1.0 2009-07-21 20:28:42 UTC 2026-05-14 16:58:58 UTC T3D3029 Sevoflurane SmallMolecule Sevoflurane (C4H3F7O) is an exogenous organic compound with an average molecular weight of 200.05 g/mol. It exists as a liquid at room temperature. Sevoflurane belongs to the ethers, a subclass of organooxygen compounds within the organic compounds. Its roles and uses include application as an inhalation anaesthetic, a platelet aggregation inhibitor, and a central nervous system depressant. It is found in 14 recorded sources, including anesthetics in healthcare, pharmaceuticals and veterinary products; food preservation in food, food processing and cookware; non-electric simulated smoking devices, soap detergents, and tobacco smoke filters in household cleaning and consumer products; and electrical and electronic equipment such as antennas, colour television systems, conductors or conductive bodies characterised by the conductive materials, electric switches, and electrically stimulated smoking devices. Recorded exposure routes include nasal and respiratory pathways, with inhalation supported by literature (PMC11894927, PMC4310588, PMC6299439). Sevoflurane interacts with 30 recorded protein targets, including Calcium-transporting ATPase type 2C member 1 (ATP2C1), NADH-ubiquinone oxidoreductase chain 1 (MT-ND1), Glycine receptor subunit alpha-1 (GLRA1), and Glutamate receptor 1 (GRIA1). It acts as an activator, agonist, or inhibitor of Gamma-aminobutyric acid receptor subunits pi (GABRP), delta (GABRD), beta-1 (GABRB1), gamma-2 (GABRG2), and 19 other proteins. Sevoflurane induces a reduction in junctional conductance by decreasing gap junction channel opening times and increasing gap junction channel closing times. It activates calcium dependent ATPase in the sarcoplasmic reticulum by increasing the fluidity of the lipid membrane. Additionally, it appears to bind the D subunit of ATP synthase and NADH dehydogenase, and binds to the GABA receptor, the large conductance Ca2+ activated potassium channel, the glutamate receptor, and the glycine receptor. Drug Synthetic Toxin Organic Compound Organofluoride Ether Drug Anesthetic, Inhalation Metabolite Platelet Aggregation Inhibitor Synthetic Compound Human Neurotoxin 1,1,1,3,3,3-Hexafluoro-2-(fluoromethoxy)propane Sevofluran Sevoflurano Sevofluranum Sevorane Sojourn Ultane C4H3F7O 200.0548 200.007212153 1,1,1,3,3,3-hexafluoro-2-(fluoromethoxy)propane sevoflurane 28523-86-6 FCOC(C(F)(F)F)C(F)(F)F InChI=1S/C4H3F7O/c5-1-12-2(3(6,7)8)4(9,10)11/h2H,1H2 DFEYYRMXOJXZRJ-UHFFFAOYSA-N Organic compounds Organic oxygen compounds Organooxygen compounds Ethers Dialkyl ethers Alkyl fluorides Hydrocarbon derivatives Organofluorides Aliphatic acyclic compound Alkyl fluoride Alkyl halide Dialkyl ether Hydrocarbon derivative Organofluoride Organohalogen compound Aliphatic acyclic compounds ether organofluorine compound Detected and Not Quantified Exogenous Cytoplasm Extracellular Membrane Sevoflurane GABA(A) Anesthetic Action Pathway SMP0126170 Sevoflurane Drug Metabolism Action Pathway SMP0143654 Liquid melting_point < 25°C boiling_point 58.5°C solubility Very slightly soluble logp 2.4 logp 2.44 ALOGPS logs -2.13 ALOGPS solubility 1.48e+00 g/l ALOGPS logp 2.27 ChemAxon pka_strongest_acidic 15.07 ChemAxon pka_strongest_basic -4.5 ChemAxon iupac 1,1,1,3,3,3-hexafluoro-2-(fluoromethoxy)propane ChemAxon average_mass 200.0548 ChemAxon mono_mass 200.007212153 ChemAxon smiles FCOC(C(F)(F)F)C(F)(F)F ChemAxon formula C4H3F7O ChemAxon inchi InChI=1S/C4H3F7O/c5-1-12-2(3(6,7)8)4(9,10)11/h2H,1H2 ChemAxon inchikey DFEYYRMXOJXZRJ-UHFFFAOYSA-N ChemAxon polar_surface_area 9.23 ChemAxon refractivity 23.3 ChemAxon polarizability 9.83 ChemAxon rotatable_bond_count 4 ChemAxon acceptor_count 1 ChemAxon donor_count 0 ChemAxon physiological_charge 0 ChemAxon formal_charge 0 ChemAxon Rapidly absorbed into circulation via the lungs, however solubility in the blood is low. Sevoflurane induces a reduction in junctional conductance by decreasing gap junction channel opening times and increasing gap junction channel closing times. Sevoflurane also activates calcium dependent ATPase in the sarcoplasmic reticulum by increasing the fluidity of the lipid membrane. It also appears to bind the D subunit of ATP synthase and NADH dehydogenase and also binds to the GABA receptor, the large conductance Ca²⁺ activated potassium channel, the glutamate receptor, and the glycine receptor. Relatively little biotransformation, only 5% is metabolized by cytochrome P450 CYP2E1 to hexafluoroisopropanol (HFIP) with release of inorganic fluoride and CO2. No other metabolic pathways have been identified for sevoflurane. Route of Elimination: The low solubility of sevoflurane facilitates rapid elimination via the lungs. In vivo metabolism studies suggest that approximately 5% of the sevoflurane dose may be metabolized. Up to 3.5% of the sevoflurane dose appears in the urine as inorganic fluoride. Half Life: 15-23 hours LD50: 10.8 g/kg (Rat) (A308) LC50: 49881 ppm/hr (Inhalation, Rat) (A308) No indication of carcinogenicity to humans (not listed by IARC). Used for induction and maintenance of general anesthesia in adult and pediatric patients for inpatient and outpatient surgery. #<HealthEffect::ActiveRecord_Associations_CollectionProxy:0x00007f7226c56f58> In the event of overdosage, or what may appear to be overdosage, the following action should be taken: discontinue administration of sevoflurane, maintain a patent airway, initiate assisted or controlled ventilation with oxygen, and maintain adequate cardiovascular function. (L1712) DB01236 HMDB15366 5206 CHEMBL1200694 5017 C07520 9130 Sevoflurane Sevoflurane 18048412 Drugs.com: http://www.drugs.com/cons/Sevoflurane.html RxList: The Internet Drug Index (2009).: http://www.rxlist.com/ BE0000484 Sevoflurane induces a reduction in junctional conductance by decreasing gap junction channel opening times and increasing gap junction channel closing times. Sevoflurane also activates calcium dependent ATPase in the sarcoplasmic reticulum by increasing the fluidity of the lipid membrane. It also appears to bind the D subunit of ATP synthase and NADH dehydogenase and also binds to the GABA receptor, the large conductance Ca²⁺ activated potassium channel, the glutamate receptor, and the glycine receptor. BE0000218 Sevoflurane induces a reduction in junctional conductance by decreasing gap junction channel opening times and increasing gap junction channel closing times. Sevoflurane also activates calcium dependent ATPase in the sarcoplasmic reticulum by increasing the fluidity of the lipid membrane. It also appears to bind the D subunit of ATP synthase and NADH dehydogenase and also binds to the GABA receptor, the large conductance Ca²⁺ activated potassium channel, the glutamate receptor, and the glycine receptor. BE0000795 Sevoflurane induces a reduction in junctional conductance by decreasing gap junction channel opening times and increasing gap junction channel closing times. Sevoflurane also activates calcium dependent ATPase in the sarcoplasmic reticulum by increasing the fluidity of the lipid membrane. It also appears to bind the D subunit of ATP synthase and NADH dehydogenase and also binds to the GABA receptor, the large conductance Ca²⁺ activated potassium channel, the glutamate receptor, and the glycine receptor. BE0000640 Sevoflurane induces a reduction in junctional conductance by decreasing gap junction channel opening times and increasing gap junction channel closing times. Sevoflurane also activates calcium dependent ATPase in the sarcoplasmic reticulum by increasing the fluidity of the lipid membrane. It also appears to bind the D subunit of ATP synthase and NADH dehydogenase and also binds to the GABA receptor, the large conductance Ca²⁺ activated potassium channel, the glutamate receptor, and the glycine receptor. BE0000433 Sevoflurane induces a reduction in junctional conductance by decreasing gap junction channel opening times and increasing gap junction channel closing times. Sevoflurane also activates calcium dependent ATPase in the sarcoplasmic reticulum by increasing the fluidity of the lipid membrane. It also appears to bind the D subunit of ATP synthase and NADH dehydogenase and also binds to the GABA receptor, the large conductance Ca²⁺ activated potassium channel, the glutamate receptor, and the glycine receptor. BE0000503 Sevoflurane induces a reduction in junctional conductance by decreasing gap junction channel opening times and increasing gap junction channel closing times. Sevoflurane also activates calcium dependent ATPase in the sarcoplasmic reticulum by increasing the fluidity of the lipid membrane. It also appears to bind the D subunit of ATP synthase and NADH dehydogenase and also binds to the GABA receptor, the large conductance Ca²⁺ activated potassium channel, the glutamate receptor, and the glycine receptor. BE0000781 Sevoflurane induces a reduction in junctional conductance by decreasing gap junction channel opening times and increasing gap junction channel closing times. Sevoflurane also activates calcium dependent ATPase in the sarcoplasmic reticulum by increasing the fluidity of the lipid membrane. It also appears to bind the D subunit of ATP synthase and NADH dehydogenase and also binds to the GABA receptor, the large conductance Ca²⁺ activated potassium channel, the glutamate receptor, and the glycine receptor. BE0004797 BE0003596 BE0003599 BE0002344 BE0003592 BE0002345 BE0000471 BE0000523 BE0000381 BE0002346 BE0000478 BE0003595 BE0000764 BE0003593 BE0003594 BE0003597 BE0009966 BE0003888 BE0010001 BE0003477 BE0009968 BE0009971 BE0009969 BE0009970