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Identification
NameCelecoxib
Accession NumberDB00482  (APRD00373)
Typesmall molecule
Groupsapproved, investigational
Description

Celecoxib is a non-steroidal anti-inflammatory drug (NSAID) used in the treatment of osteoarthritis, rheumatoid arthritis, acute pain, painful menstruation and menstrual symptoms, and to reduce numbers of colon and rectum polyps in patients with familial adenomatous polyposis. It is marketed by Pfizer under the brand name Celebrex. In some countries, it is branded Celebra. Celecoxib is available by prescription in capsule form.

Structure
Thumb
Synonyms
SynonymLanguageCode
CelebrexNot AvailableNot Available
CelecoxibGerman/SpanishINN
CélécoxibFrenchINN
CelecoxibumLatin INN
P-(5-P-Tolyl-3-(trifluoromethyl)pyrazol-1-yl)benzenesulfonamideNot AvailableNot Available
SaltsNot Available
Brand names
NameCompany
ArticoxKeyfarm
ArticoxibNabiqasim
ArtiflexStandpharm
ArtilogPfizer
ArtixPharmalab
ArtrixibIntipharma
BlocktenInfarmasa
CaditarFarmindustria
CefinixFarmacoop
CelactSun
CelebraPfizer
CelebrexPfizer
OnsenalPfizer
ValdynePfizer
Brand mixtures
Brand NameIngredients
Caditar FlexCelecoxib and Orphenadrine
CategoriesNot Available
CAS number169590-42-5
WeightAverage: 381.372
Monoisotopic: 381.075882012
Chemical FormulaC17H14F3N3O2S
InChI KeyRZEKVGVHFLEQIL-UHFFFAOYSA-N
InChI
InChI=1S/C17H14F3N3O2S/c1-11-2-4-12(5-3-11)15-10-16(17(18,19)20)22-23(15)13-6-8-14(9-7-13)26(21,24)25/h2-10H,1H3,(H2,21,24,25)
IUPAC Name
4-[5-(4-methylphenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]benzene-1-sulfonamide
SMILES
CC1=CC=C(C=C1)C1=CC(=NN1C1=CC=C(C=C1)S(N)(=O)=O)C(F)(F)F
Mass SpecNot Available
Taxonomy
KingdomOrganic Compounds
SuperclassHeterocyclic Compounds
ClassAzoles
SubclassPyrazoles
Direct parentPhenylpyrazoles
Alternative parentsAminobenzenesulfonamides; Toluenes; Sulfonamides; Sulfonyls; Polyamines; Organofluorides; Alkyl Fluorides
Substituentstoluene; benzene; sulfonic acid derivative; sulfonamide; sulfonyl; polyamine; organonitrogen compound; amine; organofluoride; organohalogen; alkyl halide; alkyl fluoride
Classification descriptionThis compound belongs to the phenylpyrazoles. These are compounds containing a phenylpyrazole skeleton, which consists of a pyrazole bound to a phenyl group.
Pharmacology
IndicationFor relief and management of osteoarthritis (OA), rheumatoid arthritis (RA), juvenile rheumatoid arthritis (JRA), ankylosing spondylitis, acute pain, primary dysmenorrhea and oral adjunct to usual care for patients with familial adenomatous polyposis
PharmacodynamicsCelecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, is classified as a nonsteroidal anti-inflammatory drug (NSAID). Celecoxib is used to treat rheumatoid arthritis, osteoarthritis, and familial adenomatous polyposis (FAP). Because of its lack of platelet effects, celecoxib is not a substitute for aspirin for cardiovascular prophylaxis. It is not known if there are any effects of celecoxib on platelets that may contribute to the increased risk of serious cardiovascular thrombotic adverse events associated with the use of celecoxib. Inhibition of PGE2 synthesis may lead to sodium and water retention through increased fluid reabsorption in the renal medullary thick ascending loop of Henle and perhaps other segments of the distal nephron. In the collecting ducts, PGE2 appears to inhibit water reabsorption by counteracting the action of antidiuretic hormone.
Mechanism of actionThe mechanism of action of celecoxib is believed to be due to inhibition of prostaglandin synthesis. Unlike most NSAIDs, which inhibit both types of cyclooxygenases (COX-1 and COX-2), celecoxib is a selective noncompetitive inhibitor of cyclooxygenase-2 (COX-2) enzyme. It binds with its polar sulfonamide side chain to a hydrophilic side pocket region close to the active COX-2 binding site. Both COX-1 and COX-2 catalyze the conversion of arachidonic acid to prostaglandin (PG) H2, the precursor of PGs and thromboxane.
AbsorptionWell absorbed in the gastrointestinal tract. When a single dose of 200 mg is given to healthy subjects, peak plasma levels occur 3 hours after an oral dose. The peak plasma level is 705 ng/mL. Absolute bioavailability studies have not been conducted. When multiple doses are given, steady-state is reached on or before Day 5. When taken with a high fat meal, peak plasma levels are delayed for about 1 to 2 hours with an increase in total absorption (AUC) of 10% to 20%.
Volume of distribution

Apparent volume of distribution at steady state (Vdss/F), 200 mg single dose, healthy subjects = 429 L

Protein binding97%, primarily to albumin and, to a lesser extent, a1-acid glycoprotein. Celecoxib is not preferentially bound to red blood cells.
Metabolism

Hepatic. Celecoxib metabolism is primarily mediated via cytochrome P450 2C9. Three metabolites, a primary alcohol, the corresponding carboxylic acid and its glucuronide conjugate, have been identified in human plasma. CYP3A4 is also involved in the hydroxylation of celecoxib but to a lesser extent. These metabolites are inactive as COX-1 or COX-2 inhibitors.

SubstrateEnzymesProduct
Celecoxib
HydroxycelecoxibDetails
Hydroxycelecoxib
CarboxycelecoxibDetails
Carboxycelecoxib
Celecoxib glucuronideDetails
Route of eliminationCelecoxib is eliminated predominantly by hepatic metabolism with little (<3%) unchanged drug recovered in the urine and feces. 57% of the oral dose is excreted in the feces and 27% is excreted into the urine. The primary metabolite in urine and feces was the carboxylic acid metabolite (73%). The amount of glucuronide in the urine is low.
Half lifeThe effective half-life is approximately 11 hours when a single 200 mg dose is given to healthy subjects. Terminal half-life is generally variable because of the low solubility of the drug thus prolonging absorption.
Clearance

Apparent clearance (CL/F), single oral 200 mg dose, healthy subjects = 27.7 L/hr.

ToxicitySymptoms of overdose include breathing difficulties, coma, drowsiness, gastrointestinal bleeding, high blood pressure, kidney failure, nausea, sluggishness, stomach pain, and vomiting.
Affected organisms
  • Humans and other mammals
PathwaysNot Available
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
SNP Mediated Adverse Drug ReactionsNot Available
ADMET
Predicted ADMET features
Property Value Probability
Human Intestinal Absorption + 1.0
Blood Brain Barrier + 0.9713
Caco-2 permeable + 0.8866
P-glycoprotein substrate Non-substrate 0.9287
P-glycoprotein inhibitor I Non-inhibitor 0.8619
P-glycoprotein inhibitor II Non-inhibitor 0.792
Renal organic cation transporter Non-inhibitor 0.8582
CYP450 2C9 substrate Non-substrate 0.6237
CYP450 2D6 substrate Substrate 0.8919
CYP450 3A4 substrate Non-substrate 0.5751
CYP450 1A2 substrate Inhibitor 0.7805
CYP450 2C9 substrate Inhibitor 0.6172
CYP450 2D6 substrate Non-inhibitor 0.8594
CYP450 2C19 substrate Inhibitor 0.7169
CYP450 3A4 substrate Inhibitor 0.7959
CYP450 inhibitory promiscuity High CYP Inhibitory Promiscuity 0.7392
Ames test Non AMES toxic 0.7185
Carcinogenicity Non-carcinogens 0.7905
Biodegradation Not ready biodegradable 1.0
Rat acute toxicity 2.3719 LD50, mol/kg Not applicable
hERG inhibition (predictor I) Weak inhibitor 0.9856
hERG inhibition (predictor II) Non-inhibitor 0.8419
Pharmacoeconomics
Manufacturers
  • Gd searle llc
Packagers
Dosage forms
FormRouteStrength
CapsuleOral50 mg, 100 mg, 200 mg, 400 mg
Prices
Unit descriptionCostUnit
Celebrex 400 mg capsule6.78USDcapsule
Celebrex 200 mg capsule4.52USDcapsule
Celebrex 100 mg capsule2.75USDcapsule
Celebrex 50 mg capsule1.26USDcapsule
DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.
Patents
CountryPatent NumberApprovedExpires (estimated)
United States59729861998-04-142018-04-14
United States54668231993-11-302013-11-30
Canada22671862002-05-142017-10-14
Canada21775761999-10-262014-11-14
Properties
Statesolid
Experimental Properties
PropertyValueSource
melting point158 °CPhysProp
water solubilityVery low water solubility (3.3 mg/L)Not Available
logP3.9Not Available
Predicted Properties
PropertyValueSource
water solubility5.03e-03 g/lALOGPS
logP3.99ALOGPS
logP4.01ChemAxon
logS-4.9ALOGPS
pKa (strongest acidic)10.7ChemAxon
pKa (strongest basic)-0.42ChemAxon
physiological charge0ChemAxon
hydrogen acceptor count3ChemAxon
hydrogen donor count1ChemAxon
polar surface area77.98ChemAxon
rotatable bond count4ChemAxon
refractivity92.23ChemAxon
polarizability35.2ChemAxon
number of rings3ChemAxon
bioavailability1ChemAxon
rule of fiveYesChemAxon
Ghose filterYesChemAxon
Veber's ruleNoChemAxon
MDDR-like ruleNoChemAxon
Spectra
SpectraNot Available
References
Synthesis Reference

DrugSyn.org

US5466823
General Reference
  1. Malhotra S, Shafiq N, Pandhi P: COX-2 inhibitors: a CLASS act or Just VIGORously promoted. MedGenMed. 2004 Mar 23;6(1):6. Pubmed
  2. Silverstein FE, Faich G, Goldstein JL, Simon LS, Pincus T, Whelton A, Makuch R, Eisen G, Agrawal NM, Stenson WF, Burr AM, Zhao WW, Kent JD, Lefkowith JB, Verburg KM, Geis GS: Gastrointestinal toxicity with celecoxib vs nonsteroidal anti-inflammatory drugs for osteoarthritis and rheumatoid arthritis: the CLASS study: A randomized controlled trial. Celecoxib Long-term Arthritis Safety Study. JAMA. 2000 Sep 13;284(10):1247-55. Pubmed
  3. Solomon SD, McMurray JJ, Pfeffer MA, Wittes J, Fowler R, Finn P, Anderson WF, Zauber A, Hawk E, Bertagnolli M: Cardiovascular risk associated with celecoxib in a clinical trial for colorectal adenoma prevention. N Engl J Med. 2005 Mar 17;352(11):1071-80. Epub 2005 Feb 15. Pubmed
  4. Yelland MJ, Nikles CJ, McNairn N, Del Mar CB, Schluter PJ, Brown RM: Celecoxib compared with sustained-release paracetamol for osteoarthritis: a series of n-of-1 trials. Rheumatology (Oxford). 2007 Jan;46(1):135-40. Epub 2006 Jun 15. Pubmed
  5. Bertagnolli MM, Eagle CJ, Zauber AG, Redston M, Solomon SD, Kim K, Tang J, Rosenstein RB, Wittes J, Corle D, Hess TM, Woloj GM, Boisserie F, Anderson WF, Viner JL, Bagheri D, Burn J, Chung DC, Dewar T, Foley TR, Hoffman N, Macrae F, Pruitt RE, Saltzman JR, Salzberg B, Sylwestrowicz T, Gordon GB, Hawk ET: Celecoxib for the prevention of sporadic colorectal adenomas. N Engl J Med. 2006 Aug 31;355(9):873-84. Pubmed
  6. FDA label
  7. Sandberg M, Yasar U, Stromberg P, Hoog JO, Eliasson E: Oxidation of celecoxib by polymorphic cytochrome P450 2C9 and alcohol dehydrogenase. Br J Clin Pharmacol. 2002 Oct;54(4):423-9. Pubmed
External Links
ResourceLink
KEGG DrugD00567
KEGG CompoundC07589
PubChem Compound2662
PubChem Substance46505596
ChemSpider2562
BindingDB11639
ChEBI3520
ChEMBLCHEMBL118
Therapeutic Targets DatabaseDAP000737
PharmGKBPA448871
HETCEL
Drug Product Database2239941
RxListhttp://www.rxlist.com/cgi/generic/coxib.htm
Drugs.comhttp://www.drugs.com/celecoxib.html
WikipediaCelecoxib
ATC CodesL01XX33M01AH01
AHFS Codes
  • 28:08.04.08
PDB EntriesNot Available
FDA labelshow(174 KB)
MSDSshow(102 KB)
Interactions
Drug Interactions
Drug
AcenocoumarolCelecoxib may increase the anticoagulant effect of acenocoumarol.
AnisindioneCelecoxib may increase the anticoagulant effect of anisindione.
Azilsartan medoxomilIncreases toxicity of each. May deteriorate renal function, particularly in volume depleted or elderly patients. Decreases effects of azilsartan by antagonism.
ColesevelamBile acid sequestrants may decrease the absorption of Nonsteroidal Anti-Inflammatory Agents. Monitor for decreased serum concentrations/therapeutic effects of nonsteroidal anti-inflammatory agents (NSAID) if coadministered with bile acid sequestrants. Separating the administration of doses by 2 or more hours may reduce (but not eliminate) the risk of interaction. The manufacturer of colesevelam recommends that drugs should be administered at least 1 hour before or 4 hours after colesevelam.
DicoumarolCelecoxib may increase the anticoagulant effect of dicumarol.
EltrombopagEltrombopag increases levels of Celecoxib via metabolism decrease.
FluconazoleFluconazole may increase the effect of celecoxib.
LithiumThe COX-2 inhibitor increases serum levels of lithium
PralatrexateNSAIDs increase the risk of toxicity due to impairment of renal clearance of pralatrexate thus increasing exposure. Monitor for adverse effects or adjust dose of pralatrexate.
RifampicinRifampin, a strong CYP2C9 inducer, may decrease the serum levels of celecoxib by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects if rifampin is initiated, discontinued or dose changed.
TelmisartanConcomitant use of Telmisartan and Celecoxib may increase the risk of acute renal failure and hyperkalemia. Monitor renal function at the beginning and during treatment.
TimololThe NSAID, Celecoxib, may antagonize the antihypertensive effect of Timolol.
TolbutamideTolbutamide, a strong CYP2C9 inhibitor, may decrease the metabolism and clearance of Celecoxib. Consider alternate therapy or monitor for changes in Celecobix therapeutic and adverse effects if Tolbutamide is initiated, discontinued or dose changed.
TrandolaprilThe NSAID, Celecoxib, may reduce the antihypertensive effect of Trandolapril. Consider alternate therapy or monitor for changes in Trandolapril efficacy if Celecoxib is initiated, discontinued or dose changed.
TreprostinilThe prostacyclin analogue, Treprostinil, may increase the risk of bleeding when combined with the NSAID, Celecoxib. Monitor for increased bleeding during concomitant thearpy.
TretinoinThe moderate CYP2C8 inhibitor, Celecoxib, may decrease the metabolism and clearance of oral Tretinoin. Monitor for changes in Tretinoin effectiveness and adverse/toxic effects if Celecoxib is initiated, discontinued to dose changed.
VilazodoneSelective Serotonin Reuptake Inhibitors may enhance the antiplatelet effect of NSAID (COX-2 Inhibitor). To minimize the risk of bleeding associated with this combination, consider using alternative analgesics, when appropriate, and/or addition of an gastroprotective agent, such as a proton pump inhibitor for the time that combined selective serotonin reuptake inhibitor (SSRIs) and nonsteroidal anti-inflammatory drugs (NSAIDs) is necessary.
WarfarinCelecoxib may increase the anticoagulant effect of warfarin.
Food Interactions
  • Take without regard to meals.
  • Taking this product with a high-fat meal will delay the Cmax, but total absorption will be increased by 10 to 20%.

Targets

1. 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. Sigthorsson G, Simpson RJ, Walley M, Anthony A, Foster R, Hotz-Behoftsitz C, Palizban A, Pombo J, Watts J, Morham SG, Bjarnason I: COX-1 and 2, intestinal integrity, and pathogenesis of nonsteroidal anti-inflammatory drug enteropathy in mice. Gastroenterology. 2002 Jun;122(7):1913-23. Pubmed
  2. Scheiman JM: Outcomes studies of the gastrointestinal safety of cyclooxygenase-2 inhibitors. Cleve Clin J Med. 2002;69 Suppl 1:SI40-6. Pubmed
  3. Reddy BS, Rao CV: Novel approaches for colon cancer prevention by cyclooxygenase-2 inhibitors. J Environ Pathol Toxicol Oncol. 2002;21(2):155-64. Pubmed
  4. Ahmad SR, Kortepeter C, Brinker A, Chen M, Beitz J: Renal failure associated with the use of celecoxib and rofecoxib. Drug Saf. 2002;25(7):537-44. Pubmed
  5. Lu S, Zhang X, Badawi AF, El-Sohemy A, Archer MC: Cyclooxygenase-2 inhibitor celecoxib inhibits promotion of mammary tumorigenesis in rats fed a high fat diet rich in n-6 polyunsaturated fatty acids. Cancer Lett. 2002 Oct 8;184(1):7-12. Pubmed
  6. Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. Pubmed

2. 3-phosphoinositide-dependent protein kinase 1

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: inhibitor

Components

Name UniProt ID Details
3-phosphoinositide-dependent protein kinase 1 O15530 Details

References:

  1. Kulp SK, Yang YT, Hung CC, Chen KF, Lai JP, Tseng PH, Fowble JW, Ward PJ, Chen CS: 3-phosphoinositide-dependent protein kinase-1/Akt signaling represents a major cyclooxygenase-2-independent target for celecoxib in prostate cancer cells. Cancer Res. 2004 Feb 15;64(4):1444-51. Pubmed
  2. Zhu J, Huang JW, Tseng PH, Yang YT, Fowble J, Shiau CW, Shaw YJ, Kulp SK, Chen CS: From the cyclooxygenase-2 inhibitor celecoxib to a novel class of 3-phosphoinositide-dependent protein kinase-1 inhibitors. Cancer Res. 2004 Jun 15;64(12):4309-18. Pubmed
  3. Tong Z, Wu X, Ovcharenko D, Zhu J, Chen CS, Kehrer JP: Neutrophil gelatinase-associated lipocalin as a survival factor. Biochem J. 2005 Oct 15;391(Pt 2):441-8. Pubmed
  4. Li J, Zhu J, Melvin WS, Bekaii-Saab TS, Chen CS, Muscarella P: A structurally optimized celecoxib derivative inhibits human pancreatic cancer cell growth. J Gastrointest Surg. 2006 Feb;10(2):207-14. Pubmed
  5. Tseng PH, Wang YC, Weng SC, Weng JR, Chen CS, Brueggemeier RW, Shapiro CL, Chen CY, Dunn SE, Pollak M, Chen CS: Overcoming trastuzumab resistance in HER2-overexpressing breast cancer cells by using a novel celecoxib-derived phosphoinositide-dependent kinase-1 inhibitor. Mol Pharmacol. 2006 Nov;70(5):1534-41. Epub 2006 Aug 3. Pubmed

Enzymes

1. Cytochrome P450 2C9

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: substrate

Components

Name UniProt ID Details
Cytochrome P450 2C9 P11712 Details

References:

  1. Davies NM, McLachlan AJ, Day RO, Williams KM: Clinical pharmacokinetics and pharmacodynamics of celecoxib: a selective cyclo-oxygenase-2 inhibitor. Clin Pharmacokinet. 2000 Mar;38(3):225-42. Pubmed
  2. Zhou SF, Zhou ZW, Yang LP, Cai JP: Substrates, inducers, inhibitors and structure-activity relationships of human Cytochrome P450 2C9 and implications in drug development. Curr Med Chem. 2009;16(27):3480-675. Epub 2009 Sep 1. Pubmed
  3. Mo SL, Zhou ZW, Yang LP, Wei MQ, Zhou SF: New insights into the structural features and functional relevance of human cytochrome P450 2C9. Part I. Curr Drug Metab. 2009 Dec;10(10):1075-126. Pubmed
  4. Flockhart DA. Drug Interactions: Cytochrome P450 Drug Interaction Table. Indiana University School of Medicine (2007). Accessed May 28, 2010.
  5. 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
  6. Lin Y, Lu P, Tang C, Mei Q, Sandig G, Rodrigues AD, Rushmore TH, Shou M: Substrate inhibition kinetics for cytochrome P450-catalyzed reactions. Drug Metab Dispos. 2001 Apr;29(4 Pt 1):368-74. Pubmed
  7. Rodrigues AD: Impact of CYP2C9 genotype on pharmacokinetics: are all cyclooxygenase inhibitors the same? Drug Metab Dispos. 2005 Nov;33(11):1567-75. Epub 2005 Aug 23. Pubmed

2. Cytochrome P450 3A4

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: substrate

Components

Name UniProt ID Details
Cytochrome P450 3A4 P08684 Details

References:

  1. Zhou SF, Zhou ZW, Yang LP, Cai JP: Substrates, inducers, inhibitors and structure-activity relationships of human Cytochrome P450 2C9 and implications in drug development. Curr Med Chem. 2009;16(27):3480-675. Epub 2009 Sep 1. Pubmed
  2. 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 2D6

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: inhibitor

Components

Name UniProt ID Details
Cytochrome P450 2D6 P10635 Details

References:

  1. Werner U, Werner D, Rau T, Fromm MF, Hinz B, Brune K: Celecoxib inhibits metabolism of cytochrome P450 2D6 substrate metoprolol in humans. Clin Pharmacol Ther. 2003 Aug;74(2):130-7. Pubmed
  2. Flockhart DA. Drug Interactions: Cytochrome P450 Drug Interaction Table. Indiana University School of Medicine (2007). Accessed May 28, 2010.
  3. 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

Carriers

1. Serum albumin

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: substrate

Components

Name UniProt ID Details
Serum albumin P02768 Details

References:

  1. FDA label

2. Alpha-1-acid glycoprotein 1

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: substrate

Components

Name UniProt ID Details
Alpha-1-acid glycoprotein 1 P02763 Details

References:

  1. FDA label

Transporters

1. Multidrug resistance-associated protein 4

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: inhibitor

Components

Name UniProt ID Details
Multidrug resistance-associated protein 4 O15439 Details

References:

  1. Reid G, Wielinga P, Zelcer N, van der Heijden I, Kuil A, de Haas M, Wijnholds J, Borst P: The human multidrug resistance protein MRP4 functions as a prostaglandin efflux transporter and is inhibited by nonsteroidal antiinflammatory drugs. Proc Natl Acad Sci U S A. 2003 Aug 5;100(16):9244-9. Epub 2003 Jun 30. Pubmed

Comments
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Drug created on June 13, 2005 07:24 / Updated on October 08, 2013 14:22