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Identification
Name Acetylsalicylic acid
Accession Number DB00945 (APRD00264, EXPT00475)
Type small molecule
Groups approved
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
Download: MOL | SDF | SMILES | InChI
Display: 2D Structure | 3D Structure
Synonyms
2-Acetoxybenzenecarboxylic acid
2-Acetoxybenzoic acid
2-Carboxyphenyl acetate
A.S.A.
Acetilsalicilico
Acetilum acidulatum
Acetosalic acid
Acetoxybenzoic acid
Acetylsalicylate
Acetylsalicylsaure (GERMAN)
Acetysalicylic acid
Acide acetylsalicylique (FRENCH)
Acido acetilsalicilico
Acido O-acetil-benzoico
Acidum acetylsalicylicum
ASA
Kyselina 2-acetoxybenzoova
Kyselina acetylsalicylova
O-accetylsalicylic acid
o-Acetoxybenzoic acid
O-Acetylsalicylic acid
o-Carboxyphenyl acetate
Salicylic acid acetate
Salicylic acid, acetate
First Prev Next Last
Salts Not Available
Brand names
Name Company
8-hour Bayer
A.S.A. Empirin
Acenterine
Acesal
Acetal
Aceticyl
Acetisal
Acetol
Acetonyl
Acetophen
Acetosal
Acetosalin
Acetylin
Acetylsal
Acimetten
Acisal
Acylpyrin
Adiro
Asagran
Asatard
Ascoden-30
Aspalon
Aspec
Aspergum
Aspirdrops
Aspirin Bayer
Aspirine
Aspro
Asteric
Bayer Extra Strength Aspirin For Migraine Pain
Benaspir
Bi-prin
Bialpirina
Bialpirinia
Bufferin
Cemirit
Claradin
Clariprin
Colfarit
Contrheuma retard
Coricidin
Crystar
Decaten
Delgesic
Dolean pH 8
Duramax
Easprin
ECM
Ecolen
Ecotrin
Empirin
Endydol
Entericin
Enterophen
Enterosarein
Enterosarine
Entrophen
Extren
Globentyl
Globoid
Helicon
Idragin
Levius
Measurin
Micristin
Neuronika
Novid
Nu-seals
Nu-seals aspirin
Persistin
Pharmacin
Pirseal
Polopiryna
Premaspin
Rheumintabletten
Rhodine
Rhonal
Salacetin
Salcetogen
Saletin
Solfrin
Solprin
Solprin acid
Solpyron
Spira-Dine
St. Joseph
St. Joseph Aspirin for Adults
Supac
Tasprin
Temperal
Triple-sal
Xaxa
Yasta
First Prev Next Last
Brand mixtures
Brand Name Ingredients
Aspirin Plus Stomach Guard Acetylsalicylic Acid + Calcium Carbonate + Magnesium Carbonate + Magnesium Oxide
Aspirin Plus Stomach Guard Ext.Stgth.Caplet Acetylsalicylic Acid + Calcium Carbonate + Magnesium Carbonate + Magnesium Oxide
Aspirin Plus Stomach Guard Extra Strength Acetylsalicylic Acid + Calcium Carbonate + Magnesium Carbonate + Magnesium Oxide
Aspirin Plus Stomach Guard Tab Acetylsalicylic Acid + Calcium Carbonate + Magnesium Carbonate + Magnesium Oxide
Aspirin with Stomach Guard Acetylsalicylic Acid + Calcium Carbonate + Magnesium Carbonate + Magnesium Oxide
Aspirin with Stomach Guard Extra Strength - Tab Acetylsalicylic Acid + Calcium Carbonate + Magnesium Carbonate + Magnesium Oxide
Extra Strength Aspirin Backache Acetylsalicylic Acid + Methocarbamol
Categories
  • Anticoagulants
  • Cyclooxygenase Inhibitors
  • Platelet Aggregation Inhibitors
  • Fibrinolytic Agents
  • Salicylates
CAS number 50-78-2
Weight Average: 180.1574
Monoisotopic: 180.042258744
Chemical Formula C9H8O4
InChI Key InChIKey=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)
Plain Text
IUPAC Name
2-(acetyloxy)benzoic acid
SMILES
CC(=O)OC1=CC=CC=C1C(O)=O
Plain Text
Mass Spec show (8.27 KB)
Taxonomy
Kingdom Organic
Classes
  • Benzoates
  • Salicylates and Derivatives
  • Phenylacetates
Substructures
  • Carboxylic Acids and Derivatives
  • Hydroxy Compounds
  • Benzyl Alcohols and Derivatives
  • Acetates
  • Benzoates
  • Salicylates and Derivatives
  • Phenols and Derivatives
  • Phenylacetates
  • Ethers
  • Benzene and Derivatives
  • Aromatic compounds
  • Anisoles
  • Benzoyl Derivatives
  • Phenyl Esters
Pharmacology
Indication For 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.
Pharmacodynamics Acetylsalicylic 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 action The 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.
Absorption Absorption 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 distribution Not Available
Protein binding High (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.
Route of elimination Not Available
Half life The 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.
Clearance Not Available
Toxicity Oral, 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
Pathway Name SMPDB ID
Smp00083 Acetylsalicylic Acid Pathway SMP00083
Pharmacoeconomics
Manufacturers
  • Bayer healthcare llc
Packagers
Dosage forms
Form Route Strength
Gum Oral
Liquid Oral
Powder Oral
Solution / drops Oral
Suppository Rectal
Tablet Oral
Tablet, chewable Oral
Tablet, coated Oral
Tablet, delayed release Oral
Prices
Unit description Cost Unit
Entrophen 10 650 mg Enteric-Coated Tablet 0.09 USD tablet
DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.
Patents Not Available
Properties
State solid
Experimental Properties
Property Value Source
melting point 135 °C PhysProp
boiling point 140 °C Not Available
water solubility 4600 mg/L (at 25 °C) YALKOWSKY,SH & DANNENFELSER,RM (1992)
logP 1.19 HANSCH,C ET AL. (1995)
Caco2 permeability -5.06 ADME Research, USCD
pKa 3.49 (at 25 °C) MERCK INDEX (1983)
Predicted Properties
Property Value Source
water solubility 1.46e+00 g/l ALOGPS
logP 1.43 ALOGPS
logP 1.24 ChemAxon
logS -2.1 ALOGPS
pKa (strongest acidic) 3.41 ChemAxon
pKa (strongest basic) -7.1 ChemAxon
physiological charge -1 ChemAxon
hydrogen acceptor count 3 ChemAxon
hydrogen donor count 1 ChemAxon
polar surface area 63.6 ChemAxon
rotatable bond count 3 ChemAxon
refractivity 44.45 ChemAxon
polarizability 17.1 ChemAxon
References
Synthesis Reference Not Available
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
Resource Link
KEGG Drug D00109 Link_out
KEGG Compound C01405 Link_out
PubChem Compound 2244 Link_out
PubChem Substance 46505803 Link_out
ChemSpider 2157 Link_out
BindingDB 22360 Link_out
ChEBI 15365 Link_out
ChEMBL 15365 Link_out
Therapeutic Targets Database DAP000843 Link_out
PharmGKB PA448497 Link_out
IUPHAR 4139 Link_out
Guide to Pharmacology 4139 Link_out
HET AIN Link_out
Drug Product Database 2237900 Link_out
RxList http://www.rxlist.com/cgi/generic/asa.htm Link_out
Drugs.com http://www.drugs.com/aspirin.html Link_out
PDRhealth http://www.pdrhealth.com/drug_info/rxdrugprofiles/drugs/asp1033.shtml Link_out
Wikipedia http://en.wikipedia.org/wiki/Aspirin Link_out
ATC Codes
  • A01AD05
  • B01AC06
  • N02BA01
AHFS Codes
  • 28:08.04.24
  • 92:02.00*
PDB Entries Not Available
FDA label show (889 KB)
MSDS show (18.9 KB)
Interactions
Drug Interactions
Drug Interaction
Acenocoumarol Acetylsalicylic acid increases the effect of the anticoagulant, acenocoumarol.
Acetazolamide Acetylsalicylic acid at high dose increases the effect of the carbonic anhydrase inhibitor, acetazolamide.
Acetohexamide Acetylsalicylic acid increases the effect of sulfonylurea, acetohexamide.
Anisindione Acetylsalicylic acid increases effect of the anticoagulant, anisindione.
Azilsartan medoxomil Increases toxicity of each. May deteriorate renal function, particularly in volume depleted or elderly patients. Decreases effects of azilsartan by antagonism.
Betamethasone The corticosteroid, betamethasone, may decrease the effect of the salicylate, acetylsalicylic acid.
Chlorpropamide Acetylsalicylic acid may increase the effect of the sulfonylurea, chlorpropamide.
Cortisone acetate The corticosteroid, cortisone acetate, may decrease the effect of the salicylate, acetylsalicylic acid.
Dexamethasone The corticosteroid, dexamethasone, may decrease the effect of the salicylate, acetylsalicylic acid.
Dichlorphenamide Acetylsalicylic acid at high dose increases the effect of the carbonic anhydrase inhibitor, dichlorphenamide.
Dicumarol Acetylsalicylic acid increases effect of the anticoagulant, dicumarol.
Eltrombopag Decreases metabolism, will increase effect/level of eltrombopag.
Fludrocortisone The corticosteroid, fludrocortisone, may decrease the effect of the salicylate, acetylsalicylic acid.
Ginkgo biloba Additive anticoagulant/antiplatelet effects may increase bleed risk. Concomitant therapy should be avoided.
Gliclazide Acetylsalicylic acid increases the effect of the sulfonylurea, gliclazide.
Glipizide Acetylsalicylic acid increases the effect of the sulfonylurea, glipizide.
Glisoxepide Acetylsalicylic acid increases the effect of the sulfonylurea, glisoxepide.
Glyburide Acetylsalicylic acid increases the effect of the sulfonylurea, glibenclamide.
Glycodiazine Acetylsalicylic acid increases the effect of sulfonylurea, glycodiazine.
Griseofulvin Griseofulvin may decrease the efficacy of acetylsalicylic acid.
Heparin Increased risk of bleeding.
Hydrocortisone The corticosteroid, hydrocortisone, may decrease the effect of the salicylate, acetylsalicylic acid.
Ibuprofen Concomitant 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.
Ketoprofen Concomitant 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.
Ketorolac Acetylsalicylic acid may increase the adverse GI effects ketorolac.
Methazolamide Acetylsalicylic acid at high dose increases the effect of the carbonic anhydrase inhibitor, methazolamide.
Methotrexate Acetylsalicylic acid increases the effect and toxicity of methotrexate.
Methylprednisolone The corticosteroid, methylprednisolone, may decrease the effect of the salicylate, acetylsalicylic acid.
Paramethasone The corticosteroid, paramethasone, may decrease the effect of the salicylate, acetylsalicylic acid.
Prednisolone The corticosteroid, prednisolone, may decrease the effect of the salicylate, acetylsalicylic acid.
Prednisone The corticosteroid, prednisone, may decrease the effect of the salicylate, acetylsalicylic acid.
Probenecid Acetylsalicylic acid decreases the uricosuric effect of probenecid.
Sulindac Risk 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.
Telmisartan Concomitant 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 acid Increased risk of gastrointestinal bleeding.
Ticlopidine Increased effect of ticlopidine
Tolazamide Acetylsalicylic acid increases the effect of the sulfonylurea, tolazamide.
Tolbutamide Acetylsalicylic acid increases the effect of the sulfonylurea, tolbutamide.
Tolmetin Additive 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.
Trandolapril Acetylsalicylic acid may reduce the efficacy of Trandolapril. Monitor for changes in Trandolapril efficacy if Acetylsalicylic acid is initiated, discontinued or dose changed.
Treprostinil The prostacyclin analogue, Treprostinil, increases the risk of bleeding when combined with the antiplatelet agent, Acetylsalicylic acid. Monitor for increased bleeding during concomitant thearpy.
Triamcinolone The corticosteroid, triamcinolone, may decrease the effect of the salicylate, acetylsalicylic acid.
Valproic Acid Acetylsalicylic acid increases the effect of valproic acid.
Warfarin The 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.
Targets

1. Prostaglandin G/H synthase 1

Pharmacological action: yes
Actions: inhibitor

May play an important role in regulating or promoting cell proliferation in some normal and neoplastically transformed cells

Organism class: human
UniProt ID: P23219 Link_out
Gene: PTGS1 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

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

Pharmacological action: yes
Actions: inhibitor

May have a role as a major mediator of inflammation and/or a role for prostanoid signaling in activity-dependent plasticity

Organism class: human
UniProt ID: P35354 Link_out
Gene: PTGS2 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

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

Pharmacological action: unknown
Actions: inhibitor

Converts progesterone to its inactive form, 20alpha- dihydroxyprogesterone (20alpha-OHP). In the liver and intestine, may have a role in the transport of bile. May have a role in monitoring the intrahepatic bile acid concentration. May play a role in myelin formation

Organism class: human
UniProt ID: Q04828 Link_out
Gene: AKR1C1 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

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
Enzymes

1. Cytochrome P450 2C19

Actions: inducer

Responsible for the metabolism of a number of therapeutic agents such as the anticonvulsant drug S-mephenytoin, omeprazole, proguanil, certain barbiturates, diazepam, propranolol, citalopram and imipramine

UniProt ID: P33261 Link_out
Gene: CYP2C19 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

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

Actions: substrate

Cytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It oxidizes a variety of structurally unrelated compounds, including steroids, fatty acids, and xenobiotics. In the epoxidation of arachidonic acid it generates only 14,15- and 11,12-cis-epoxyeicosatrienoic acids. It is the principal enzyme responsible for the metabolism the anti- cancer drug paclitaxel (taxol)

UniProt ID: P10632 Link_out
Gene: CYP2C8
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

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

Actions: substrate

Cytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It oxidizes a variety of structurally unrelated compounds, including steroids, fatty acids, and xenobiotics. This enzyme contributes to the wide pharmacokinetics variability of the metabolism of drugs such as S- warfarin, diclofenac, phenytoin, tolbutamide and losartan

UniProt ID: P11712 Link_out
Gene: CYP2C9
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

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
Transporters

1. Solute carrier family 22 member 6

Actions: inhibitor
UniProt ID: Q4U2R8 Link_out
Gene: hROAT1 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

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

Actions: substrate

Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells

UniProt ID: P08183 Link_out
Gene: ABCB1 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

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

Actions: substrate

Mediates sodium-independent multispecific organic anion transport. Transport of prostaglandin E2, prostaglandin F2, tetracycline, bumetanide, estrone sulfate, glutarate, dehydroepiandrosterone sulfate, allopurinol, 5-fluorouracil, paclitaxel, L-ascorbic acid, salicylate, ethotrexate, and alpha- ketoglutarate

UniProt ID: Q9Y694 Link_out
Gene: SLC22A7 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

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
Carriers

1. Serum albumin

Actions: other/unknown

Serum albumin, the main protein of plasma, has a good binding capacity for water, Ca(2+), Na(+), K(+), fatty acids, hormones, bilirubin and drugs. Its main function is the regulation of the colloidal osmotic pressure of blood

UniProt ID: P02768 Link_out
Gene: ALB Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

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
Comments
Drug created on June 13, 2005 07:24 / Updated on February 08, 2013 16:19