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Identification
NameAcetylsalicylic acid
Accession NumberDB00945  (APRD00264, EXPT00475)
Typesmall molecule
Groupsapproved
Description

The prototypical analgesic used in the treatment of mild to moderate pain. It has anti-inflammatory and antipyretic properties and acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Acetylsalicylic acid also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5)

Structure
Thumb
Synonyms
SynonymLanguageCode
2-Acetoxybenzenecarboxylic acidNot AvailableNot Available
2-Acetoxybenzoic acidNot AvailableNot Available
AcetylsalicylateNot AvailableNot Available
Acide acétylsalicyliqueFrenchINN
ácido acetilsalicílicoSpanishINN
Acidum acetylsalicylicumLatinINN
ASANot AvailableNot Available
AspirinNot AvailableUSAN
AzetylsalizylsäureGermanNot Available
o-acetoxybenzoic acidNot AvailableNot Available
O-acetylsalicylic acidNot AvailableNot Available
o-carboxyphenyl acetateNot AvailableNot Available
PolopirynaPolishNot Available
SaltsNot Available
Brand names
NameCompany
AcenterineNot Available
AcetophenMerck
AdiroNot Available
AspergumNot Available
AspirinBayer HealthCare LLC.
AsproNot Available
Bayer AspirinBayer HealthCare LLC.
EasprinNot Available
EcotrinNot Available
EmpirinNot Available
EntrophenNot Available
Nu-sealsNot Available
RhodineNot Available
RhonalNot Available
SolprinNot Available
Solprin acidNot Available
St. Joseph Aspirin for AdultsNot Available
TasprinNot Available
Brand mixtures
Brand NameIngredients
Aspirin with Stomach GuardAcetylsalicylic Acid + Calcium Carbonate + Magnesium Carbonate + Magnesium Oxide
Extra Strength Aspirin BackacheAcetylsalicylic Acid + Methocarbamol
Categories
CAS number50-78-2
WeightAverage: 180.1574
Monoisotopic: 180.042258744
Chemical FormulaC9H8O4
InChI KeyInChIKey=BSYNRYMUTXBXSQ-UHFFFAOYSA-N
InChI
InChI=1S/C9H8O4/c1-6(10)13-8-5-3-2-4-7(8)9(11)12/h2-5H,1H3,(H,11,12)
IUPAC Name
2-(acetyloxy)benzoic acid
SMILES
CC(=O)OC1=CC=CC=C1C(O)=O
Mass Specshow(8.27 KB)
Taxonomy
KingdomOrganic Compounds
SuperclassBenzenoids
ClassBenzene and Substituted Derivatives
SubclassPhenol Esters
Direct parentPhenol Esters
Alternative parentsSalicylic Acids; Benzoic Acids; Phenol Ethers; Benzoyl Derivatives; Alkyl Aryl Ethers; Dicarboxylic Acids and Derivatives; Carboxylic Acid Esters; Enolates; Polyamines; Carboxylic Acids
Substituentsbenzoyl; phenol ether; alkyl aryl ether; dicarboxylic acid derivative; carboxylic acid ester; ether; carboxylic acid; carboxylic acid derivative; polyamine; enolate
Classification descriptionThis compound belongs to the phenol esters. These are aromatic compounds containing a benzene ring substituted by an hydroxyl group and an ester group.
Pharmacology
IndicationFor use in the temporary relief of various forms of pain, inflammation associated with various conditions (including rheumatoid arthritis, juvenile rheumatoid arthritis, systemic lupus erythematosus, osteoarthritis, and ankylosing spondylitis), and is also used to reduce the risk of death and/or nonfatal myocardial infarction in patients with a previous infarction or unstable angina pectoris.
PharmacodynamicsAcetylsalicylic acid is an analgesic, antipyretic, antirheumatic, and anti-inflammatory agent. Acetylsalicylic acid's mode of action as an antiinflammatory and antirheumatic agent may be due to inhibition of synthesis and release of prostaglandins. Acetylsalicylic acid appears to produce analgesia by virtue of both a peripheral and CNS effect. Peripherally, acetylsalicylic acid acts by inhibiting the synthesis and release of prostaglandins. Acting centrally, it would appear to produce analgesia at a hypothalamic site in the brain, although the mode of action is not known. Acetylsalicylic acid also acts on the hypothalamus to produce antipyresis; heat dissipation is increased as a result of vasodilation and increased peripheral blood flow. Acetylsalicylic acid's antipyretic activity may also be related to inhibition of synthesis and release of prostaglandins.
Mechanism of actionThe analgesic, antipyretic, and anti-inflammatory effects of acetylsalicylic acid are due to actions by both the acetyl and the salicylate portions of the intact molecule as well as by the active salicylate metabolite. Acetylsalicylic acid directly and irreversibly inhibits the activity of both types of cyclooxygenase (COX-1 and COX-2) to decrease the formation of precursors of prostaglandins and thromboxanes from arachidonic acid. This makes acetylsalicylic acid different from other NSAIDS (such as diclofenac and ibuprofen) which are reversible inhibitors. Salicylate may competitively inhibit prostaglandin formation. Acetylsalicylic acid's antirheumatic (nonsteroidal anti-inflammatory) actions are a result of its analgesic and anti-inflammatory mechanisms; the therapeutic effects are not due to pituitary-adrenal stimulation. The platelet aggregation-inhibiting effect of acetylsalicylic acid specifically involves the compound's ability to act as an acetyl donor to cyclooxygenase; the nonacetylated salicylates have no clinically significant effect on platelet aggregation. Irreversible acetylation renders cyclooxygenase inactive, thereby preventing the formation of the aggregating agent thromboxane A2 in platelets. Since platelets lack the ability to synthesize new proteins, the effects persist for the life of the exposed platelets (7-10 days). Acetylsalicylic acid may also inhibit production of the platelet aggregation inhibitor, prostacyclin (prostaglandin I2), by blood vessel endothelial cells; however, inhibition prostacyclin production is not permanent as endothelial cells can produce more cyclooxygenase to replace the non-functional enzyme.
AbsorptionAbsorption is generally rapid and complete following oral administration but may vary according to specific salicylate used, dosage form, and other factors such as tablet dissolution rate and gastric or intraluminal pH.
Volume of distributionNot Available
Protein bindingHigh (99.5%) to albumin. Decreases as plasma salicylate concentration increases, with reduced plasma albumin concentration or renal dysfunction, and during pregnancy.
Metabolism

Acetylsalicylic acid is rapidly hydrolyzed primarily in the liver to salicylic acid, which is conjugated with glycine (forming salicyluric acid) and glucuronic acid and excreted largely in the urine.

SubstrateEnzymesProduct
Acetylsalicylic acid
    1-Salicylate glucuronideDetails
    Route of eliminationNot Available
    Half lifeThe plasma half-life is approximately 15 minutes; that for salicylate lengthens as the dose increases: doses of 300 to 650 mg have a half-life of 3.1 to 3.2 hours; with doses of 1 gram, the half-life is increased to 5 hours and with 2 grams it is increased to about 9 hours.
    ClearanceNot Available
    ToxicityOral, mouse: LD50 = 250 mg/kg; Oral, rabbit: LD50 = 1010 mg/kg; Oral, rat: LD50 = 200 mg/kg. Effects of overdose include: tinnitus, abdominal pain, hypokalemia, hypoglycemia, pyrexia, hyperventilation, dysrhythmia, hypotension, hallucination, renal failure, confusion, seizure, coma, and death.
    Affected organisms
    • Humans and other mammals
    Pathways
    PathwayCategorySMPDB ID
    Acetylsalicylic Acid Action PathwayDrug actionSMP00083
    SNP Mediated Effects
    Interacting Gene/EnzymeSNP RS IDAllele nameDefining changeEffectReference(s)
    Cytochrome P450 2C9
    Gene symbol: CYP2C9
    UniProt: P11712
    rs1057910 CYP2C9*1C AllelePoor drug metabolizer, lower dose requirements12893985
    Integrin beta-3
    Gene symbol: ITGB3
    UniProt: P05106
    rs5918 Not AvailableT > CPatients are more resistant to the anti-thrombotic effects of aspirin11723016
    SNP Mediated Adverse Drug Reactions
    Interacting Gene/EnzymeSNP RS IDAllele nameDefining changeAdverse ReactionReference(s)
    Leukotriene C4 synthase
    Gene symbol: LTC4S
    UniProt: Q16873
    rs730012 Not AvailableC alleleAspirin-induced urticaria16433794
    ADMET
    Predicted ADMET features
    Property Value Probability
    Human Intestinal Absorption + 0.9645
    Blood Brain Barrier + 0.9376
    Caco-2 permeable - 0.6607
    P-glycoprotein substrate Non-substrate 0.685
    P-glycoprotein inhibitor I Non-inhibitor 0.9118
    P-glycoprotein inhibitor II Non-inhibitor 0.9615
    Renal organic cation transporter Non-inhibitor 0.914
    CYP450 2C9 substrate Non-substrate 0.7518
    CYP450 2D6 substrate Non-substrate 0.9116
    CYP450 3A4 substrate Non-substrate 0.7225
    CYP450 1A2 substrate Non-inhibitor 0.9046
    CYP450 2C9 substrate Non-inhibitor 0.9071
    CYP450 2D6 substrate Non-inhibitor 0.9576
    CYP450 2C19 substrate Non-inhibitor 0.9445
    CYP450 3A4 substrate Non-inhibitor 0.9611
    CYP450 inhibitory promiscuity Low CYP Inhibitory Promiscuity 0.9557
    Ames test Non AMES toxic 0.9326
    Carcinogenicity Non-carcinogens 0.8356
    Biodegradation Ready biodegradable 0.9067
    Rat acute toxicity 2.6386 LD50, mol/kg Not applicable
    hERG inhibition (predictor I) Weak inhibitor 0.9433
    hERG inhibition (predictor II) Non-inhibitor 0.9799
    Pharmacoeconomics
    Manufacturers
    • Bayer healthcare llc
    Packagers
    Dosage forms
    FormRouteStrength
    GumOral
    LiquidOral
    PowderOral
    Solution / dropsOral
    SuppositoryRectal
    TabletOral
    Tablet, chewableOral
    Tablet, coatedOral
    Tablet, delayed releaseOral
    Prices
    Unit descriptionCostUnit
    Entrophen 10 650 mg Enteric-Coated Tablet0.09USDtablet
    DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.
    PatentsNot Available
    Properties
    Statesolid
    Experimental Properties
    PropertyValueSource
    melting point135 °CPhysProp
    boiling point140 °CNot Available
    water solubility4600 mg/L (at 25 °C)YALKOWSKY,SH & DANNENFELSER,RM (1992)
    logP1.19HANSCH,C ET AL. (1995)
    Caco2 permeability-5.06ADME Research, USCD
    pKa3.49 (at 25 °C)MERCK INDEX (1983)
    Predicted Properties
    PropertyValueSource
    water solubility1.46e+00 g/lALOGPS
    logP1.43ALOGPS
    logP1.24ChemAxon
    logS-2.1ALOGPS
    pKa (strongest acidic)3.41ChemAxon
    pKa (strongest basic)-7.1ChemAxon
    physiological charge-1ChemAxon
    hydrogen acceptor count3ChemAxon
    hydrogen donor count1ChemAxon
    polar surface area63.6ChemAxon
    rotatable bond count3ChemAxon
    refractivity44.45ChemAxon
    polarizability17.1ChemAxon
    number of rings1ChemAxon
    bioavailability1ChemAxon
    rule of fiveYesChemAxon
    Ghose filterYesChemAxon
    Veber's ruleNoChemAxon
    MDDR-like ruleNoChemAxon
    Spectra
    Spectra
    References
    Synthesis Reference

    Marino Gobetti, Guido Vandoni, “Acetylsalicylic acid thioesters, a process for their preparation and pharmaceutical compositions containing them.” U.S. Patent US4563443, issued March, 1981.

    US4563443
    General Reference
    1. Macdonald S: Aspirin use to be banned in under 16 year olds. BMJ. 2002 Nov 2;325(7371):988. Pubmed
    2. Sneader W: The discovery of aspirin: a reappraisal. BMJ. 2000 Dec 23-30;321(7276):1591-4. Pubmed
    3. Aukerman G, Knutson D, Miser WF: Management of the acute migraine headache. Am Fam Physician. 2002 Dec 1;66(11):2123-30. Pubmed
    4. Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. ISIS-2 (Second International Study of Infarct Survival) Collaborative Group. Lancet. 1988 Aug 13;2(8607):349-60. Pubmed
    5. Dorsch MP, Lee JS, Lynch DR, Dunn SP, Rodgers JE, Schwartz T, Colby E, Montague D, Smyth SS: Aspirin resistance in patients with stable coronary artery disease with and without a history of myocardial infarction. Ann Pharmacother. 2007 May;41(5):737-41. Epub 2007 Apr 24. Pubmed
    External Links
    ResourceLink
    KEGG DrugD00109
    KEGG CompoundC01405
    PubChem Compound2244
    PubChem Substance46505803
    ChemSpider2157
    BindingDB22360
    ChEBI15365
    ChEMBLCHEMBL25
    Therapeutic Targets DatabaseDAP000843
    PharmGKBPA448497
    IUPHAR4139
    Guide to Pharmacology4139
    HETAIN
    Drug Product Database2237900
    RxListhttp://www.rxlist.com/cgi/generic/asa.htm
    Drugs.comhttp://www.drugs.com/aspirin.html
    PDRhealthhttp://www.pdrhealth.com/drug_info/rxdrugprofiles/drugs/asp1033.shtml
    WikipediaAspirin
    ATC CodesA01AD05B01AC06N02BA01
    AHFS Codes
    • 28:08.04.24
    • 92:02.00*
    PDB EntriesNot Available
    FDA labelshow(889 KB)
    MSDSshow(18.9 KB)
    Interactions
    Drug Interactions
    Drug
    AcenocoumarolAcetylsalicylic acid increases the effect of the anticoagulant, acenocoumarol.
    AcetazolamideAcetylsalicylic acid at high dose increases the effect of the carbonic anhydrase inhibitor, acetazolamide.
    AcetohexamideAcetylsalicylic acid increases the effect of sulfonylurea, acetohexamide.
    AnisindioneAcetylsalicylic acid increases effect of the anticoagulant, anisindione.
    Azilsartan medoxomilIncreases toxicity of each. May deteriorate renal function, particularly in volume depleted or elderly patients. Decreases effects of azilsartan by antagonism.
    BetamethasoneThe corticosteroid, betamethasone, may decrease the effect of the salicylate, acetylsalicylic acid.
    ChlorpropamideAcetylsalicylic acid may increase the effect of the sulfonylurea, chlorpropamide.
    Cortisone acetateThe corticosteroid, cortisone acetate, may decrease the effect of the salicylate, acetylsalicylic acid.
    DexamethasoneThe corticosteroid, dexamethasone, may decrease the effect of the salicylate, acetylsalicylic acid.
    DiclofenamideAcetylsalicylic acid at high dose increases the effect of the carbonic anhydrase inhibitor, dichlorphenamide.
    DicoumarolAcetylsalicylic acid increases effect of the anticoagulant, dicumarol.
    EltrombopagDecreases metabolism, will increase effect/level of eltrombopag.
    FludrocortisoneThe corticosteroid, fludrocortisone, may decrease the effect of the salicylate, acetylsalicylic acid.
    Ginkgo bilobaAdditive anticoagulant/antiplatelet effects may increase bleed risk. Concomitant therapy should be avoided.
    GliclazideAcetylsalicylic acid increases the effect of the sulfonylurea, gliclazide.
    GlipizideAcetylsalicylic acid increases the effect of the sulfonylurea, glipizide.
    GlisoxepideAcetylsalicylic acid increases the effect of the sulfonylurea, glisoxepide.
    GlyburideAcetylsalicylic acid increases the effect of the sulfonylurea, glibenclamide.
    GlycodiazineAcetylsalicylic acid increases the effect of sulfonylurea, glycodiazine.
    GriseofulvinGriseofulvin may decrease the efficacy of acetylsalicylic acid.
    HeparinIncreased risk of bleeding.
    HomoharringtonineAvoid combination with acetylsalicylic acid due to the potential enhancement of homoharringtonine associated bleeding-related adverse effects. Specifically it is suggested to avoid this combination in patients with a platelet count of less than 50,000/uL.
    HydrocortisoneThe corticosteroid, hydrocortisone, may decrease the effect of the salicylate, acetylsalicylic acid.
    IbuprofenConcomitant therapy of the NSAID, ketoprofen, and acetylsalicylic acid may result in additive adverse/toxic effects (e.g. GI bleeding). The NSAID may also limit the cardioprotective effect of acetylsalicylic acid. Occasional concomitant use may not cause clinically significant problems, but regular, frequent concomitant therapy is not recommended.
    KetoprofenConcomitant therapy of the NSAID, ketoprofen, and acetylsalicylic acid may result in additive adverse/toxic effects (e.g. GI bleeding). The NSAID may also limit the cardioprotective effect of acetylsalicylic acid. Occasional concomitant use may not cause clinically significant problems, but regular, frequent concomitant therapy is not recommended.
    KetorolacAcetylsalicylic acid may increase the adverse GI effects ketorolac.
    MethazolamideAcetylsalicylic acid at high dose increases the effect of the carbonic anhydrase inhibitor, methazolamide.
    MethotrexateAcetylsalicylic acid increases the effect and toxicity of methotrexate.
    MethylprednisoloneThe corticosteroid, methylprednisolone, may decrease the effect of the salicylate, acetylsalicylic acid.
    ParamethasoneThe corticosteroid, paramethasone, may decrease the effect of the salicylate, acetylsalicylic acid.
    PrednisoloneThe corticosteroid, prednisolone, may decrease the effect of the salicylate, acetylsalicylic acid.
    PrednisoneThe corticosteroid, prednisone, may decrease the effect of the salicylate, acetylsalicylic acid.
    ProbenecidAcetylsalicylic acid decreases the uricosuric effect of probenecid.
    SulindacRisk of additive toxicity (e.g. bleed risk). Acetylsalicylic acid may decrease the serum concentration of sulindac. Sulindac may counteract the cardioprotective effects of acetylsalicylic acid. Consider alternate therapy or monitor for changes in the therapeutic and adverse effects of both agents if the interacting agent is initiated, discontinued or dose changed.
    TelmisartanConcomitant use of Telmisartan and Acetylsalicylic acid may increase the risk of acute renal failure and hyperkalemia. Monitor renal function at the beginning and during treatment.
    Tiaprofenic acidIncreased risk of gastrointestinal bleeding.
    TiclopidineIncreased effect of ticlopidine
    TolazamideAcetylsalicylic acid increases the effect of the sulfonylurea, tolazamide.
    TolbutamideAcetylsalicylic acid increases the effect of the sulfonylurea, tolbutamide.
    TolmetinAdditive adverse effects increase the risk of gastrointestinal bleeding. Possible decrease in the cardioprotective effect of acetylsalicylic acid. Monitor for increased bleeding risk during concomitant therapy.
    TrandolaprilAcetylsalicylic acid may reduce the efficacy of Trandolapril. Monitor for changes in Trandolapril efficacy if Acetylsalicylic acid is initiated, discontinued or dose changed.
    TreprostinilThe prostacyclin analogue, Treprostinil, increases the risk of bleeding when combined with the antiplatelet agent, Acetylsalicylic acid. Monitor for increased bleeding during concomitant thearpy.
    TriamcinoloneThe corticosteroid, triamcinolone, may decrease the effect of the salicylate, acetylsalicylic acid.
    Valproic AcidAcetylsalicylic acid increases the effect of valproic acid.
    WarfarinThe antiplatelet effects of acetylsalicylic acid may increase the bleed risk associated with warfarin.
    Food Interactions
    • Avoid alcohol, alcohol appears to cause a 50 to 100% increases in ASA serum levels.
    • Take with a full glass of water.
    • Take with food to reduce gastric irritation.

    1. Prostaglandin G/H synthase 1

    Kind: protein

    Organism: Human

    Pharmacological action: yes

    Actions: inhibitor

    Components

    Name UniProt ID Details
    Prostaglandin G/H synthase 1 P23219 Details

    References:

    1. Stevenson DD, Szczeklik A: Clinical and pathologic perspectives on aspirin sensitivity and asthma. J Allergy Clin Immunol. 2006 Oct;118(4):773-86; quiz 787-8. Epub 2006 Sep 1. Pubmed
    2. Flipo RM: [Are the NSAIDs able to compromising the cardio-preventive efficacy of aspirin?] Presse Med. 2006 Sep;35(9 Spec No 1):1S53-60. Pubmed
    3. Schwartz KA: Aspirin resistance: a review of diagnostic methodology, mechanisms, and clinical utility. Adv Clin Chem. 2006;42:81-110. Pubmed
    4. Birnbaum Y, Ye Y, Lin Y, Freeberg SY, Huang MH, Perez-Polo JR, Uretsky BF: Aspirin augments 15-epi-lipoxin A4 production by lipopolysaccharide, but blocks the pioglitazone and atorvastatin induction of 15-epi-lipoxin A4 in the rat heart. Prostaglandins Other Lipid Mediat. 2007 Feb;83(1-2):89-98. Epub 2006 Nov 7. Pubmed
    5. Guthikonda S, Lev EI, Patel R, DeLao T, Bergeron AL, Dong JF, Kleiman NS: Reticulated platelets and uninhibited COX-1 and COX-2 decrease the antiplatelet effects of aspirin. J Thromb Haemost. 2007 Mar;5(3):490-6. Pubmed
    6. Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. Pubmed

    2. Prostaglandin G/H synthase 2

    Kind: protein

    Organism: Human

    Pharmacological action: yes

    Actions: inhibitor

    Components

    Name UniProt ID Details
    Prostaglandin G/H synthase 2 P35354 Details

    References:

    1. Brzozowski T, Konturek PC, Sliwowski Z, Kwiecien S, Drozdowicz D, Pawlik M, Mach K, Konturek SJ, Pawlik WW: Interaction of nonsteroidal anti – inflammatory drugs (NSAID) with Helicobacter pylori in the stomach of humans and experimental animals. J Physiol Pharmacol. 2006 Sep;57 Suppl 3:67-79. Pubmed
    2. Wang HJ, Liu XJ, Yang KX, Luo FM, Lou JY, Peng ZL: [Effects of nonsteroidal anti-inflammatory drug celecoxib on expression of cyclooxygenase-2 (COX-2) in ovarian carcinoma cell] Sichuan Da Xue Xue Bao Yi Xue Ban. 2006 Sep;37(5):757-60. Pubmed
    3. Shen J, Gammon MD, Terry MB, Teitelbaum SL, Neugut AI, Santella RM: Genetic polymorphisms in the cyclooxygenase-2 gene, use of nonsteroidal anti-inflammatory drugs, and breast cancer risk. Breast Cancer Res. 2006;8(6):R71. Pubmed
    4. Nakano M, Denda N, Matsumoto M, Kawamura M, Kawakubo Y, Hatanaka K, Hiramoto Y, Sato Y, Noshiro M, Harada Y: Interaction between cyclooxygenase (COX)-1- and COX-2-products modulates COX-2 expression in the late phase of acute inflammation. Eur J Pharmacol. 2007 Mar 22;559(2-3):210-8. Epub 2006 Dec 16. Pubmed
    5. Hall MN, Campos H, Li H, Sesso HD, Stampfer MJ, Willett WC, Ma J: Blood levels of long-chain polyunsaturated fatty acids, aspirin, and the risk of colorectal cancer. Cancer Epidemiol Biomarkers Prev. 2007 Feb;16(2):314-21. Pubmed
    6. Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. Pubmed

    3. Aldo-keto reductase family 1 member C1

    Kind: protein

    Organism: Human

    Pharmacological action: unknown

    Actions: inhibitor

    Components

    Name UniProt ID Details
    Aldo-keto reductase family 1 member C1 Q04828 Details

    References:

    1. Dhagat U, Carbone V, Chung RP, Matsunaga T, Endo S, Hara A, El-Kabbani O: A salicylic acid-based analogue discovered from virtual screening as a potent inhibitor of human 20alpha-hydroxysteroid dehydrogenase. Med Chem. 2007 Nov;3(6):546-50. Pubmed

    1. Cytochrome P450 2C19

    Kind: protein

    Organism: Human

    Pharmacological action: unknown

    Actions: inducer

    Components

    Name UniProt ID Details
    Cytochrome P450 2C19 P33261 Details

    References:

    1. Preissner S, Kroll K, Dunkel M, Senger C, Goldsobel G, Kuzman D, Guenther S, Winnenburg R, Schroeder M, Preissner R: SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids Res. 2010 Jan;38(Database issue):D237-43. Epub 2009 Nov 24. Pubmed

    2. Cytochrome P450 2C8

    Kind: protein

    Organism: Human

    Pharmacological action: unknown

    Actions: substrate

    Components

    Name UniProt ID Details
    Cytochrome P450 2C8 P10632 Details

    References:

    1. Preissner S, Kroll K, Dunkel M, Senger C, Goldsobel G, Kuzman D, Guenther S, Winnenburg R, Schroeder M, Preissner R: SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids Res. 2010 Jan;38(Database issue):D237-43. Epub 2009 Nov 24. Pubmed

    3. Cytochrome P450 2C9

    Kind: protein

    Organism: Human

    Pharmacological action: unknown

    Actions: substrate

    Components

    Name UniProt ID Details
    Cytochrome P450 2C9 P11712 Details

    References:

    1. Preissner S, Kroll K, Dunkel M, Senger C, Goldsobel G, Kuzman D, Guenther S, Winnenburg R, Schroeder M, Preissner R: SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids Res. 2010 Jan;38(Database issue):D237-43. Epub 2009 Nov 24. Pubmed

    1. Serum albumin

    Kind: protein

    Organism: Human

    Pharmacological action: no

    Actions: other/unknown

    Components

    Name UniProt ID Details
    Serum albumin P02768 Details

    References:

    1. Sulkowska A, Bojko B, Rownicka J, Sulkowski WW: Competition of cytarabine and aspirin in binding to serum albumin in multidrug therapy. Biopolymers. 2006 Apr 15;81(6):464-72. Pubmed
    2. Dundee JW, Halliday NJ, McMurray TJ: Aspirin and probenecid pretreatment influences the potency of thiopentone and the onset of action of midazolam. Eur J Anaesthesiol. 1986 May;3(3):247-51. Pubmed

    1. Solute carrier family 22 member 6

    Kind: protein

    Organism: Human

    Pharmacological action: unknown

    Actions: inhibitor

    Components

    Name UniProt ID Details
    Solute carrier family 22 member 6 Q4U2R8 Details

    References:

    1. Apiwattanakul N, Sekine T, Chairoungdua A, Kanai Y, Nakajima N, Sophasan S, Endou H: Transport properties of nonsteroidal anti-inflammatory drugs by organic anion transporter 1 expressed in Xenopus laevis oocytes. Mol Pharmacol. 1999 May;55(5):847-54. Pubmed

    2. Multidrug resistance protein 1

    Kind: protein

    Organism: Human

    Pharmacological action: unknown

    Actions: substrate

    Components

    Name UniProt ID Details
    Multidrug resistance protein 1 P08183 Details

    References:

    1. Faassen F, Vogel G, Spanings H, Vromans H: Caco-2 permeability, P-glycoprotein transport ratios and brain penetration of heterocyclic drugs. Int J Pharm. 2003 Sep 16;263(1-2):113-22. Pubmed

    3. Solute carrier family 22 member 7

    Kind: protein

    Organism: Human

    Pharmacological action: unknown

    Actions: substrate

    Components

    Name UniProt ID Details
    Solute carrier family 22 member 7 Q9Y694 Details

    References:

    1. Sekine T, Cha SH, Tsuda M, Apiwattanakul N, Nakajima N, Kanai Y, Endou H: Identification of multispecific organic anion transporter 2 expressed predominantly in the liver. FEBS Lett. 1998 Jun 12;429(2):179-82. Pubmed

    Comments
    Drug created on June 13, 2005 07:24 / Updated on September 16, 2013 17:12