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1. Alyrane
2. Enfran
3. Enlirane
4. Ethrane
5. Etran
1. 13838-16-9
2. Methylflurether
3. 2-chloro-1-(difluoromethoxy)-1,1,2-trifluoroethane
4. Efrane
5. Ethrane
6. Alyrane
7. 2-chloro-1,1,2-trifluoroethyl Difluoromethyl Ether
8. Compound 347
9. Anesthetic 347
10. Anesthetic Compound No. 347
11. Ohio 347
12. Enflurano
13. Enfluranum [inn-latin]
14. Enflurano [inn-spanish]
15. Nsc-115944
16. Ethane, 2-chloro-1-(difluoromethoxy)-1,1,2-trifluoro-
17. C 347
18. Ether, 2-chloro-1,1,2-trifluoroethyl Difluoromethyl
19. Chebi:4792
20. 91i69l5ay5
21. R-e-235ca2
22. Ncgc00167422-01
23. Enfluranum
24. Dsstox_cid_562
25. Dsstox_rid_75661
26. Dsstox_gsid_20562
27. Ethrane (tn)
28. Cas-13838-16-9
29. Einecs 237-553-4
30. Brn 1903921
31. Unii-91i69l5ay5
32. Hsdb 7909
33. Enflurane [anaesthetics, Volatile]
34. Enflurane [usan:usp:inn:ban:jan]
35. (+-)-2-chloro-1,1,2-trifluoroethyl Difluoromethyl Ether
36. Wln: Gyfxffoyff
37. Enflurane [inn]
38. Enflurane [jan]
39. Enflurane [mi]
40. Enflurane [usan]
41. Enflurane [vandf]
42. Enflurane [mart.]
43. Enflurane [usp-rs]
44. Enflurane [who-dd]
45. Chembl1257
46. Schembl61712
47. Enflurane (jp17/usp/inn)
48. Enflurane [green Book]
49. Gtpl7175
50. Enflurane [orange Book]
51. Dtxsid1020562
52. Enflurane [usp Impurity]
53. Enflurane [usp Monograph]
54. Act02934
55. Amy14276
56. Ethane, 2-chloro-1-(difluoromethoxy)-1,1,2-trifluoro-, (+-)-
57. Tox21_112426
58. Tox21_200166
59. Mfcd00069095
60. Nsc115944
61. Akos015853043
62. Db00228
63. Ether,1,2-trifluoroethyl Difluoromethyl
64. 4-chloro-1h,4h-perfluoro(2-oxabutane)
65. Ncgc00167422-02
66. Ncgc00257720-01
67. As-69470
68. Db-042426
69. Ft-0625662
70. C07516
71. D00543
72. D83877
73. 2-chloro-1,1,2-trifluoroethyldifluoromethylether
74. 2-chloro-1,2-trifluoroethyl Difluoromethyl Ether
75. 2-chloro-1-(difluoromethoxy)-1,2-trifluoroethane
76. Q416740
77. Sr-01000944966
78. 2-chloro-1,1,2-difluoroethane, 1-difluoromethoxy-
79. Sr-01000944966-1
80. 2- Chloro-1,1,2-trifluoroethyl Difluoromethyl Ether
81. 2-chloro-1-(difluoromethoxy)-1,1,2-trifluoro-ethane
82. 2-chloro-1,1,2-trifluoroethyl Difluoromethyl Ether, Aldrichcpr
83. (+/-)-2-chloro-1,1,2-trifluoroethyl Difluoromethyl Ether
84. Ethane, 2-chloro-1-(difluoromethoxy)-1,1,2-trifluoro-, (+/-)-
| Molecular Weight | 184.49 g/mol |
|---|---|
| Molecular Formula | C3H2ClF5O |
| XLogP3 | 2.1 |
| Hydrogen Bond Donor Count | 0 |
| Hydrogen Bond Acceptor Count | 6 |
| Rotatable Bond Count | 3 |
| Exact Mass | 183.9714332 g/mol |
| Monoisotopic Mass | 183.9714332 g/mol |
| Topological Polar Surface Area | 9.2 Ų |
| Heavy Atom Count | 10 |
| Formal Charge | 0 |
| Complexity | 107 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 0 |
| Undefined Atom Stereocenter Count | 1 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
| 1 of 4 | |
|---|---|
| Drug Name | Enflurane |
| Drug Label | Enflurane, USP, a nonflammable liquid administered by vaporizing, is a general inhalation anesthetic drug. It is 2-chloro-1,1,2-trifluoroethyl difluoromethyl ether, (CHF2OCF2CHFCl). The boiling point is 56.5C at 760 mm Hg, and the vapor pressure (i... |
| Active Ingredient | Enflurane |
| Dosage Form | Liquid |
| Route | Inhalation |
| Strength | 99.9% |
| Market Status | Prescription |
| Company | Piramal Critical |
| 2 of 4 | |
|---|---|
| Drug Name | Ethrane |
| Active Ingredient | Enflurane |
| Dosage Form | Liquid |
| Route | Inhalation |
| Strength | 99.9% |
| Market Status | Prescription |
| Company | Baxter Hlthcare |
| 3 of 4 | |
|---|---|
| Drug Name | Enflurane |
| Drug Label | Enflurane, USP, a nonflammable liquid administered by vaporizing, is a general inhalation anesthetic drug. It is 2-chloro-1,1,2-trifluoroethyl difluoromethyl ether, (CHF2OCF2CHFCl). The boiling point is 56.5C at 760 mm Hg, and the vapor pressure (i... |
| Active Ingredient | Enflurane |
| Dosage Form | Liquid |
| Route | Inhalation |
| Strength | 99.9% |
| Market Status | Prescription |
| Company | Piramal Critical |
| 4 of 4 | |
|---|---|
| Drug Name | Ethrane |
| Active Ingredient | Enflurane |
| Dosage Form | Liquid |
| Route | Inhalation |
| Strength | 99.9% |
| Market Status | Prescription |
| Company | Baxter Hlthcare |
Anesthetics, Inhalation
National Library of Medicine; Medical Subject Headings (MeSH) (2011). Available from, as of March 10, 2011: https://www.nlm.nih.gov/mesh/2011/mesh_browser/MBrowser.html
Enflurane may be used for induction and maintenance of general anesthesia. Enflurane may be used to provide analgesia for vaginal delivery. Low concentrations of enflurane (see DOSAGE AND ADMINISTRATION) may also be used to supplement other general anesthetic agents during delivery by Cesarean section. Higher concentrations of enflurane may produce uterine relaxation and an increase in uterine bleeding. /Included in US product label/
US Natl Inst Health; DailyMed. Current Medication Information for ENFLURANE inhalant (April 2010). Available from, as of March 12, 2011: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?id=18189&CFID=55487510&CFTOKEN=245e1f8f4d81dce0-5FF4B3EE-CC3A-992F-5E755E9D27611217&jsessionid=ca30c8d8773f5f27c655
A patient developed fever and acute hepatitis shortly after enflurane anesthesia. Other causes of postoperative hepatitis were excluded. Cross-sensitization with halothane may have occurred, and the enflurane hepatitis may have been aggravated by halothane hepatitis.
PMID:7426222 Danilewitz MD et al; Brit J Anesthesia 52 (11): 1151-3 (1980)
A case of mild post operative jaundice and transient renal insufficiency associated with enflurane anesthesia ... was eventually treated vigorously and successfully. ... Although other types of viral hepatitis cannot be completely ruled out, the anesthesiologist should be aware of the potential hazard of hepatic and renal toxicity attributed to enflurane...
PMID:7425324 Bernad PG et al; Anesthesie, Analgesie, Reanimation 37 (7-8): 427-8 (1980)
A case of succinylcholine and enflurane induced rhabdomyolysis and myoglobinuric acute renal failure in a mentally retarded patient is presented. The report illustrates some principles of management and the correlation of laboratory findings with the syndrome...
PMID:3476700 Lee SC et al; J Oral Maxillofac Surg 45 (9): 789-92 (1987)
Enflurane, as well as other general anesthetics, may cause a slight decrease in intellectual function for 2 or 3 days following anesthesia. As with other anesthetics, small changes in moods and symptoms may persist for several days following administration.
US Natl Inst Health; DailyMed. Current Medication Information for ENFLURANE inhalant (April 2010). Available from, as of March 12, 2011: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?id=18189&CFID=55487510&CFTOKEN=245e1f8f4d81dce0-5FF4B3EE-CC3A-992F-5E755E9D27611217&jsessionid=ca30c8d8773f5f27c655
For more Drug Warnings (Complete) data for Enflurane (9 total), please visit the HSDB record page.
Enflurane may be used for both the induction and maintenance of general anesthesia. It can also be used to induce analgesia for vaginal delivery. Low concentrations of enflurane can also be used as an adjunct to general anesthetic drugs during delivery by Cesarean section.
Enflurane rapidly induces anesthesia via the stimulation of inhibitory neural channels and the inhibition of excitatory neural channels. Muscle relaxation, obtundation of pharyngeal and laryngeal reflexes, and lowering of blood pressure are some of the main pharmacodynamic effects of this drug. Enflurane also decreases cardiac muscle contractility. High concentrations of enflurane may lead to uterine relaxation and increase the risk of uterine bleeding during delivery. Rare but clinically significant elevations in ALT may indicate hepatoxicity from the use of enflurane. In some susceptible patients, enflurane may cause malignant hyperthermia.
Anesthetics, Inhalation
Gases or volatile liquids that vary in the rate at which they induce anesthesia; potency; the degree of circulation, respiratory, or neuromuscular depression they produce; and analgesic effects. Inhalation anesthetics have advantages over intravenous agents in that the depth of anesthesia can be changed rapidly by altering the inhaled concentration. Because of their rapid elimination, any postoperative respiratory depression is of relatively short duration. (From AMA Drug Evaluations Annual, 1994, p173) (See all compounds classified as Anesthetics, Inhalation.)
N - Nervous system
N01 - Anesthetics
N01A - Anesthetics, general
N01AB - Halogenated hydrocarbons
N01AB04 - Enflurane
Absorption
Enflurane is rapidly absorbed into the circulation through the lungs. The minimum alveolar concentration is oxygen is 1.68%.
Route of Elimination
Metabolism accounts for 5-9% of enflurane elimination, sometimes causing nephrotoxicity. Excretion through the skin is believed to be minimal.
Volume of Distribution
Enflurane distributes to the brain, blood, and subcutaneous fat.
Enflurane is metabolized by the CYP2E1 enzyme in the liver to produce inorganic fluoride ions, the major metabolite of enflurane metabolism. One reference indicates that enflurane is only 2-5% eliminated after oxidative metabolism in the liver, however more recent evidence suggests that about 9% is eliminated via hepatic oxidation.
The toxicity of the chiral fluorinated volatile anesthetics halothane, enflurane, and isoflurane is closely related to their metabolism by hepatic cytochrome P450. Although individual anesthetic enantiomers have been shown to exhibit a difference in anesthetic efficacy, metabolism of anesthetic enantiomers has not been reported. Human liver enflurane metabolism to difluoromethoxydifluoroacetic acid (DFMDFA) and inorganic fluoride is catalyzed in vivo and in vitro by cytochrome P450 2E1. The purpose of this investigation was to characterize enflurane racemate and enantiomer metabolism to test the hypothesis that fluorinated ether anesthetic metabolism by cytochrome P450 2E1 exhibits substrate stereoselectivity. Enflurane metabolism by microsomes from three human livers and by microsomes containing cDNA-expressed human P450 2E1 was measured at saturating enflurane concentrations. DFMDFA was quantitated with gas chromatography-mass spectrometry by detection of the ethanolamide derivative. In microsomes from all three livers, (R)-enflurane metabolism was significantly greater than that of (S)-enflurane, whereas rates of racemic enflurane metabolism were generally between those seen for the R- and S-enantiomers. The ratio of (R)-enflurane to (S)-enflurane metabolism in the three livers studied was 2.1:1, 1.9:1, and 1.4:1. (R)-, (S)-, and racemic enflurane were all metabolized by expressed P450 2E1. The ratio of (R)-enflurane to (S)-enflurane metabolism was 1.9:1. The metabolic enantiomeric selectivity of human liver P450 2E1 for (R)-enflurane suggests that enflurane metabolism by P450 2E1 occurs by direct substrate oxidation, rather than indirectly through the generation of a P450-dependent reactive oxygen species, and supports the hypothesis that the P450 2E1 active site is somewhat restrictive and capable of stereochemical discrimination.
PMID:8689955 Garton KJ et al; Drug Metab Dispos 23 (12): 1426-30 (1995)
Difluoromethoxydifluoroacetic acid (CHF2OCF2CO2H) has been identified as a metabolite of enflurane (CHF2OCF2CHCIF) in rat liver microsomes in vitro and in human urine by gas chromatography mass spectrometry. The formation of the metabolite in rat liver microsomes was dependent upon the presence of NADPH and O2, and was inhibited when SKF 525-A or CO/O2 (8:2, v/v) were present in the reaction mixture. When the C-H bonds of the CHCIF group of enflurane or of the CHCI group of isoflurane (CHF2OCHCICF3) were replaced with a C-CI bond, virtually no fluoride ion was produced from either derivative in rat liver microsomes. These results indicate that cytochrome P-450 catalyzes the oxidative dehalogenation of CHF2OCF2CHCIF at its CHCIF group to form CHF2OCF2CO2H and chloride and fluoride ions. In contrast, the CHF2 group does not appear to be appreciably susceptible to metabolic oxidative dehalogenation...
PMID:6111426 Burke TR et al; Drug Metab Dispos 9 (1): 19-24 (1981)
Enflurane is a fluorinated volatile anesthetic, mostly eliminated unchanged in exhaled air. About 10% of inhaled enflurane undergoes oxidative metabolism in liver via mixed function oxidase.
PMID:10445395 Kolarovic J et al; Exptl Toxicol Pathol 51 (4-5): 347-51 (1999)
Fluorinated ether anesthetic hepatotoxicity and nephrotoxicity are mediated by cytochrome P450-catalyzed oxidative metabolism. Metabolism of the volatile anesthetic enflurane to inorganic fluoride ion by human liver microsomes in vitro is catalyzed predominantly by the cytochrome P450 isoform CYP2E1.
PMID:8162670 Kharasch ED et al; Clin Pharmacol Therap 55 (4): 434-40 (1994)
Rats exposed to enflurane (100 ppm) ... in a closed all glass-system eliminated /enflurane/ from the atmosphere of the system with a half-life of 6.84 hr... . 24 hr-fasting had no influence on /the elimination half-life/. ... Pretreatment with diethyl maleate (1 mL/kg ip), dimethylsulfoxide (DMSO, 1 g/kg ip) or dithiocarb (100 mg/kg ip) prolonged the elimination half-life... . An accelerated metabolic elimination was only observed in DDT-pretreated rats exposed to enflurane; other inducers of the microsomal mixed-function oxidase system like phenobarbital or rifampicine had no significant influence on the in vivo metabolism ...
PMID:7224135 Siegers CP et al; Der Anaesthesist 30 (2): 83-7 (1981)
The mechanism of action of enflurane is not completely established. Studies on rats indicate that enflurane binds to GABAA and glycine receptors, causing depressant effects at the ventral neural horn. It has been reported that 30% of the central nervous system depressant effects on the spinal cord after enflurane is administered are caused by the (GABA-A) receptor while binding to glycine receptors is responsible for about 20 % of the depressant effects. The relevance of these findings to humans is unknown. Other studies have found that enflurane binds to the calcium channels in the cardiac sarcoplasmic reticulum causing cardio depressant effects. Other studies support that this drug potentiates glycine receptors, which results in central nervous system depressant effects.
Renal toxicity has occasionally been observed after enflurane anesthesia. Although originally attributed to its oxidative metabolism to inorganic fluoride, serum levels of inorganic fluoride appear to be small to explain these renal effects. Formation of potentially nephrotoxic halogenated alkenes during alkaline degradation in carbon dioxide absorbers and subsequent bioactivation via the glutathione conjugation pathway may be considered as an alternative mechanism for renal toxicity. ... Alkaline degradation products of enflurane can be conjugated to thiol compounds, forming S-conjugates that could theoretically contribute to adverse renal effects observed occasionally with enflurane anesthesia. The N-acetyl-L-cysteine S-conjugates identified may be biomarkers to assess exposure of humans to alkaline degradation products of enflurane.
PMID:11465554 Orhan H et al; Anesthesiology 95 (1): 165-75 (2001)
Clinical case reports of unexplained hepatic dysfunction following enflurane and isoflurane anesthesia led to the hypothesis that oxidative metabolism of these drugs by cytochromes P-450 produces immunoreactive, covalently bound acylated protein adducts similar to those implicated in the genesis of halothane-induced hepatic necrosis. Microsomal adducts were detected by enzyme-linked immunosorbent assay and immunoblotting techniques utilizing specific anti-trifluoroacetyl (TFA) IgG hapten antibodies in rat liver following enflurane, isoflurane, or halothane administration. Preincubation of the antibodies with microsomes from halothane-pretreated rats or with 500 uM TFA-lysine, markedly inhibited adduct recognition, while preincubation with 500 uM acetyllysine had no effect. The relative amounts of immunoreactive protein adducts formed were halothane much greater than enflurane much greater than isoflurane and correlates directly with the relative extents of metabolism of these agents. These results support the view that acyl metabolites of the volatile anesthetics may become covalently bound to hepatic proteins, thus serving as antigens, and thereby account for the apparent cross-sensitization and idiosyncratic hepatotoxicity reported for these drugs.
PMID:2894942 Christ DD et al; Drug Metab Dispos 16 (1): 135-40 (1988)
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