You are using an unsupported browser. Please upgrade your browser to a newer version to get the best experience on DrugBank.
Identification
NameButabarbital
Accession NumberDB00237  (APRD00752)
TypeSmall Molecule
GroupsApproved, Illicit
Description

Butabarbital (trade name Butisol) is a prescription barbiturate sleep aid. Butabarbital has a particularly fast onset of effects and short duration of action compared to other barbiturates, which makes it useful for certain applications such as treating severe insomnia and relieving anxiety before surgical procedures; however it is also relatively dangerous particularly when combined with alcohol, and so is now rarely used, although it is still prescribed in some Eastern European and South American countries. Its short duration of action gives butabarbital a high abuse potential, comparable to secobarbital. [Wikipedia]

Structure
Thumb
Synonyms
SynonymLanguageCode
5-Ethyl-5-(1-methylpropyl)-2,4,6(1H,3H,5H)-pyrimidinetrioneNot AvailableNot Available
5-Ethyl-5-(1-methylpropyl)barbituric acidNot AvailableNot Available
5-Sec-butyl-5-ethyl-2,4,6(1H,3H,5H)-pyrimidinetrioneNot AvailableNot Available
5-Sec-butyl-5-ethylbarbituric acidNot AvailableNot Available
5-Sec-butyl-5-ethylpyrimidine-2,4,6(1H,3H,5H)-trioneNot AvailableNot Available
ButabarbitalNot AvailableNot Available
ButisolNot AvailableNot Available
SecbutabarbitalNot AvailableNot Available
Prescription Products
NameDosageStrengthRouteLabellerMarketing StartMarketing End
Butisol Sodiumtablet30 mgoralMeda Pharmaceuticals Inc.1939-08-01Not AvailableUs 0a2ef1ad1c84951dc1392a8bbe1f3cb241c91ed59e44ad8268635315440d978c
Generic Prescription ProductsNot Available
Over the Counter ProductsNot Available
International Brands
NameCompany
ButalanNot Available
ButisolNot Available
Sarisol No. 2Not Available
Brand mixturesNot Available
Salts
Name/CASStructureProperties
Butabarbital Sodium
Thumb
  • InChI Key: QORQZMBCPRBCAB-UHFFFAOYNA-M
  • Monoisotopic Mass: 234.098037031
  • Average Mass: 234.2275
DBSALT000312
Categories
CAS number125-40-6
WeightAverage: 212.2456
Monoisotopic: 212.116092388
Chemical FormulaC10H16N2O3
InChI KeyZRIHAIZYIMGOAB-UHFFFAOYSA-N
InChI
InChI=1S/C10H16N2O3/c1-4-6(3)10(5-2)7(13)11-9(15)12-8(10)14/h6H,4-5H2,1-3H3,(H2,11,12,13,14,15)
IUPAC Name
5-(butan-2-yl)-5-ethyl-1,3-diazinane-2,4,6-trione
SMILES
CCC(C)C1(CC)C(=O)NC(=O)NC1=O
Taxonomy
DescriptionThis compound belongs to the class of organic compounds known as barbituric acid derivatives. These are compounds containing a perhydropyrimidine ring substituted at C-2, -4 and -6 by oxo groups.
KingdomOrganic compounds
Super ClassOrganoheterocyclic compounds
ClassDiazines
Sub ClassPyrimidines and pyrimidine derivatives
Direct ParentBarbituric acid derivatives
Alternative Parents
Substituents
  • Barbiturate
  • Ureide
  • 1,3-diazinane
  • Urea
  • Carboxamide group
  • Azacycle
  • Carboxylic acid derivative
  • Hydrocarbon derivative
  • Organooxygen compound
  • Organonitrogen compound
  • Carbonyl group
  • Aliphatic heteromonocyclic compound
Molecular FrameworkAliphatic heteromonocyclic compounds
External DescriptorsNot Available
Pharmacology
IndicationFor short-term treatment of insomnia and anxiety disorders
PharmacodynamicsButabarbital, a barbiturate, is used for the treatment of short term insomnia. It belongs to a group of medicines called central nervous system (CNS) depressants that induce drowsiness and relieve tension or nervousness. Little analgesia is conferred by barbiturates; their use in the presence of pain may result in excitation.
Mechanism of actionButabarbital binds at a distinct binding site associated with a Cl- ionopore at the GABAA receptor, increasing the duration of time for which the Cl- ionopore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged. All of these effects are associated with marked decreases in GABA-sensitive neuronal calcium conductance (gCa). The net result of barbiturate action is acute potentiation of inhibitory GABAergic tone. Barbiturates also act through potent (if less well characterized) and direct inhibition of excitatory AMPA-type glutamate receptors, resulting in a profound suppression of glutamatergic neurotransmission.
AbsorptionNot Available
Volume of distributionNot Available
Protein bindingNot Available
MetabolismNot Available
Route of eliminationBarbiturates are metabolized primarily by the hepatic microsomal enzyme system, and most metabolic products are excreted in the urine.
Half lifeNot Available
ClearanceNot Available
ToxicitySigns of overdose include confusion (severe), decrease in or loss of reflexes, drowsiness (severe), fever, irritability (continuing), low body temperature, poor judgment, shortness of breath or slow or troubled breathing, slow heartbeat, slurred speech, staggering, trouble in sleeping, unusual movements of the eyes, weakness (severe).
Affected organisms
  • Humans and other mammals
PathwaysNot Available
SNP Mediated EffectsNot Available
SNP Mediated Adverse Drug ReactionsNot Available
ADMET
Predicted ADMET features
PropertyValueProbability
Human Intestinal Absorption+0.9324
Blood Brain Barrier+0.9782
Caco-2 permeable-0.6013
P-glycoprotein substrateSubstrate0.5938
P-glycoprotein inhibitor INon-inhibitor0.617
P-glycoprotein inhibitor IINon-inhibitor0.961
Renal organic cation transporterNon-inhibitor0.9465
CYP450 2C9 substrateNon-substrate0.7719
CYP450 2D6 substrateNon-substrate0.9014
CYP450 3A4 substrateNon-substrate0.7098
CYP450 1A2 substrateNon-inhibitor0.8775
CYP450 2C9 substrateNon-inhibitor0.821
CYP450 2D6 substrateNon-inhibitor0.933
CYP450 2C19 substrateNon-inhibitor0.7828
CYP450 3A4 substrateNon-inhibitor0.9203
CYP450 inhibitory promiscuityLow CYP Inhibitory Promiscuity0.9458
Ames testNon AMES toxic0.6458
CarcinogenicityNon-carcinogens0.8533
BiodegradationNot ready biodegradable0.9759
Rat acute toxicity3.6803 LD50, mol/kg Not applicable
hERG inhibition (predictor I)Weak inhibitor0.99
hERG inhibition (predictor II)Non-inhibitor0.9233
Pharmacoeconomics
Manufacturers
  • Medpointe pharmaceuticals medpointe healthcare inc
  • Alpharma us pharmaceuticals division
  • Wockhardt eu operations (swiss) ag
  • Lannett co inc
  • Meda pharmaceuticals inc
  • Halsey drug co inc
  • Cm bundy co
  • Sandoz inc
  • Solvay pharmaceuticals
  • Teva pharmaceuticals usa inc
  • Watson laboratories inc
  • Whiteworth towne paulsen inc
  • Ivax pharmaceuticals inc sub teva pharmaceuticals usa
  • Marshall pharmacal corp
  • West ward pharmaceutical corp
Packagers
Dosage forms
FormRouteStrength
Tabletoral30 mg
Prices
Unit descriptionCostUnit
Butisol sodium 50 mg tablet2.46USD tablet
Butisol sodium 30 mg tablet1.89USD tablet
DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.
PatentsNot Available
Properties
StateSolid
Experimental Properties
PropertyValueSource
melting point166.5 °CPhysProp
water solubility1360 mg/LNot Available
logP1.65WONG,O & MCKEOWN,RH (1988)
Predicted Properties
PropertyValueSource
Water Solubility1.39 mg/mLALOGPS
logP1.7ALOGPS
logP1.45ChemAxon
logS-2.2ALOGPS
pKa (Strongest Acidic)8.48ChemAxon
Physiological Charge0ChemAxon
Hydrogen Acceptor Count3ChemAxon
Hydrogen Donor Count2ChemAxon
Polar Surface Area75.27 Å2ChemAxon
Rotatable Bond Count3ChemAxon
Refractivity53.4 m3·mol-1ChemAxon
Polarizability21.41 Å3ChemAxon
Number of Rings1ChemAxon
Bioavailability1ChemAxon
Rule of FiveYesChemAxon
Ghose FilterYesChemAxon
Veber's RuleYesChemAxon
MDDR-like RuleYesChemAxon
Spectra
Mass Spec (NIST)Not Available
SpectraMS
References
Synthesis ReferenceNot Available
General ReferenceNot Available
External Links
ATC CodesNot Available
AHFS CodesNot Available
PDB EntriesNot Available
FDA labelNot Available
MSDSNot Available
Interactions
Drug Interactions
Drug
AcebutololMay decrease the serum concentration of Beta-Blockers.
AcenocoumarolMay increase the metabolism of Vitamin K Antagonists.
AcetaminophenBarbiturates may increase the metabolism of Acetaminophen. This may 1) diminish the effect of acetaminophen; and 2) increase the risk of liver damage.
AcetazolamideMay enhance the hypotensive effect of Hypotensive Agents.
AldesleukinMay enhance the hypotensive effect of Hypotensive Agents.
AliskirenMay enhance the hypotensive effect of Hypotensive Agents.
AmilorideMay enhance the hypotensive effect of Hypotensive Agents.
AminophyllineMay decrease the serum concentration of Theophylline Derivatives.
AmitriptylineMay increase the metabolism of Tricyclic Antidepressants.
AmlodipineBarbiturates may increase the metabolism of Calcium Channel Blockers.
AmoxapineMay increase the metabolism of Tricyclic Antidepressants.
AmrinoneBarbiturates may increase the metabolism of Calcium Channel Blockers.
Amyl NitriteMay enhance the hypotensive effect of Hypotensive Agents.
ApraclonidineMay enhance the hypotensive effect of Hypotensive Agents.
AtenololMay enhance the hypotensive effect of Hypotensive Agents.
Azilsartan medoxomilMay enhance the orthostatic hypotensive effect of Thiazide Diuretics.
BenazeprilMay enhance the hypotensive effect of Hypotensive Agents.
BendroflumethiazideMay enhance the orthostatic hypotensive effect of Thiazide Diuretics.
BepridilBarbiturates may increase the metabolism of Calcium Channel Blockers.
BetaxololMay decrease the serum concentration of Beta-Blockers.
BisoprololMay decrease the serum concentration of Beta-Blockers.
BretyliumMay enhance the hypotensive effect of Hypotensive Agents.
BrimonidineMay enhance the hypotensive effect of Hypotensive Agents.
BumetanideMay enhance the hypotensive effect of Hypotensive Agents.
BuprenorphineCNS Depressants may enhance the CNS depressant effect of Buprenorphine.
ButalbitalMay increase the metabolism of Acetaminophen. This may 1) diminish the effect of acetaminophen; and 2) increase the risk of liver damage.
CanagliflozinMay enhance the hypotensive effect of Hypotensive Agents.
CandesartanMay enhance the hypotensive effect of Hypotensive Agents.
CaptoprilMay enhance the hypotensive effect of Hypotensive Agents.
CarteololMay decrease the serum concentration of Beta-Blockers.
CarvedilolMay decrease the serum concentration of Beta-Blockers.
ChloramphenicolBarbiturates may increase the metabolism of Chloramphenicol. Chloramphenicol may decrease the metabolism of Barbiturates.
ChlorothiazideMay enhance the orthostatic hypotensive effect of Thiazide Diuretics.
ChlorthalidoneMay enhance the orthostatic hypotensive effect of Thiazide Diuretics.
CilazaprilMay enhance the hypotensive effect of Hypotensive Agents.
ClevidipineMay enhance the hypotensive effect of Hypotensive Agents.
ClomipramineMay increase the metabolism of Tricyclic Antidepressants.
ClonidineMay enhance the hypotensive effect of Hypotensive Agents.
DapagliflozinMay enhance the hypotensive effect of Hypotensive Agents.
DesipramineMay increase the metabolism of Tricyclic Antidepressants.
DesogestrelMay diminish the therapeutic effect of Contraceptives (Estrogens). Contraceptive failure is possible.
DihydrocodeineMay increase the metabolism of Acetaminophen. This may 1) diminish the effect of acetaminophen; and 2) increase the risk of liver damage.
DiltiazemMay increase the metabolism of Calcium Channel Blockers.
DipyridamoleMay enhance the hypotensive effect of Hypotensive Agents.
DoxazosinMay enhance the hypotensive effect of Hypotensive Agents.
DoxycyclineBarbiturates may decrease the serum concentration of Doxycycline.
DoxylamineMay enhance the CNS depressant effect of CNS Depressants.
DronabinolMay enhance the CNS depressant effect of CNS Depressants.
DroperidolMay enhance the CNS depressant effect of CNS Depressants.
DrospirenoneMay diminish the therapeutic effect of Contraceptives (Progestins). Contraceptive failure is possible.
EmpagliflozinMay enhance the hypotensive effect of Hypotensive Agents.
EnalaprilMay enhance the hypotensive effect of Hypotensive Agents.
EplerenoneMay enhance the hypotensive effect of Hypotensive Agents.
EprosartanMay enhance the hypotensive effect of Hypotensive Agents.
EsmololMay decrease the serum concentration of Beta-Blockers.
Ethacrynic acidMay enhance the hypotensive effect of Hypotensive Agents.
Ethinyl EstradiolMay diminish the therapeutic effect of Contraceptives (Estrogens). Contraceptive failure is possible.
EthynodiolMay diminish the therapeutic effect of Contraceptives (Estrogens). Contraceptive failure is possible.
EtonogestrelMay diminish the therapeutic effect of Contraceptives (Progestins). Contraceptive failure is possible.
EtoposideBarbiturates may decrease the serum concentration of Etoposide.
FelbamateBarbiturates may decrease the serum concentration of Felbamate. Felbamate may increase the serum concentration of Barbiturates.
FelodipineBarbiturates may increase the metabolism of Calcium Channel Blockers.
FlunarizineBarbiturates may increase the metabolism of Calcium Channel Blockers.
FosinoprilMay enhance the hypotensive effect of Hypotensive Agents.
FurosemideMay enhance the hypotensive effect of Hypotensive Agents.
GabapentinBarbiturates may increase the metabolism of Calcium Channel Blockers.
GriseofulvinBarbiturates may decrease the serum concentration of Griseofulvin.
GuanfacineMay enhance the hypotensive effect of Hypotensive Agents.
HydralazineMay enhance the hypotensive effect of Hypotensive Agents.
HydrochlorothiazideMay enhance the orthostatic hypotensive effect of Thiazide Diuretics.
HydrocodoneCNS Depressants may enhance the CNS depressant effect of Hydrocodone.
HydroxyzineMay enhance the CNS depressant effect of Barbiturates.
ImipramineMay increase the metabolism of Tricyclic Antidepressants.
IndapamideMay enhance the orthostatic hypotensive effect of Thiazide Diuretics.
IrbesartanMay enhance the hypotensive effect of Hypotensive Agents.
IsomethepteneMay increase the metabolism of Acetaminophen. This may 1) diminish the effect of acetaminophen; and 2) increase the risk of liver damage.
Isosorbide DinitrateMay enhance the hypotensive effect of Hypotensive Agents.
Isosorbide MononitrateMay enhance the hypotensive effect of Hypotensive Agents.
IsoxsuprineMay enhance the hypotensive effect of Hypotensive Agents.
IsradipineBarbiturates may increase the metabolism of Calcium Channel Blockers.
LabetalolMay decrease the serum concentration of Beta-Blockers.
LamotrigineBarbiturates may increase the metabolism of Calcium Channel Blockers.
LercanidipineBarbiturates may increase the metabolism of Calcium Channel Blockers.
LevobunololMay enhance the hypotensive effect of Hypotensive Agents.
LevonorgestrelMay diminish the therapeutic effect of Contraceptives (Progestins). Contraceptive failure is possible.
LisinoprilMay enhance the hypotensive effect of Hypotensive Agents.
LosartanMay enhance the hypotensive effect of Hypotensive Agents.
Magnesium SulfateBarbiturates may increase the metabolism of Calcium Channel Blockers.
MannitolMay enhance the hypotensive effect of Hypotensive Agents.
Medroxyprogesterone AcetateMay diminish the therapeutic effect of Contraceptives (Progestins). Contraceptive failure is possible.
MestranolMay diminish the therapeutic effect of Contraceptives (Estrogens). Contraceptive failure is possible.
MethazolamideMay enhance the hypotensive effect of Hypotensive Agents.
MethotrimeprazineCNS Depressants may enhance the CNS depressant effect of Methotrimeprazine. Methotrimeprazine may enhance the CNS depressant effect of CNS Depressants.
MethyclothiazideMay enhance the orthostatic hypotensive effect of Thiazide Diuretics.
MethyldopaMay enhance the hypotensive effect of Hypotensive Agents.
MetipranololMay enhance the hypotensive effect of Hypotensive Agents.
MetolazoneMay enhance the orthostatic hypotensive effect of Thiazide Diuretics.
MetoprololMay decrease the serum concentration of Beta-Blockers.
MetyrosineCNS Depressants may enhance the sedative effect of Metyrosine.
MianserinMay enhance the CNS depressant effect of Barbiturates. Mianserin may diminish the therapeutic effect of Barbiturates. Barbiturates may decrease the serum concentration of Mianserin.
MirtazapineCNS Depressants may enhance the CNS depressant effect of Mirtazapine.
MoexiprilMay enhance the hypotensive effect of Hypotensive Agents.
NabiloneMay enhance the CNS depressant effect of CNS Depressants.
NadololMay enhance the hypotensive effect of Hypotensive Agents.
NebivololMay decrease the serum concentration of Beta-Blockers.
NesiritideMay enhance the hypotensive effect of Hypotensive Agents.
NicardipineBarbiturates may increase the metabolism of Calcium Channel Blockers.
NifedipineMay increase the metabolism of Calcium Channel Blockers.
NimodipineBarbiturates may increase the metabolism of Calcium Channel Blockers.
NisoldipineBarbiturates may increase the metabolism of Calcium Channel Blockers.
NitrendipineBarbiturates may increase the metabolism of Calcium Channel Blockers.
NitroglycerinMay enhance the hypotensive effect of Hypotensive Agents.
NitroprussideMay enhance the hypotensive effect of Hypotensive Agents.
NorelgestrominMay diminish the therapeutic effect of Contraceptives (Estrogens). Contraceptive failure is possible.
NorethindroneMay diminish the therapeutic effect of Contraceptives (Progestins). Contraceptive failure is possible.
NorgestimateMay diminish the therapeutic effect of Contraceptives (Progestins). Contraceptive failure is possible.
NortriptylineMay increase the metabolism of Tricyclic Antidepressants.
OlmesartanMay enhance the hypotensive effect of Hypotensive Agents.
OrphenadrineCNS Depressants may enhance the CNS depressant effect of Orphenadrine.
PapaverineMay enhance the hypotensive effect of Hypotensive Agents.
PenbutololMay decrease the serum concentration of Beta-Blockers.
PerampanelMay enhance the CNS depressant effect of CNS Depressants.
PerhexilineBarbiturates may increase the metabolism of Calcium Channel Blockers.
PerindoprilMay enhance the hypotensive effect of Hypotensive Agents.
PethidineMay enhance the CNS depressant effect of Meperidine. Barbiturates may increase serum concentrations of the active metabolite(s) of Meperidine.
PindololMay decrease the serum concentration of Beta-Blockers.
PramipexoleCNS Depressants may enhance the sedative effect of Pramipexole.
PrazosinMay enhance the hypotensive effect of Hypotensive Agents.
PrenylamineBarbiturates may increase the metabolism of Calcium Channel Blockers.
PrimidoneMay enhance the adverse/toxic effect of Barbiturates. Primidone is converted to phenobarbital, and thus becomes additive with existing barbiturate therapy.
PropafenoneBarbiturates may decrease the serum concentration of Propafenone.
PropranololMay decrease the serum concentration of Beta-Blockers.
ProtriptylineMay increase the metabolism of Tricyclic Antidepressants.
PyridoxinePyridoxine may increase the metabolism of Barbiturates. Apparent in high pyridoxine doses (eg, 200 mg/day)
QuetiapineMay enhance the hypotensive effect of Hypotensive Agents.
QuinaprilMay enhance the hypotensive effect of Hypotensive Agents.
RamiprilMay enhance the hypotensive effect of Hypotensive Agents.
ReserpineMay enhance the hypotensive effect of Hypotensive Agents.
RifampicinRifamycin Derivatives may increase the metabolism of Barbiturates.
RifapentineRifamycin Derivatives may increase the metabolism of Barbiturates.
RiociguatMay enhance the hypotensive effect of Hypotensive Agents.
RisedronateBarbiturates may increase the metabolism of Calcium Channel Blockers.
RopiniroleCNS Depressants may enhance the sedative effect of ROPINIRole.
RotigotineCNS Depressants may enhance the sedative effect of Rotigotine.
RufinamideMay enhance the adverse/toxic effect of CNS Depressants. Specifically, sleepiness and dizziness may be enhanced.
SotalolMay decrease the serum concentration of Beta-Blockers.
SpironolactoneMay enhance the hypotensive effect of Hypotensive Agents.
SuvorexantCNS Depressants may enhance the CNS depressant effect of Suvorexant.
TapentadolMay enhance the CNS depressant effect of CNS Depressants.
TelmisartanMay enhance the hypotensive effect of Hypotensive Agents.
TeniposideBarbiturates may decrease the serum concentration of Teniposide.
TerazosinMay enhance the hypotensive effect of Hypotensive Agents.
ThalidomideCNS Depressants may enhance the CNS depressant effect of Thalidomide.
TheophyllineMay decrease the serum concentration of Theophylline Derivatives.
TimololMay decrease the serum concentration of Beta-Blockers.
TizanidineMay enhance the hypotensive effect of Hypotensive Agents.
TorasemideMay enhance the hypotensive effect of Hypotensive Agents.
TrandolaprilMay enhance the hypotensive effect of Hypotensive Agents.
TriamtereneMay enhance the hypotensive effect of Hypotensive Agents.
TrimipramineMay increase the metabolism of Tricyclic Antidepressants.
UlipristalBarbiturates may decrease the serum concentration of Ulipristal.
Valproic AcidValproic Acid and Derivatives may decrease the metabolism of Barbiturates. Barbiturates may decrease the serum concentration of Valproic Acid and Derivatives.
ValsartanMay enhance the hypotensive effect of Hypotensive Agents.
VerapamilBarbiturates may increase the metabolism of Calcium Channel Blockers.
VoriconazoleBarbiturates may decrease the serum concentration of Voriconazole.
ZolpidemCNS Depressants may enhance the CNS depressant effect of Zolpidem.
Food InteractionsNot Available

Targets

1. GABA-A receptor (anion channel)

Kind: protein group

Organism: Human

Pharmacological action: yes

Actions: positive allosteric modulator

Components

Name UniProt ID Details
Gamma-aminobutyric acid receptor subunit alpha-1 P14867 Details
Gamma-aminobutyric acid receptor subunit alpha-2 P47869 Details
Gamma-aminobutyric acid receptor subunit alpha-3 P34903 Details
Gamma-aminobutyric acid receptor subunit alpha-4 P48169 Details
Gamma-aminobutyric acid receptor subunit alpha-5 P31644 Details
Gamma-aminobutyric acid receptor subunit alpha-6 Q16445 Details
Gamma-aminobutyric acid receptor subunit beta-1 P18505 Details
Gamma-aminobutyric acid receptor subunit beta-2 P47870 Details
Gamma-aminobutyric acid receptor subunit beta-3 P28472 Details
Gamma-aminobutyric acid receptor subunit delta O14764 Details
Gamma-aminobutyric acid receptor subunit epsilon P78334 Details
Gamma-aminobutyric acid receptor subunit gamma-1 Q8N1C3 Details
Gamma-aminobutyric acid receptor subunit gamma-2 P18507 Details
Gamma-aminobutyric acid receptor subunit gamma-3 Q99928 Details
Gamma-aminobutyric acid receptor subunit pi O00591 Details
Gamma-aminobutyric acid receptor subunit theta Q9UN88 Details

References:

  1. Mehta AK, Ticku MK: An update on GABAA receptors. Brain Res Brain Res Rev. 1999 Apr;29(2-3):196-217. Pubmed
  2. Yamakura T, Bertaccini E, Trudell JR, Harris RA: Anesthetics and ion channels: molecular models and sites of action. Annu Rev Pharmacol Toxicol. 2001;41:23-51. Pubmed

2. Neuronal acetylcholine receptor subunit alpha-4

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: antagonist

Components

Name UniProt ID Details
Neuronal acetylcholine receptor subunit alpha-4 P43681 Details

References:

  1. Yamakura T, Bertaccini E, Trudell JR, Harris RA: Anesthetics and ion channels: molecular models and sites of action. Annu Rev Pharmacol Toxicol. 2001;41:23-51. Pubmed
  2. Arias HR, Bhumireddy P: Anesthetics as chemical tools to study the structure and function of nicotinic acetylcholine receptors. Curr Protein Pept Sci. 2005 Oct;6(5):451-72. Pubmed
  3. Krasowski MD, Harrison NL: General anaesthetic actions on ligand-gated ion channels. Cell Mol Life Sci. 1999 Aug 15;55(10):1278-303. Pubmed

3. Neuronal acetylcholine receptor subunit alpha-7

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: antagonist

Components

Name UniProt ID Details
Neuronal acetylcholine receptor subunit alpha-7 P36544 Details

References:

  1. Yamakura T, Bertaccini E, Trudell JR, Harris RA: Anesthetics and ion channels: molecular models and sites of action. Annu Rev Pharmacol Toxicol. 2001;41:23-51. Pubmed
  2. Arias HR, Bhumireddy P: Anesthetics as chemical tools to study the structure and function of nicotinic acetylcholine receptors. Curr Protein Pept Sci. 2005 Oct;6(5):451-72. Pubmed
  3. Krasowski MD, Harrison NL: General anaesthetic actions on ligand-gated ion channels. Cell Mol Life Sci. 1999 Aug 15;55(10):1278-303. Pubmed

4. Glutamate receptor 2

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: antagonist

Components

Name UniProt ID Details
Glutamate receptor 2 P42262 Details

References:

  1. Yamakura T, Bertaccini E, Trudell JR, Harris RA: Anesthetics and ion channels: molecular models and sites of action. Annu Rev Pharmacol Toxicol. 2001;41:23-51. Pubmed
  2. Krasowski MD, Harrison NL: General anaesthetic actions on ligand-gated ion channels. Cell Mol Life Sci. 1999 Aug 15;55(10):1278-303. Pubmed

5. Glutamate receptor ionotropic, kainate 2

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: antagonist

Components

Name UniProt ID Details
Glutamate receptor ionotropic, kainate 2 Q13002 Details

References:

  1. Yamakura T, Bertaccini E, Trudell JR, Harris RA: Anesthetics and ion channels: molecular models and sites of action. Annu Rev Pharmacol Toxicol. 2001;41:23-51. Pubmed
  2. Krasowski MD, Harrison NL: General anaesthetic actions on ligand-gated ion channels. Cell Mol Life Sci. 1999 Aug 15;55(10):1278-303. Pubmed

Comments
comments powered by Disqus
Drug created on June 13, 2005 07:24 / Updated on December 03, 2013 10:09