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Identification
NameDiflunisal
Accession NumberDB00861  (APRD00922, DB06895)
TypeSmall Molecule
GroupsApproved
Description

Diflunisal, a salicylate derivative, is a nonsteroidal anti-inflammatory agent (NSAIA) with pharmacologic actions similar to other prototypical NSAIAs. Diflunisal possesses anti-inflammatory, analgesic and antipyretic activity. Though its mechanism of action has not been clearly established, most of its actions appear to be associated with inhibition of prostaglandin synthesis via the arachidonic acid pathway. Diflunisal is used to relieve pain accompanied with inflammation and in the symptomatic treatment of rheumatoid arthritis and osteoarthritis.

Structure
Thumb
Synonyms
SynonymLanguageCode
2-(Hydroxy)-5-(2,4-difluorophenyl)benzoic acidNot AvailableNot Available
2',4'-Difluoro-4-hydroxy-3-biphenylcarboxylic acidNot AvailableNot Available
5-(2,4-Difluorophenyl)salicylic acidNot AvailableNot Available
DiflunisalGermanINN
DiflunisalFrenchINN
DiflunisalSpanishINN
DiflunisalumLatinINN
DolobidNot AvailableNot Available
Prescription ProductsNot Available
Generic Prescription Products
NameDosageStrengthRouteLabellerMarketing StartMarketing End
Diflunisaltablet, film coated500 mgoralTeva Pharmaceuticals USA Inc1992-11-01Not AvailableUs 0a2ef1ad1c84951dc1392a8bbe1f3cb241c91ed59e44ad8268635315440d978c
Diflunisaltablet, film coated500 mgoralA S Medication Solutions Llc1992-11-01Not AvailableUs 0a2ef1ad1c84951dc1392a8bbe1f3cb241c91ed59e44ad8268635315440d978c
Diflunisaltablet, film coated500 mgoralPhysicians Total Care, Inc.2009-07-21Not AvailableUs 0a2ef1ad1c84951dc1392a8bbe1f3cb241c91ed59e44ad8268635315440d978c
Diflunisaltablet, film coated500 mgoralPd Rx Pharmaceuticals, Inc.2010-08-20Not AvailableUs 0a2ef1ad1c84951dc1392a8bbe1f3cb241c91ed59e44ad8268635315440d978c
Diflunisaltablet, film coated500 mgoralRising Pharmaceuticals Inc.2012-05-01Not AvailableUs 0a2ef1ad1c84951dc1392a8bbe1f3cb241c91ed59e44ad8268635315440d978c
Diflunisaltablet, film coated500 mgoralCarilion Materials Management1992-11-01Not AvailableUs 0a2ef1ad1c84951dc1392a8bbe1f3cb241c91ed59e44ad8268635315440d978c
Diflunisaltablet500 mgoralAa Pharma IncNot AvailableNot AvailableCanada 5f16b84899037e23705f146ff57e3794121879cb055f0954756d94bc690476b4
Diflunisaltablet250 mgoralAa Pharma IncNot AvailableNot AvailableCanada 5f16b84899037e23705f146ff57e3794121879cb055f0954756d94bc690476b4
Over the Counter ProductsNot Available
International Brands
NameCompany
AntonEverest
DolobidMerck
Brand mixturesNot Available
SaltsNot Available
Categories
CAS number22494-42-4
WeightAverage: 250.1976
Monoisotopic: 250.044150532
Chemical FormulaC13H8F2O3
InChI KeyHUPFGZXOMWLGNK-UHFFFAOYSA-N
InChI
InChI=1S/C13H8F2O3/c14-8-2-3-9(11(15)6-8)7-1-4-12(16)10(5-7)13(17)18/h1-6,16H,(H,17,18)
IUPAC Name
5-(2,4-difluorophenyl)-2-hydroxybenzoic acid
SMILES
OC(=O)C1=C(O)C=CC(=C1)C1=C(F)C=C(F)C=C1
Taxonomy
DescriptionThis compound belongs to the class of organic compounds known as biphenyls and derivatives. These are organic compounds containing to benzene rings linked together by a C-C bond.
KingdomOrganic compounds
Super ClassBenzenoids
ClassBenzene and substituted derivatives
Sub ClassBiphenyls and derivatives
Direct ParentBiphenyls and derivatives
Alternative Parents
Substituents
  • Biphenyl
  • Salicylic acid
  • Salicylic acid or derivatives
  • Hydroxybenzoic acid
  • Benzoic acid
  • Benzoic acid or derivatives
  • Benzoyl
  • Phenol
  • Halobenzene
  • Fluorobenzene
  • Aryl halide
  • Aryl fluoride
  • Vinylogous acid
  • Monocarboxylic acid or derivatives
  • Carboxylic acid
  • Carboxylic acid derivative
  • Hydrocarbon derivative
  • Organooxygen compound
  • Organofluoride
  • Organohalogen compound
  • Carbonyl group
  • Aromatic homomonocyclic compound
Molecular FrameworkAromatic homomonocyclic compounds
External Descriptors
Pharmacology
IndicationFor symptomatic treatment of mild to moderate pain accompanied by inflammation (e.g. musculoskeletal trauma, post-dental extraction, post-episiotomy), osteoarthritis, and rheumatoid arthritis.
PharmacodynamicsDiflunisal is a nonsteroidal drug with analgesic, anti-inflammatory and antipyretic properties. It is a peripherally-acting non-narcotic analgesic drug. Habituation, tolerance and addiction have not been reported. Diflunisal is a difluorophenyl derivative of salicylic acid. Chemically, diflunisal differs from aspirin (acetylsalicylic acid) in two respects. The first of these two is the presence of a difluorophenyl substituent at carbon 1. The second difference is the removal of the 0-acetyl group from the carbon 4 position. Diflunisal is not metabolized to salicylic acid, and the fluorine atoms are not displaced from the difluorophenyl ring structure.
Mechanism of actionThe precise mechanism of the analgesic and anti-inflammatory actions of diflunisal is not known. Diflunisal is a prostaglandin synthetase inhibitor. In animals, prostaglandins sensitize afferent nerves and potentiate the action of bradykinin in inducing pain. Since prostaglandins are known to be among the mediators of pain and inflammation, the mode of action of diflunisal may be due to a decrease of prostaglandins in peripheral tissues.
AbsorptionRapidly and completely absorbed following oral administration, with a bioavailability of 80-90%. Peak plasma concentrations are achieved 2 - 3 hours following oral administration.
Volume of distributionNot Available
Protein bindingAt least 98 to 99% of diflunisal in plasma is bound to proteins.
Metabolism

Hepatic, primarily via glucuronide conjugation (90% of administered dose).

Route of eliminationThe drug is excreted in the urine as two soluble glucuronide conjugates accounting for about 90% of the administered dose. Little or no diflunisal is excreted in the feces.
Half life8 to 12 hours
ClearanceNot Available
ToxicityOral LD50 in rat, mouse, and rabbit is 392 mg/kg, 439 mg/kg, and 603 mg/kg, respectively. Symptoms of overdose include drowsiness, nausea, vomiting, diarrhea, hyperventilation, tachycardia, sweating, tinnitus, disorientation, stupor, and coma. The lowest dose without the presence of other medicines which caused death was 15 grams.

Selective COX-2 inhibitors have been associated with increased risk of serious cardiovascular events (e.g. myocardial infarction, stroke) in some patients. Current data is insufficient to assess the cardiovascular risk of diflunisal. Short-term use does not appear to be associated with increased cardiovascular risk (except when used immediately following coronary artery bypass graft (CABG) surgery). Risk of GI toxicity including bleeding, ulceration and perforation. Risk of direct renal injury, including renal papillary necrosis. Severe hepatic reactions, including cholestasis and/or jaundice, have been reported. May cause rash or hypersensitivity syndrome.

Affected organisms
  • Humans and other mammals
Pathways
PathwayCategorySMPDB ID
Diflunisal Action PathwayDrug actionSMP00289
SNP Mediated EffectsNot Available
SNP Mediated Adverse Drug ReactionsNot Available
ADMET
Predicted ADMET features
PropertyValueProbability
Human Intestinal Absorption+0.9945
Blood Brain Barrier+0.8047
Caco-2 permeable+0.8866
P-glycoprotein substrateNon-substrate0.6927
P-glycoprotein inhibitor INon-inhibitor0.9407
P-glycoprotein inhibitor IINon-inhibitor0.9735
Renal organic cation transporterNon-inhibitor0.911
CYP450 2C9 substrateNon-substrate0.7982
CYP450 2D6 substrateNon-substrate0.9201
CYP450 3A4 substrateNon-substrate0.7145
CYP450 1A2 substrateNon-inhibitor0.9046
CYP450 2C9 substrateInhibitor0.6684
CYP450 2D6 substrateNon-inhibitor0.9357
CYP450 2C19 substrateNon-inhibitor0.9025
CYP450 3A4 substrateNon-inhibitor0.8309
CYP450 inhibitory promiscuityLow CYP Inhibitory Promiscuity0.5156
Ames testNon AMES toxic0.9666
CarcinogenicityNon-carcinogens0.7828
BiodegradationNot ready biodegradable0.988
Rat acute toxicity2.7735 LD50, mol/kg Not applicable
hERG inhibition (predictor I)Weak inhibitor0.983
hERG inhibition (predictor II)Non-inhibitor0.9178
Pharmacoeconomics
Manufacturers
  • Purepac pharmaceutical co
  • Roxane laboratories inc
  • Sandoz inc
  • Teva pharmaceuticals usa inc
  • Watson laboratories inc
  • Merck and co inc
Packagers
Dosage forms
FormRouteStrength
Tabletoral250 mg
Tabletoral500 mg
Tablet, film coatedoral500 mg
Prices
Unit descriptionCostUnit
Dolobid 60 500 mg tablet Bottle92.83USD bottle
Diflunisal 250 mg tablet1.74USD tablet
Diflunisal powder1.56USD g
Diflunisal 500 mg tablet1.46USD tablet
Apo-Diflunisal 500 mg Tablet0.75USD tablet
DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.
PatentsNot Available
Properties
StateSolid
Experimental Properties
PropertyValueSource
melting point210-211Ruyle, W.V., Jarett, L.H. and Matzuk, A.R. ; U S . Patent 3,714,226; January 30, 1973; assigned to Merck & Co., Inc.
water solubilityPractically insoluble (14.5 mg/L) at neutral or acidic pH.Not Available
logP4.44SANGSTER (1993)
Predicted Properties
PropertyValueSource
Water Solubility0.0711 mg/mLALOGPS
logP3.11ALOGPS
logP3.91ChemAxon
logS-3.5ALOGPS
pKa (Strongest Acidic)2.69ChemAxon
pKa (Strongest Basic)-6.3ChemAxon
Physiological Charge-1ChemAxon
Hydrogen Acceptor Count3ChemAxon
Hydrogen Donor Count2ChemAxon
Polar Surface Area57.53 Å2ChemAxon
Rotatable Bond Count2ChemAxon
Refractivity60.86 m3·mol-1ChemAxon
Polarizability22.29 Å3ChemAxon
Number of Rings2ChemAxon
Bioavailability1ChemAxon
Rule of FiveYesChemAxon
Ghose FilterYesChemAxon
Veber's RuleYesChemAxon
MDDR-like RuleYesChemAxon
Spectra
Mass Spec (NIST)Not Available
SpectraMS
References
Synthesis Reference

Ruyle, W.V., Jarett, L.H. and Matzuk, A.R. ; U S . Patent 3,714,226; January 30, 1973; assigned to Merck & Co., Inc.

General ReferenceNot Available
External Links
ATC CodesN02BA11
AHFS Codes
  • 28:08.04.92
PDB EntriesNot Available
FDA labelDownload (94.1 KB)
MSDSDownload (73.4 KB)
Interactions
Drug Interactions
Drug
AbciximabAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
AcenocoumarolAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
Acetylsalicylic acidNSAID (Nonselective) may enhance the adverse/toxic effect of Salicylates. An increased risk of bleeding may be associated with use of this combination. NSAID (Nonselective) may diminish the cardioprotective effect of Salicylates. Salicylates may decrease the serum concentration of NSAID (Nonselective). Exceptions: Choline Magnesium Trisalicylate.
AliskirenNonsteroidal Anti-Inflammatory Agents may diminish the antihypertensive effect of Aliskiren. Nonsteroidal Anti-Inflammatory Agents may enhance the nephrotoxic effect of Aliskiren.
AlteplaseAgents with Antiplatelet Properties may enhance the anticoagulant effect of Thrombolytic Agents.
AmikacinNonsteroidal Anti-Inflammatory Agents may decrease the excretion of Aminoglycosides. Data only in premature infants.
AnistreplaseAgents with Antiplatelet Properties may enhance the anticoagulant effect of Thrombolytic Agents.
ApixabanAgents with Antiplatelet Properties may enhance the adverse/toxic effect of Apixaban. Specifically, the risk for bleeding may be increased.
ArbekacinNonsteroidal Anti-Inflammatory Agents may decrease the excretion of Aminoglycosides. Data only in premature infants.
Citric AcidAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
ColesevelamMay decrease the absorption of Nonsteroidal Anti-Inflammatory Agents.
Dabigatran etexilateAgents with Antiplatelet Properties may enhance the anticoagulant effect of Dabigatran Etexilate. Agents with Antiplatelet Properties may increase the serum concentration of Dabigatran Etexilate. This mechanism applies specifically to clopidogrel.
DalteparinAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
DasatinibMay enhance the anticoagulant effect of Agents with Antiplatelet Properties.
DeferasiroxNonsteroidal Anti-Inflammatory Agents may enhance the adverse/toxic effect of Deferasirox. Specifically, the risk for GI ulceration/irritation or GI bleeding may be increased.
Deoxycholic AcidAgents with Antiplatelet Properties may enhance the adverse/toxic effect of Deoxycholic Acid. Specifically, the risk for bleeding or bruising in the treatment area may be increased.
DesmopressinNonsteroidal Anti-Inflammatory Agents may enhance the adverse/toxic effect of Desmopressin.
DicoumarolAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
DigoxinNonsteroidal Anti-Inflammatory Agents may increase the serum concentration of Digoxin.
Edetic AcidAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
EnoxaparinAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
EplerenoneNonsteroidal Anti-Inflammatory Agents may diminish the antihypertensive effect of Eplerenone. Nonsteroidal Anti-Inflammatory Agents may enhance the hyperkalemic effect of Eplerenone.
Ethyl biscoumacetateAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
FloctafenineMay enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents.
Fondaparinux sodiumAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
FramycetinNonsteroidal Anti-Inflammatory Agents may decrease the excretion of Aminoglycosides. Data only in premature infants.
GentamicinNonsteroidal Anti-Inflammatory Agents may decrease the excretion of Aminoglycosides. Data only in premature infants.
GlucosamineMay enhance the antiplatelet effect of Agents with Antiplatelet Properties.
HaloperidolNonsteroidal Anti-Inflammatory Agents may enhance the adverse/toxic effect of Haloperidol. Specifically including drowsiness and confusion.
HeparinAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
HydralazineNonsteroidal Anti-Inflammatory Agents may diminish the antihypertensive effect of HydrALAZINE.
IbritumomabAgents with Antiplatelet Properties may enhance the adverse/toxic effect of Ibritumomab. Both agents may contribute to impaired platelet function and an increased risk of bleeding.
KanamycinNonsteroidal Anti-Inflammatory Agents may decrease the excretion of Aminoglycosides. Data only in premature infants.
LithiumNonsteroidal Anti-Inflammatory Agents may increase the serum concentration of Lithium.
MethotrexateNonsteroidal Anti-Inflammatory Agents may increase the serum concentration of Methotrexate.
NeomycinNonsteroidal Anti-Inflammatory Agents may decrease the excretion of Aminoglycosides. Data only in premature infants.
NetilmicinNonsteroidal Anti-Inflammatory Agents may decrease the excretion of Aminoglycosides. Data only in premature infants.
ObinutuzumabAgents with Antiplatelet Properties may enhance the adverse/toxic effect of Obinutuzumab. Specifically, the risk of serious bleeding-related events may be increased.
PemetrexedNSAID (Nonselective) may increase the serum concentration of PEMEtrexed.
PentoxifyllineMay enhance the antiplatelet effect of Agents with Antiplatelet Properties.
PhenindioneAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
PhenprocoumonAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
PorfimerPhotosensitizing Agents may enhance the photosensitizing effect of Porfimer.
PralatrexateNonsteroidal Anti-Inflammatory Agents may increase the serum concentration of PRALAtrexate. More specifically, NSAIDS may decrease the renal excretion of pralatrexate.
ProbenecidMay increase the serum concentration of Nonsteroidal Anti-Inflammatory Agents.
ReteplaseAgents with Antiplatelet Properties may enhance the anticoagulant effect of Thrombolytic Agents.
RibostamycinNonsteroidal Anti-Inflammatory Agents may decrease the excretion of Aminoglycosides. Data only in premature infants.
RidogrelAgents with Antiplatelet Properties may enhance the anticoagulant effect of Thrombolytic Agents.
RivaroxabanAgents with Antiplatelet Properties may enhance the anticoagulant effect of Rivaroxaban.
Salicylate-sodiumNSAID (Nonselective) may enhance the adverse/toxic effect of Salicylates. An increased risk of bleeding may be associated with use of this combination. NSAID (Nonselective) may diminish the cardioprotective effect of Salicylates. Salicylates may decrease the serum concentration of NSAID (Nonselective). Exceptions: Choline Magnesium Trisalicylate.
SpectinomycinNonsteroidal Anti-Inflammatory Agents may decrease the excretion of Aminoglycosides. Data only in premature infants.
StreptokinaseAgents with Antiplatelet Properties may enhance the anticoagulant effect of Thrombolytic Agents.
StreptomycinNonsteroidal Anti-Inflammatory Agents may decrease the excretion of Aminoglycosides. Data only in premature infants.
SulodexideAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
TenecteplaseAgents with Antiplatelet Properties may enhance the anticoagulant effect of Thrombolytic Agents.
TenofovirNonsteroidal Anti-Inflammatory Agents may enhance the adverse/toxic effect of Tenofovir.
TipranavirMay enhance the antiplatelet effect of Agents with Antiplatelet Properties.
TobramycinNonsteroidal Anti-Inflammatory Agents may decrease the excretion of Aminoglycosides. Data only in premature infants.
TreprostinilAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
UrokinaseAgents with Antiplatelet Properties may enhance the anticoagulant effect of Thrombolytic Agents.
VancomycinNonsteroidal Anti-Inflammatory Agents may increase the serum concentration of Vancomycin.
VerteporfinPhotosensitizing Agents may enhance the photosensitizing effect of Verteporfin.
Vitamin EMay enhance the antiplatelet effect of Agents with Antiplatelet Properties.
WarfarinAgents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants.
Food Interactions
  • Avoid alcohol.
  • Food slightly delays rate of absorption with no effect on extent of absorption.
  • Take with food to reduce gastric irritation.

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. Cappon GD, Cook JC, Hurtt ME: Relationship between cyclooxygenase 1 and 2 selective inhibitors and fetal development when administered to rats and rabbits during the sensitive periods for heart development and midline closure. Birth Defects Res B Dev Reprod Toxicol. 2003 Feb;68(1):47-56. Pubmed
  2. Jeske AH: COX-2 inhibitors and dental pain control. J Gt Houst Dent Soc. 1999 Nov;71(4):39-40. Pubmed
  3. Mao H, Hajduk PJ, Craig R, Bell R, Borre T, Fesik SW: Rational design of diflunisal analogues with reduced affinity for human serum albumin. J Am Chem Soc. 2001 Oct 31;123(43):10429-35. Pubmed
  4. Moore PA, Hersh EV: Celecoxib and rofecoxib. The role of COX-2 inhibitors in dental practice. J Am Dent Assoc. 2001 Apr;132(4):451-6. Pubmed
  5. Young JM, Panah S, Satchawatcharaphong C, Cheung PS: Human whole blood assays for inhibition of prostaglandin G/H synthases-1 and -2 using A23187 and lipopolysaccharide stimulation of thromboxane B2 production. Inflamm Res. 1996 May;45(5):246-53. 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 1

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: inhibitor

Components

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

References:

  1. Cappon GD, Cook JC, Hurtt ME: Relationship between cyclooxygenase 1 and 2 selective inhibitors and fetal development when administered to rats and rabbits during the sensitive periods for heart development and midline closure. Birth Defects Res B Dev Reprod Toxicol. 2003 Feb;68(1):47-56. Pubmed
  2. Chen QH, Rao PN, Knaus EE: Design, synthesis, and biological evaluation of N-acetyl-2-carboxybenzenesulfonamides: a novel class of cyclooxygenase-2 (COX-2) inhibitors. Bioorg Med Chem. 2005 Apr 1;13(7):2459-68. Pubmed
  3. Young JM, Panah S, Satchawatcharaphong C, Cheung PS: Human whole blood assays for inhibition of prostaglandin G/H synthases-1 and -2 using A23187 and lipopolysaccharide stimulation of thromboxane B2 production. Inflamm Res. 1996 May;45(5):246-53. Pubmed

Enzymes

1. UDP-glucuronosyltransferase 1-8

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: substrate

Components

Name UniProt ID Details
UDP-glucuronosyltransferase 1-8 Q9HAW9 Details

References:

  1. Cheng Z, Radominska-Pandya A, Tephly TR: Studies on the substrate specificity of human intestinal UDP- lucuronosyltransferases 1A8 and 1A10. Drug Metab Dispos. 1999 Oct;27(10):1165-70. Pubmed

Carriers

1. Transthyretin

Kind: protein

Organism: Human

Pharmacological action: unknown

Components

Name UniProt ID Details
Transthyretin P02766 Details

References:

  1. Adamski-Werner SL, Palaninathan SK, Sacchettini JC, Kelly JW: Diflunisal analogues stabilize the native state of transthyretin. Potent inhibition of amyloidogenesis. J Med Chem. 2004 Jan 15;47(2):355-74. Pubmed
  2. Almeida MR, Macedo B, Cardoso I, Alves I, Valencia G, Arsequell G, Planas A, Saraiva MJ: Selective binding to transthyretin and tetramer stabilization in serum from patients with familial amyloidotic polyneuropathy by an iodinated diflunisal derivative. Biochem J. 2004 Jul 15;381(Pt 2):351-6. Pubmed
  3. Gales L, Macedo-Ribeiro S, Arsequell G, Valencia G, Saraiva MJ, Damas AM: Human transthyretin in complex with iododiflunisal: structural features associated with a potent amyloid inhibitor. Biochem J. 2005 Jun 1;388(Pt 2):615-21. Pubmed
  4. Miller SR, Sekijima Y, Kelly JW: Native state stabilization by NSAIDs inhibits transthyretin amyloidogenesis from the most common familial disease variants. Lab Invest. 2004 May;84(5):545-52. Pubmed
  5. Tojo K, Sekijima Y, Kelly JW, Ikeda S: Diflunisal stabilizes familial amyloid polyneuropathy-associated transthyretin variant tetramers in serum against dissociation required for amyloidogenesis. Neurosci Res. 2006 Dec;56(4):441-9. Epub 2006 Oct 6. Pubmed

2. Serum albumin

Kind: protein

Organism: Human

Pharmacological action: unknown

Components

Name UniProt ID Details
Serum albumin P02768 Details

References:

  1. Davilas A, Koupparis M, Macheras P, Valsami G: In-vitro study on the competitive binding of diflunisal and uraemic toxins to serum albumin and human plasma using a potentiometric ion-probe technique. J Pharm Pharmacol. 2006 Nov;58(11):1467-74. Pubmed
  2. Mao H, Hajduk PJ, Craig R, Bell R, Borre T, Fesik SW: Rational design of diflunisal analogues with reduced affinity for human serum albumin. J Am Chem Soc. 2001 Oct 31;123(43):10429-35. Pubmed
  3. Rehse K, Fiedler B: [Determination of the protein binding of drugs by continuous ultrafiltration. 9. Comparison of the binding of nonsteroid antirheumatics to human serum albumin and their interaction with phenprocoumon] Arch Pharm (Weinheim). 1989 Apr;322(4):241-3. Pubmed
  4. Verbeeck RK, De Schepper PJ: Influence of chronic renal failure and hemodialysis on diflunisal plasma protein binding. Clin Pharmacol Ther. 1980 May;27(5):628-35. Pubmed

Transporters

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. Mulato AS, Ho ES, Cihlar T: Nonsteroidal anti-inflammatory drugs efficiently reduce the transport and cytotoxicity of adefovir mediated by the human renal organic anion transporter 1. J Pharmacol Exp Ther. 2000 Oct;295(1):10-5. Pubmed
  2. 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

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Drug created on June 13, 2005 07:24 / Updated on April 14, 2014 12:54