Welcome to DrugBank 4.0! If you prefer, you can still go back to version 3.0.
Identification
NameSulindac
Accession NumberDB00605  (APRD01243)
Typesmall molecule
Groupsapproved
Description

Sulindac is a nonsteroidal anti-inflammatory agent (NSAIA) of the arylalkanoic acid class that is marketed in the U.S. by Merck as Clinoril. Like other NSAIAs, it may be used in the treatment of acute or chronic inflammatory conditions. Sulindac is a prodrug, derived from sulfinylindene, that is converted in vivo to an active sulfide compound by liver enzymes. The sulfide metabolite then undergoes enterohepatic circulation; it is excreted in the bile and then reabsorbed from the intestine. This is thought to help maintain constant blood levels with reduced gastrointestinal side effects. Some studies have shown sulindac to be relatively less irritating to the stomach than other NSAIA’s except for drugs of the cyclooxygenase-2 (COX-2) inhibitor class. The exact mechanism of its NSAIA properties is unknown, but it is thought to act on enzymes COX-1 and COX-2, inhibiting prostaglandin synthesis.

Structure
Thumb
SynonymsNot Available
SaltsNot Available
Brand names
NameCompany
ClinorilMerck
Brand mixturesNot Available
CategoriesNot Available
CAS number38194-50-2
WeightAverage: 356.411
Monoisotopic: 356.088243305
Chemical FormulaC20H17FO3S
InChI KeyInChIKey=MLKXDPUZXIRXEP-MFOYZWKCSA-N
InChI
InChI=1S/C20H17FO3S/c1-12-17(9-13-3-6-15(7-4-13)25(2)24)16-8-5-14(21)10-19(16)18(12)11-20(22)23/h3-10H,11H2,1-2H3,(H,22,23)/b17-9-
IUPAC Name
2-[(1Z)-5-fluoro-1-[(4-methanesulfinylphenyl)methylidene]-2-methyl-1H-inden-3-yl]acetic acid
SMILES
CC1=C(CC(O)=O)C2=CC(F)=CC=C2\C1=C/C1=CC=C(C=C1)S(C)=O
Mass SpecNot Available
Taxonomy
KingdomOrganic Compounds
SuperclassPhenylpropanoids and Polyketides
ClassStilbenes
SubclassNot Available
Direct parentStilbenes
Alternative parentsIndenes and Isoindenes; Fluorobenzenes; Aryl Fluorides; Sulfoxides; Enolates; Polyamines; Carboxylic Acids; Organofluorides
Substituentsindene; fluorobenzene; aryl fluoride; aryl halide; benzene; sulfoxide; enolate; carboxylic acid derivative; carboxylic acid; polyamine; organofluoride; organohalogen
Classification descriptionThis compound belongs to the stilbenes. These are organic compounds containing a 1,2-diphenylethylene moiety. Stilbenes (C6-C2-C6 ) are derived from the common phenylpropene (C6-C3) skeleton building block. The introduction of one or more hydroxyl groups to a phenyl ring lead to stilbenoids.
Pharmacology
IndicationFor acute or long-term use in the relief of signs and symptoms of osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, acute painful shoulder (acute subacromial bursitis/supraspinatus tendinitis), and acute gouty arthritis.
PharmacodynamicsSulindac is a non-steroidal anti-inflammatory indene derivative, also possessing analgesic and antipyretic activities.
Mechanism of actionSulindac's exact mechanism of action is unknown. Its antiinflammatory effects are believed to be due to inhibition of both COX-1 and COX-2 which leads to the inhibition of prostaglandin synthesis. Antipyretic effects may be due to action on the hypothalamus, resulting in an increased peripheral blood flow, vasodilation, and subsequent heat dissipation.
AbsorptionApproximately 90% absorbed in humans following oral administration.
Volume of distributionNot Available
Protein bindingAt 1 mcg/ml concentrations, approximately 93% sulindac and 98% of its sulfide metabolite are bound to human serum albumin.
Metabolism

Undergoes two major biotransformations: reversible reduction to the sulfide metabolite, and irreversible oxidation to the sulfone metabolite. Sulindac and its sulfide and sulfone metabolites undergo extensive enterohepatic circulation. Available evidence indicates that the biological activity resides with the sulfide metabolite. Side chain hydroxylation and hydration of the double bond also occur.

SubstrateEnzymesProduct
Sulindac
    Sulindac sulfideDetails
    Sulindac
      Sulindac sulfoneDetails
      Route of eliminationSulindac is excreted in rat milk; concentrations in milk were 10 to 20% of those levels in plasma. It is not known if sulindac is excreted in human milk. Approximately 50% of the administered dose of sulindac is excreted in the urine with the conjugated sulfone metabolite accounting for the major portion. Hepatic metabolism is an important elimination pathway.
      Half lifeThe mean half-life of sulindac is 7.8 hours while the mean half-life of the sulfide metabolite is 16.4 hours.
      Clearance
      • Renal cl=68.12 +/- 27.56 mL/min [NORMAL (19-41 yrs)]
      ToxicityAcute oral toxicity (LD50) in rats is 264 mg/kg. Cases of overdose have been reported and rarely, deaths have occurred. The following signs and symptoms may be observed following overdose: stupor, coma, diminished urine output and hypotension.
      Affected organisms
      • Humans and other mammals
      Pathways
      PathwayCategorySMPDB ID
      Sulindac Action PathwayDrug actionSMP00094
      SNP Mediated EffectsNot Available
      SNP Mediated Adverse Drug ReactionsNot Available
      ADMET
      Predicted ADMET features
      Property Value Probability
      Human Intestinal Absorption + 0.9937
      Blood Brain Barrier + 0.8325
      Caco-2 permeable - 0.8957
      P-glycoprotein substrate Non-substrate 0.5904
      P-glycoprotein inhibitor I Non-inhibitor 0.5847
      P-glycoprotein inhibitor II Non-inhibitor 0.9949
      Renal organic cation transporter Non-inhibitor 0.8753
      CYP450 2C9 substrate Non-substrate 0.7715
      CYP450 2D6 substrate Non-substrate 0.8961
      CYP450 3A4 substrate Non-substrate 0.5629
      CYP450 1A2 substrate Inhibitor 0.9107
      CYP450 2C9 substrate Non-inhibitor 0.9071
      CYP450 2D6 substrate Non-inhibitor 0.9231
      CYP450 2C19 substrate Non-inhibitor 0.9025
      CYP450 3A4 substrate Non-inhibitor 0.8309
      CYP450 inhibitory promiscuity Low CYP Inhibitory Promiscuity 0.5789
      Ames test Non AMES toxic 0.5451
      Carcinogenicity Non-carcinogens 0.6516
      Biodegradation Not ready biodegradable 1.0
      Rat acute toxicity 3.0989 LD50, mol/kg Not applicable
      hERG inhibition (predictor I) Weak inhibitor 0.9768
      hERG inhibition (predictor II) Non-inhibitor 0.8671
      Pharmacoeconomics
      Manufacturers
      • Merck research laboratories div merck co inc
      • Epic pharma llc
      • Heritage pharmaceuticals inc
      • Mutual pharmaceutical co inc
      • Mylan pharmaceuticals inc
      • Sandoz inc
      • Teva pharmaceuticals usa inc
      • Watson laboratories inc
      Packagers
      Dosage forms
      FormRouteStrength
      TabletOral150 mg
      TabletOral200 mg
      Prices
      Unit descriptionCostUnit
      Sulindac powder17.36USDg
      Clinoril 200 mg tablet1.58USDtablet
      Sulindac 200 mg tablet1.23USDtablet
      Sulindac 150 mg tablet1.0USDtablet
      Apo-Sulin 200 mg Tablet0.51USDtablet
      Novo-Sundac 200 mg Tablet0.51USDtablet
      Nu-Sulindac 200 mg Tablet0.51USDtablet
      Apo-Sulin 150 mg Tablet0.4USDtablet
      Novo-Sundac 150 mg Tablet0.4USDtablet
      Nu-Sulindac 150 mg Tablet0.4USDtablet
      DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.
      PatentsNot Available
      Properties
      Statesolid
      Experimental Properties
      PropertyValueSource
      melting point183 °CPhysProp
      water solubility3000 mg/LMERCK INDEX (1996); pH 7
      logP3.42SANGSTER (1993)
      pKa4.7MERCK INDEX (1996)
      Predicted Properties
      PropertyValueSource
      water solubility2.51e-02 g/lALOGPS
      logP2.96ALOGPS
      logP2.93ChemAxon
      logS-4.2ALOGPS
      pKa (strongest acidic)4.09ChemAxon
      pKa (strongest basic)-6.7ChemAxon
      physiological charge-1ChemAxon
      hydrogen acceptor count3ChemAxon
      hydrogen donor count1ChemAxon
      polar surface area54.37ChemAxon
      rotatable bond count4ChemAxon
      refractivity99.56ChemAxon
      polarizability37.2ChemAxon
      number of rings3ChemAxon
      bioavailability1ChemAxon
      rule of fiveYesChemAxon
      Ghose filterYesChemAxon
      Veber's ruleNoChemAxon
      MDDR-like ruleNoChemAxon
      Spectra
      SpectraNot Available
      References
      Synthesis Reference

      Gary Piazza, Robert Reynolds, “Derivatives of sulindac, use thereof and preparation thereof.” U.S. Patent US20070244122, issued October 18, 2007.

      US20070244122
      General ReferenceNot Available
      External Links
      ResourceLink
      KEGG DrugD00120
      KEGG CompoundC01531
      ChEBI9352
      ChEMBLCHEMBL15770
      Therapeutic Targets DatabaseDAP000569
      PharmGKBPA451565
      Drug Product Database808636
      RxListhttp://www.rxlist.com/cgi/generic3/sulindac.htm
      Drugs.comhttp://www.drugs.com/cdi/sulindac.html
      PDRhealthhttp://www.pdrhealth.com/drug_info/rxdrugprofiles/drugs/cli1087.shtml
      WikipediaSulindac
      ATC CodesM01AB02
      AHFS Codes
      • 28:08.04.92
      PDB EntriesNot Available
      FDA labelshow(106 KB)
      MSDSshow(73.2 KB)
      Interactions
      Drug Interactions
      Drug
      AcenocoumarolThe NSAID, sulindac, may increase the anticoagulant effect of acenocoumarol. Consider alternate therapy or monitor for signs and symptoms of bleeding during concomitant therapy.
      Acetylsalicylic acidRisk 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.
      Aminosalicylic AcidRisk of additive toxicity (e.g. bleed risk). Aminosalicylic acid may decrease the serum concentration of sulindac. Consider alternate therapy or monitor for changes in the therapeutic effects of sulindac and adverse effects of both agents if the interacting agent is initiated, discontinued or dose changed.
      Azilsartan medoxomilIncreases toxicity of each. May deteriorate renal function, particularly in volume depleted or elderly patients. Decreases effects of azilsartan by antagonism.
      BumetanideThe NSAID, sulindac, decreases the diuretic and antihypertensive effects of the loop diuretic, bumetanide.
      CholestyramineThe bile acid sequestrant, cholestyramine, may decrease the absorption of the NSAID, sulindac. Monitor for changes in the therapeutic and adverse effects of sulindac if cholestyramine is initiated, discontinued or dose changed. Administering the two agents 2 or more hours apart may reduce, but not eliminate, the risk of this interactions.
      ColesevelamThe bile acid sequestrant, colesevelam, may decrease the absorption of the NSAID, sulindac. Sulindac should be administered at least 1 hour before or 4 hours after colesevelam. Monitor for changes in the therapeutic and adverse effects of sulindac if colesevelam is initiated, discontinued or dose changed.
      ColestipolThe bile acid sequestrant, colestipol, may decrease the absorption of the NSAID, sulindac. Monitor for changes in the therapeutic and adverse effects of sulindac if colestipol is initiated, discontinued or dose changed. Administering the two agents 2 or more hours apart may reduce, but not eliminate, the risk of this interactions.
      CyclosporineThe NSAID, sulindac, may increase the nephrotoxic effect of cyclosporine. Sulindac may increase the serum concentration of cyclosporine. Consider alternate therapy or monitor for increased cyclosporine levels and nephrotoxicity during concomitant therapy.
      Ethacrynic acidThe NSAID, sulindac, may decrease the diuretic and antihypertensive effects of the loop diuretic, ethacryninc acid.
      FurosemideThe NSAID, sulindac, may decrease the diuretic and antihypertensive effects of the loop diuretic, furosemide.
      Ginkgo bilobaGinkgo biloba may enhance the anticoagulant effect of sulindac. Increased risk of bleeding, bruising and altered mental status due to CNS bleeds. Concomitant therapy should be avoided.
      GinsengGinseng may enhance the anticoagulant effect of sulindac. Increased risk of bleeding, bruising and altered mental status due to CNS bleeds. Concomitant therapy should be avoided.
      KetorolacMay cause additive or synergistic NSAID toxicities (e.g. GI bleeding, renal dysfunction, etc.). Concomitant therapy is contraindicated.
      MethotrexateThe NSAID, sulindac, may decrease the clearance methotrexate. Consider alternate therapy, especially in patients receiving high antineoplastic doses of methotrexate. Otherwise, monitor for hematologic and renal toxicities.
      PemetrexedThe NSAID, sulindac, may increase the serum concentration of pemetrexed by decreasing its elimination. This interaction more prevalent in patients with mild to moderate renal insufficiency. Consider alternate therapy or monitor for pemetrexed toxicity during concomitant therapy.
      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.
      S-AdenosylmethionineS-adenosylmethionine may enhance the anticoagulant effect of sulindac. Increased risk of bleeding, bruising and altered mental status due to CNS bleeds. Concomitant therapy should be avoided.
      Salicylate-sodiumRisk of additive toxicity (e.g. bleed risk). Salicylate-sodium may decrease the serum concentration of sulindac. Consider alternate therapy or monitor for changes in the therapeutic effects of sulindac and adverse effects of both agents if the interacting agent is initiated, discontinued or dose changed.
      SalsalateRisk of additive toxicity (e.g. bleed risk). Salsalate may decrease the serum concentration of sulindac. Consider alternate therapy or monitor for changes in the therapeutic effects of sulindac and adverse effects of both agents if the interacting agent is initiated, discontinued or dose changed.
      TelmisartanConcomitant use of Telmisartan and Sulindac may increase the risk of acute renal failure and hyperkalemia. Monitor renal function at the beginning and during treatment.
      TimololThe NSAID, Sulindac, may antagonize the antihypertensive effect of Timolol.
      TrandolaprilThe NSAID, Sulindac, may reduce the antihypertensive effect of Trandolapril. Consider alternate therapy or monitor for changes in Trandolapril efficacy if Sulindac is initiated, discontinued or dose changed.
      TreprostinilThe prostacyclin analogue, Treprostinil, may increase the risk of bleeding when combined with the NSAID, Sulindac. Monitor for increased bleeding during concomitant thearpy.
      WarfarinThe antiplatelet effects of sulindac may increase the bleed risk associated with warfarin. Consider alternate therapy or monitor for signs and symptoms of bleeding during concomitant therapy.
      Food InteractionsNot Available

      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. Giuliano F, Warner TD: Ex vivo assay to determine the cyclooxygenase selectivity of non-steroidal anti-inflammatory drugs. Br J Pharmacol. 1999 Apr;126(8):1824-30. Pubmed
      2. Molina MA, Sitja-Arnau M, Lemoine MG, Frazier ML, Sinicrope FA: Increased cyclooxygenase-2 expression in human pancreatic carcinomas and cell lines: growth inhibition by nonsteroidal anti-inflammatory drugs. Cancer Res. 1999 Sep 1;59(17):4356-62. Pubmed
      3. Yip-Schneider MT, Barnard DS, Billings SD, Cheng L, Heilman DK, Lin A, Marshall SJ, Crowell PL, Marshall MS, Sweeney CJ: Cyclooxygenase-2 expression in human pancreatic adenocarcinomas. Carcinogenesis. 2000 Feb;21(2):139-46. Pubmed
      4. Fosslien E: Biochemistry of cyclooxygenase (COX)-2 inhibitors and molecular pathology of COX-2 in neoplasia. Crit Rev Clin Lab Sci. 2000 Oct;37(5):431-502. Pubmed
      5. Taylor MT, Lawson KR, Ignatenko NA, Marek SE, Stringer DE, Skovan BA, Gerner EW: Sulindac sulfone inhibits K-ras-dependent cyclooxygenase-2 expression in human colon cancer cells. Cancer Res. 2000 Dec 1;60(23):6607-10. Pubmed

      2. Prostaglandin G/H synthase 1

      Kind: protein

      Organism: Human

      Pharmacological action: unknown

      Actions: inhibitor

      Components

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

      References:

      1. Giuliano F, Warner TD: Ex vivo assay to determine the cyclooxygenase selectivity of non-steroidal anti-inflammatory drugs. Br J Pharmacol. 1999 Apr;126(8):1824-30. Pubmed
      2. Lim JT, Piazza GA, Han EK, Delohery TM, Li H, Finn TS, Buttyan R, Yamamoto H, Sperl GJ, Brendel K, Gross PH, Pamukcu R, Weinstein IB: Sulindac derivatives inhibit growth and induce apoptosis in human prostate cancer cell lines. Biochem Pharmacol. 1999 Oct 1;58(7):1097-107. Pubmed
      3. Soriano AF, Helfrich B, Chan DC, Heasley LE, Bunn PA Jr, Chou TC: Synergistic effects of new chemopreventive agents and conventional cytotoxic agents against human lung cancer cell lines. Cancer Res. 1999 Dec 15;59(24):6178-84. Pubmed
      4. Cheng ZJ, Tikkanen I, Vapaatalo H, Mervaala EM: Vascular effects of COX inhibition and AT1 receptor blockade in transgenic rats harboring mouse renin-2 gene. J Physiol Pharmacol. 2002 Dec;53(4 Pt 1):597-613. Pubmed
      5. Cheng ZJ, Finckenberg P, Louhelainen M, Merasto S, Tikkanen I, Vapaatalo H, Mervaala EM: Cardiovascular and renal effects of cyclooxygenase inhibition in transgenic rats harboring mouse renin-2 gene (TGR[mREN2]27). Eur J Pharmacol. 2003 Feb 14;461(2-3):159-69. Pubmed

      3. Aldose reductase

      Kind: protein

      Organism: Human

      Pharmacological action: unknown

      Actions: inhibitor

      Components

      Name UniProt ID Details
      Aldose reductase P15121 Details

      References:

      1. Sharma YR, Vajpayee RB, Bhatnagar R, Mohan M, Azad RV, Kumar M, Nath R: Topical sulindac therapy in diabetic senile cataracts: cataract-IV. Indian J Ophthalmol. 1989 Jul-Sep;37(3):127-33. Pubmed
      2. Crabbe MJ, Freeman G, Halder AB, Bron AJ: The inhibition of bovine lens aldose reductase by Clinoril, its absorption into the human red cell and its effect on human red cell aldose reductase activity. Ophthalmic Res. 1985;17(2):85-9. Pubmed
      3. Chaudhry PS, Cabrera J, Juliani HR, Varma SD: Inhibition of human lens aldose reductase by flavonoids, sulindac and indomethacin. Biochem Pharmacol. 1983 Jul 1;32(13):1995-8. Pubmed
      4. Jacobson M, Sharma YR, Cotlier E, Hollander JD: Diabetic complications in lens and nerve and their prevention by sulindac or sorbinil: two novel aldose reductase inhibitors. Invest Ophthalmol Vis Sci. 1983 Oct;24(10):1426-9. Pubmed
      5. van der Sloot P, Mizisin A, Zochodne D: Sulindac in established experimental diabetes: a follow-up study. Can J Neurol Sci. 1995 Aug;22(3):198-201. Pubmed
      6. Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. Pubmed

      4. Mitogen-activated protein kinase 3

      Kind: protein

      Organism: Human

      Pharmacological action: unknown

      Actions: inhibitor

      Components

      Name UniProt ID Details
      Mitogen-activated protein kinase 3 P27361 Details

      References:

      1. Rice PL, Goldberg RJ, Ray EC, Driggers LJ, Ahnen DJ: Inhibition of extracellular signal-regulated kinase 1/2 phosphorylation and induction of apoptosis by sulindac metabolites. Cancer Res. 2001 Feb 15;61(4):1541-7. Pubmed
      2. Rice PL, Washington M, Schleman S, Beard KS, Driggers LJ, Ahnen DJ: Sulindac sulfide inhibits epidermal growth factor-induced phosphorylation of extracellular-regulated kinase 1/2 and Bad in human colon cancer cells. Cancer Res. 2003 Feb 1;63(3):616-20. Pubmed
      3. Rice PL, Beard KS, Driggers LJ, Ahnen DJ: Inhibition of extracellular-signal regulated kinases 1/2 is required for apoptosis of human colon cancer cells in vitro by sulindac metabolites. Cancer Res. 2004 Nov 15;64(22):8148-51. Pubmed
      4. Pangburn HA, Kraus H, Ahnen DJ, Rice PL: Sulindac metabolites inhibit epidermal growth factor receptor activation and expression. J Carcinog. 2005 Sep 2;4:16. Pubmed
      5. Rice PL, Peters SL, Beard KS, Ahnen DJ: Sulindac independently modulates extracellular signal-regulated kinase 1/2 and cyclic GMP-dependent protein kinase signaling pathways. Mol Cancer Ther. 2006 Mar;5(3):746-54. Pubmed

      5. Peroxisome proliferator-activated receptor delta

      Kind: protein

      Organism: Human

      Pharmacological action: unknown

      Actions: negative modulator

      Components

      Name UniProt ID Details
      Peroxisome proliferator-activated receptor delta Q03181 Details

      References:

      1. He TC, Chan TA, Vogelstein B, Kinzler KW: PPARdelta is an APC-regulated target of nonsteroidal anti-inflammatory drugs. Cell. 1999 Oct 29;99(3):335-45. Pubmed
      2. Babbar N, Ignatenko NA, Casero RA Jr, Gerner EW: Cyclooxygenase-independent induction of apoptosis by sulindac sulfone is mediated by polyamines in colon cancer. J Biol Chem. 2003 Nov 28;278(48):47762-75. Epub 2003 Sep 23. Pubmed
      3. Jarvis MC, Gray TJ, Palmer CN: Both PPARgamma and PPARdelta influence sulindac sulfide-mediated p21WAF1/CIP1 upregulation in a human prostate epithelial cell line. Oncogene. 2005 Dec 8;24(55):8211-5. Pubmed
      4. Kim DJ, Prabhu KS, Gonzalez FJ, Peters JM: Inhibition of chemically induced skin carcinogenesis by sulindac is independent of peroxisome proliferator-activated receptor-beta/delta (PPARbeta/delta). Carcinogenesis. 2006 May;27(5):1105-12. Epub 2006 Jan 16. Pubmed
      5. Liou JY, Ghelani D, Yeh S, Wu KK: Nonsteroidal anti-inflammatory drugs induce colorectal cancer cell apoptosis by suppressing 14-3-3epsilon. Cancer Res. 2007 Apr 1;67(7):3185-91. Pubmed

      6. Prostaglandin D2 receptor 2

      Kind: protein

      Organism: Human

      Pharmacological action: unknown

      Actions: antagonist

      Components

      Name UniProt ID Details
      Prostaglandin D2 receptor 2 Q9Y5Y4 Details

      References:

      1. Hata AN, Lybrand TP, Marnett LJ, Breyer RM: Structural determinants of arylacetic acid nonsteroidal anti-inflammatory drugs necessary for binding and activation of the prostaglandin D2 receptor CRTH2. Mol Pharmacol. 2005 Mar;67(3):640-7. Epub 2004 Nov 24. Pubmed

      1. Cytochrome P450 1A1

      Kind: protein

      Organism: Human

      Pharmacological action: unknown

      Actions: inhibitor

      Components

      Name UniProt ID Details
      Cytochrome P450 1A1 P04798 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 1A2

      Kind: protein

      Organism: Human

      Pharmacological action: unknown

      Actions: inhibitor

      Components

      Name UniProt ID Details
      Cytochrome P450 1A2 P05177 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: unknown

      Components

      Name UniProt ID Details
      Serum albumin P02768 Details

      References:

      1. Russeva VN, Zhivkova ZD: Molecular basis of sulindac competition with specific markers for the major binding sites on human serum albumin. Arzneimittelforschung. 2003;53(3):174-81. Pubmed
      2. Shams-Eldeen MA, Vallner JJ, Needham TE: Interaction of sulindac and metabolite with human serum albumin. J Pharm Sci. 1978 Aug;67(8):1077-80. Pubmed
      3. Zhivkova ZD, Russeva VN: Thermodynamic characterization of the binding process of sulindac to human serum albumin. Arzneimittelforschung. 2003;53(1):53-6. 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. Kuze K, Graves P, Leahy A, Wilson P, Stuhlmann H, You G: Heterologous expression and functional characterization of a mouse renal organic anion transporter in mammalian cells. J Biol Chem. 1999 Jan 15;274(3):1519-24. Pubmed

      Comments
      Drug created on June 13, 2005 07:24 / Updated on September 16, 2013 17:11