides rapid and effective pain relief for acute trauma, consistently outperforming placebo and standard treatments and improving patient and clinician satisfaction.
Abstract licence: CC BY
Hyldmo PK, Rehn M, Dahl Friesgaard K, et al.
2024
- Analgesics
- Emergency Medical Services
- Pain Management
BackgroundMany prehospital emergency patients receive suboptimal treatment for their moderate to severe pain. Various factors may contribute. We aim to systematically review literature pertaining to prehospital emergency adult patients with acute pain and the pain-reducing effects, adverse events (AEs), and safety issues associated with inhaled analgetic agents compared with other prehospital analgesic agents.MethodsAs part of an initiative from the Scandinavian Society of Anaesthesia and Intensive Care Medicine, we conducted a systematic review (PROSPERO CRD42018114399), applying the PRISMA guidelines, Grading of Recommendations Assessment, Development, and Evaluation (GRADE), and Cochrane methods, searching the Cochrane Library, Epistemonikos, Centre for Reviews and Dissemination, PubMed, and EMBASE databases (updated March 2024). Inclusion criteria were the use of inhaled analgesic agents in adult patients with acute pain in the prehospital emergency care setting. All steps were performed by minimum of two individual researchers. The primary outcome was pain reduction; secondary outcomes were speed of onset, duration of effect, and relevant AEs.ResultsWe included seven studies (56,535 patients in total) that compared inhaled agents (methoxyflurane [MF] and nitrous oxide [N2O]) to other drugs or placebo. Study designs were randomized controlled trial (1; n = 60), randomized non-blinded study (1; n = 343), and randomized open-label study (1; n = 270). The remaining were prospective or retrospective observational studies. The evidence according to GRADE was of low or very low quality. No combined meta-analysis was possible. N2O may reduce pain compared to placebo, but not compared to intravenous (IV) paracetamol, and may be less effective compared to morphine and MF. MF may reduce pain compared to paracetamol, ketoprofen, tramadol, and fentanyl. Both agents may be associated with marked but primarily mild AEs.ConclusionWe found low-quality evidence suggesting that both MF and N2O are safe and may have a role in the management of pain in the prehospital setting. There is low-quality evidence to support MF as a short-acting single analgesic or as a bridge to IV access and the administration of other analgesics. There may be occupational health issues regarding the prehospital use of N2O.
Abstract licence: CC BY-NC
Sairally BZF, De Silva PM, Smith P, et al.
2025
- Methoxyflurane
- Anesthetics, Inhalation
- Ambulatory Care
Mériaux Océane, Falguière Arthur, Lesclous Philippe, et al.
Journal of Oral Medicine and Oral Surgery, 2024
2025
S. Hartshorn, P. Middleton
Trauma, 2018
A. Fabbri, A. Borobia, A. Ricard-Hibon, et al.
Journal of Pain Research, 2021
Hong Liu, Xi Fu, Yi-Feng Ren, et al.
Pain and Therapy, 2021
Michael M. Eager, G. Nolan, K. Tonks, et al.
Systematic Reviews, 2021
- Anesthetics, Inhalation
- Analgesia
- Pain
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
1 found
Half-life
Not available
Mechanism
Methoxyflurane induces a reduction in junctional conductance by decreasing gap j…
Food interactions
1 warning
Human targets
7 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Metabolism
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
In the US, methoxyflurane is one of the products that have been withdrawn or removed from the market for reasons of safety or effectiveness.[L43942]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1475 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
Proteins and enzymes this drug interacts with in the body
PMID:23909897 PMID:25489750 PMID:29950725 PMID:30602789
GABA-gated chloride channels, also named GABA(A) receptors (GABAAR), consist of five subunits arranged around a central pore and contain GABA active binding site(s) located at the alpha and beta subunit interface(s) .
PMID:29950725 PMID:30602789
When activated by GABA, GABAARs selectively allow the flow of chloride anions across the cell membrane down their electrochemical gradient .
PMID:23909897 PMID:29950725 PMID:30602789
Alpha-1/GABRA1-containing GABAARs are largely synaptic (By similarity). Chloride influx into the postsynaptic neuron following GABAAR opening decreases the neuron ability to generate a new action potential, thereby reducing nerve transmission (By similarity). GABAARs containing alpha-1 and beta-2 or -3 subunits exhibit synaptogenic activity; the gamma-2 subunit being necessary but not sufficient to induce rapid synaptic contacts formation .
PMID:23909897 PMID:25489750
GABAARs function also as histamine receptor where histamine binds at the interface of two neighboring beta subunits and potentiates GABA response (By similarity).
GABAARs containing alpha, beta and epsilon subunits also permit spontaneous chloride channel activity while preserving the structural information required for GABA-gated openings (By similarity). Alpha-1-mediated plasticity in the orbitofrontal cortex regulates context-dependent action selection (By similarity). Together with rho subunits, may also control neuronal and glial GABAergic transmission in the cerebellum (By similarity)
PMID:1311100 PMID:20805473 PMID:21172611 PMID:28628100 PMID:35675825
L-glutamate acts as an excitatory neurotransmitter at many synapses in the central nervous system. Binding of the excitatory neurotransmitter L-glutamate induces a conformation change, leading to the opening of the cation channel, and thereby converts the chemical signal to an electrical impulse upon entry of monovalent and divalent cations such as sodium and calcium. The receptor then desensitizes rapidly and enters in a transient inactive state, characterized by the presence of bound agonist (By similarity).
In the presence of CACNG2 or CACNG4 or CACNG7 or CACNG8, shows resensitization which is characterized by a delayed accumulation of current flux upon continued application of L-glutamate .
PMID:21172611
Resensitization is blocked by CNIH2 through interaction with CACNG8 in the CACNG8-containing AMPA receptors complex .
PMID:21172611
Calcium (Ca(2+)) permeability depends on subunits composition and, heteromeric channels containing edited GRIA2 subunit are calcium-impermeable. Also permeable to other divalents cations such as strontium(2+) and magnesium(2+) and monovalent cations such as potassium(1+) and lithium(1+) (By similarity)
PMID:14551753 PMID:23994010 PMID:25730860 PMID:37821459
Plays an important role in the down-regulation of neuronal excitability .
PMID:8298642 PMID:9009272
Contributes to the generation of inhibitory postsynaptic currents .
PMID:25445488
Channel activity is potentiated by ethanol .
PMID:25973519
Potentiation of channel activity by intoxicating levels of ethanol contribute to the sedative effects of ethanol (By similarity)
PMID:19903818 PMID:8845167
Contributes to the regulation of the membrane potential and nerve signaling, and prevents neuronal hyperexcitability .
PMID:17156368
Forms tetrameric potassium-selective channels through which potassium ions pass in accordance with their electrochemical gradient. The channel alternates between opened and closed conformations in response to the voltage difference across the membrane .
PMID:19912772
Can form functional homotetrameric channels and heterotetrameric channels that contain variable proportions of KCNA1, KCNA2, KCNA4, KCNA5, KCNA6, KCNA7, and possibly other family members as well; channel properties depend on the type of alpha subunits that are part of the channel .
PMID:12077175 PMID:17156368
Channel properties are modulated by cytoplasmic beta subunits that regulate the subcellular location of the alpha subunits and promote rapid inactivation of delayed rectifier potassium channels .
PMID:12077175 PMID:17156368
In vivo, membranes probably contain a mixture of heteromeric potassium channel complexes, making it difficult to assign currents observed in intact tissues to any particular potassium channel family member. Homotetrameric KCNA1 forms a delayed-rectifier potassium channel that opens in response to membrane depolarization, followed by slow spontaneous channel closure .
PMID:19307729 PMID:19903818 PMID:19912772 PMID:19968958
In contrast, a heterotetrameric channel formed by KCNA1 and KCNA4 shows rapid inactivation .
PMID:17156368
Regulates neuronal excitability in hippocampus, especially in mossy fibers and medial perforant path axons, preventing neuronal hyperexcitability.
Response to toxins that are selective for KCNA1, respectively for KCNA2, suggests that heteromeric potassium channels composed of both KCNA1 and KCNA2 play a role in pacemaking and regulate the output of deep cerebellar nuclear neurons (By similarity). May function as down-stream effector for G protein-coupled receptors and inhibit GABAergic inputs to basolateral amygdala neurons (By similarity). May contribute to the regulation of neurotransmitter release, such as gamma-aminobutyric acid (GABA) release (By similarity).
Plays a role in regulating the generation of action potentials and preventing hyperexcitability in myelinated axons of the vagus nerve, and thereby contributes to the regulation of heart contraction (By similarity). Required for normal neuromuscular responses .
PMID:11026449 PMID:17136396
Regulates the frequency of neuronal action potential firing in response to mechanical stimuli, and plays a role in the perception of pain caused by mechanical stimuli, but does not play a role in the perception of pain due to heat stimuli (By similarity). Required for normal responses to auditory stimuli and precise location of sound sources, but not for sound perception (By similarity).
The use of toxins that block specific channels suggest that it contributes to the regulation of the axonal release of the neurotransmitter dopamine (By similarity). Required for normal postnatal brain development and normal proliferation of neuronal precursor cells in the brain (By similarity). Plays a role in the reabsorption of Mg(2+) in the distal convoluted tubules in the kidney and in magnesium ion homeostasis, probably via its effect on the membrane potential PMID:19307729 PMID:23903368
PMID:10449790 PMID:16412217
GABA-gated chloride channels, also named GABA(A) receptors (GABAAR), consist of five subunits arranged around a central pore and contain GABA active binding site(s) located at the alpha and beta subunit interfaces (By similarity). When activated by GABA, GABAARs selectively allow the flow of chloride anions across the cell membrane down their electrochemical gradient PMID:10449790 PMID:16412217
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC N02BG09
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Methoxyflurane
Additional database identifiers
Drugs Product Database (DPD)
10032
ChemSpider
3973
ZINC
ZINC000000896988
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4075
GenAtlas
GABRA1
GeneCards
GABRA1
GenBank Gene Database
X13584
GenBank Protein Database
31631
Guide to Pharmacology
404
UniProt Accession
GBRA1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4571
GenAtlas
GRIA1
GeneCards
GRIA1
GenBank Gene Database
M64752
GenBank Protein Database
183281
Guide to Pharmacology
444
UniProt Accession
GRIA1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4326
GenAtlas
GLRA1
GeneCards
GLRA1
GenBank Gene Database
X52009
GenBank Protein Database
31851
Guide to Pharmacology
423
UniProt Accession
GLRA1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6218
GenAtlas
KCNA1
GeneCards
KCNA1
GenBank Gene Database
L02750
GenBank Protein Database
186663
Guide to Pharmacology
538
UniProt Accession
KCNA1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4075
GenAtlas
GABRA1
GeneCards
GABRA1
GenBank Gene Database
X13584
GenBank Protein Database
31631
Guide to Pharmacology
404
UniProt Accession
GBRA1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4076
GenAtlas
GABRA2
GeneCards
GABRA2
GenBank Gene Database
S62907
GenBank Protein Database
386422
Guide to Pharmacology
405
UniProt Accession
GBRA2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4077
GenAtlas
GABRA3
GeneCards
GABRA3
GenBank Gene Database
S62908
GenBank Protein Database
386424
Guide to Pharmacology
406
UniProt Accession
GBRA3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4078
GenAtlas
GABRA4
GeneCards
GABRA4
GenBank Gene Database
U30461
GenBank Protein Database
905393
Guide to Pharmacology
407
UniProt Accession
GBRA4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4079
GenAtlas
GABRA5
GeneCards
GABRA5
GenBank Gene Database
L08485
GenBank Protein Database
182916
Guide to Pharmacology
408
UniProt Accession
GBRA5_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4080
GenAtlas
GABRA6
GeneCards
GABRA6
GenBank Gene Database
S81944
GenBank Protein Database
1470364
Guide to Pharmacology
409
UniProt Accession
GBRA6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4081
GenAtlas
GABRB1
GeneCards
GABRB1
GenBank Gene Database
X14767
GenBank Protein Database
31635
UniProt Accession
GBRB1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4082
GenAtlas
GABRB2
GeneCards
GABRB2
GenBank Gene Database
S67368
GenBank Protein Database
455946
UniProt Accession
GBRB2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4083
GenAtlas
GABRB3
GeneCards
GABRB3
GenBank Gene Database
M82919
GenBank Protein Database
182925
Guide to Pharmacology
412
UniProt Accession
GBRB3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4084
GeneCards
GABRD
GenBank Gene Database
AF016917
GenBank Protein Database
2388693
UniProt Accession
GBRD_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4085
GeneCards
GABRE
GenBank Gene Database
U66661
GenBank Protein Database
1857126
UniProt Accession
GBRE_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4086
GeneCards
GABRG1
GenBank Gene Database
AK122845
GenBank Protein Database
193783776
UniProt Accession
GBRG1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4087
GeneCards
GABRG2
GenBank Gene Database
X15376
GenBank Protein Database
31637
UniProt Accession
GBRG2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4088
GeneCards
GABRG3
GenBank Gene Database
S82769
GenBank Protein Database
1754749
UniProt Accession
GBRG3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4089
GeneCards
GABRP
GenBank Gene Database
U95367
GenBank Protein Database
2197001
UniProt Accession
GBRP_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:14454
GeneCards
GABRQ
GenBank Gene Database
AF189259
GenBank Protein Database
7861736
UniProt Accession
GBRT_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:13211
GenAtlas
ATP2C1
GeneCards
ATP2C1
GenBank Gene Database
AF181120
GenBank Protein Database
6715131
UniProt Accession
AT2C1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:7455
GenAtlas
MT-ND1
GeneCards
MT-ND1
GenBank Gene Database
V00662
GenBank Protein Database
13004
UniProt Accession
NU1M_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2596
GenAtlas
CYP1A2
GeneCards
CYP1A2
GenBank Gene Database
Z00036
Guide to Pharmacology
1319
UniProt Accession
CP1A2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2610
GenAtlas
CYP2A6
GeneCards
CYP2A6
GenBank Gene Database
X13897
Guide to Pharmacology
1321
UniProt Accession
CP2A6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2615
GeneCards
CYP2B6
GenBank Gene Database
M29874
GenBank Protein Database
181296
Guide to Pharmacology
1324
UniProt Accession
CP2B6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2623
GenAtlas
CYP2C9
GeneCards
CYP2C9
GenBank Gene Database
AY341248
Guide to Pharmacology
1326
UniProt Accession
CP2C9_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2625
GenAtlas
CYP2D6
GeneCards
CYP2D6
GenBank Gene Database
M20403
GenBank Protein Database
181350
Guide to Pharmacology
1329
UniProt Accession
CP2D6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2631
GeneCards
CYP2E1
GenBank Gene Database
J02625
GenBank Protein Database
181360
Guide to Pharmacology
1330
UniProt Accession
CP2E1_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
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Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q411594), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication. WHO INN from the World Health Organization.