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Identification
NameSalicylate-sodium
Accession NumberDB01398
TypeSmall Molecule
GroupsApproved
Description

Sodium salicylate is a sodium salt of salicylic acid. It can be prepared from sodium phenolate and carbon dioxide under higher temperature and pressure.

It is used in medicine as an analgesic and antipyretic. Sodium salicylate also acts as non-steroidal anti-inflammatory drug (NSAID) and induces apoptosis in cancer cells. It is also potential replacement for aspirin for people sensitive to it.

Structure
Thumb
Synonyms
SynonymLanguageCode
SalsoninNot AvailableNot Available
SaltsNot Available
Brand namesNot Available
Brand mixturesNot Available
Categories
CAS numberNot Available
WeightAverage: 160.1026
Monoisotopic: 160.013638701
Chemical FormulaC7H5NaO3
InChI KeyABBQHOQBGMUPJH-UHFFFAOYSA-M
InChI
InChI=1S/C7H6O3.Na/c8-6-4-2-1-3-5(6)7(9)10;/h1-4,8H,(H,9,10);/q;+1/p-1
IUPAC Name
sodium 2-hydroxybenzoate
SMILES
[Na+].OC1=CC=CC=C1C([O-])=O
Mass SpecNot Available
Taxonomy
KingdomOrganic Compounds
SuperclassBenzenoids
ClassBenzene and Substituted Derivatives
SubclassBenzoic Acid and Derivatives
Direct parentSalicylic Acids
Alternative parentsBenzoic Acids; Benzoyl Derivatives; Phenols and Derivatives; Enolates; Carboxylic Acid Salts; Enols; Polyamines
Substituentsbenzoyl; phenol derivative; enol; polyamine; carboxylic acid salt; carboxylic acid derivative; enolate
Classification descriptionThis compound belongs to the salicylic acids. These are ortho-hydroxylated benzoic acids.
Pharmacology
IndicationIt is used in medicine as an analgesic and antipyretic. Sodium salicylate also acts as non-steroidal anti-inflammatory drug (NSAID)
PharmacodynamicsNon-steroidal anti-inflammatory drugs such as Salicylate-sodium work by inhibiting the enzyme cyclooxygenase (COX), which converts arachidonic acid to prostaglandin H2 (PGH2). PGH2, in turn, is converted by other enzymes to several other prostaglandins (which are mediators of pain, inflammation, and fever)
Mechanism of actionSalicylate-sodium is considered a non-selective COX inhibitor—that is, it inhibits two isoforms of cyclooxygenase, COX-1 and COX-2. The analgesic, antipyretic, and anti-inflammatory activity of NSAIDs appears to be achieved mainly through inhibition of COX-2, whereas inhibition of COX-1 would be responsible for unwanted effects on platelet aggregation and the gastrointestinal tract. However, the role of the individual COX isoforms in the analgesic, anti-inflammatory, and gastric damage effects of NSAIDs is uncertain and different compounds cause different degrees of analgesia and gastric damage. Salicylate-sodium directly and irreversibly inhibits the activity of both types of cyclo-oxygenases (COX-1 and COX-2) to decrease the formation of precursors of prostaglandins and thromboxanes from arachidonic acid. Salicylate may competitively inhibit prostaglandin formation. Salicylate's antirheumatic (nonsteroidal anti-inflammatory) actions are a result of its analgesic and anti-inflammatory mechanisms.
AbsorptionNot Available
Volume of distributionNot Available
Protein bindingNot Available
Metabolism
Route of eliminationNot Available
Half lifeNot Available
ClearanceNot Available
ToxicityNot Available
Affected organismsNot Available
Pathways
PathwayCategorySMPDB ID
Salicylate-sodium Action PathwayDrug actionSMP00708
SNP Mediated EffectsNot Available
SNP Mediated Adverse Drug ReactionsNot Available
ADMET
Predicted ADMET features
Property Value Probability
Human Intestinal Absorption + 0.9253
Blood Brain Barrier + 0.8725
Caco-2 permeable + 0.8102
P-glycoprotein substrate Non-substrate 0.8015
P-glycoprotein inhibitor I Non-inhibitor 0.9806
P-glycoprotein inhibitor II Non-inhibitor 0.9938
Renal organic cation transporter Non-inhibitor 0.9134
CYP450 2C9 substrate Non-substrate 0.7949
CYP450 2D6 substrate Non-substrate 0.9035
CYP450 3A4 substrate Non-substrate 0.7619
CYP450 1A2 substrate Non-inhibitor 0.9298
CYP450 2C9 substrate Non-inhibitor 0.9595
CYP450 2D6 substrate Non-inhibitor 0.95
CYP450 2C19 substrate Non-inhibitor 0.8808
CYP450 3A4 substrate Non-inhibitor 0.9693
CYP450 inhibitory promiscuity Low CYP Inhibitory Promiscuity 0.9586
Ames test Non AMES toxic 0.9448
Carcinogenicity Non-carcinogens 0.854
Biodegradation Ready biodegradable 0.9624
Rat acute toxicity 2.3171 LD50, mol/kg Not applicable
hERG inhibition (predictor I) Weak inhibitor 0.9461
hERG inhibition (predictor II) Non-inhibitor 0.9832
Pharmacoeconomics
ManufacturersNot Available
Packagers
Dosage formsNot Available
Prices
Unit descriptionCostUnit
Sodium salicylate crystals0.09USDg
DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.
PatentsNot Available
Properties
Statesolid
Experimental PropertiesNot Available
Predicted Properties
PropertyValueSource
Water Solubility48.1ALOGPS
logP1.36ALOGPS
logP1.98ChemAxon
logS-0.52ALOGPS
pKa (Strongest Acidic)2.79ChemAxon
pKa (Strongest Basic)-6.3ChemAxon
Physiological Charge-1ChemAxon
Hydrogen Acceptor Count3ChemAxon
Hydrogen Donor Count1ChemAxon
Polar Surface Area60.36 Å2ChemAxon
Rotatable Bond Count1ChemAxon
Refractivity46.13 m3·mol-1ChemAxon
Polarizability12.38 Å3ChemAxon
Number of Rings1ChemAxon
Bioavailability1ChemAxon
Rule of FiveYesChemAxon
Ghose FilterNoChemAxon
Veber's RuleNoChemAxon
MDDR-like RuleNoChemAxon
Spectra
SpectraNot Available
References
Synthesis ReferenceNot Available
General ReferenceNot Available
External Links
ResourceLink
KEGG DrugD00566
PharmGKBPA451428
WikipediaSodium_salicylate
ATC CodesD01AE12S01BC08
AHFS CodesNot Available
PDB EntriesNot Available
FDA labelNot Available
MSDSNot Available
Interactions
Drug Interactions
Drug
BetamethasoneThe corticosteroid, betamethasone, may decrease the effect of the salicylate, salicylate-sodium.
FludrocortisoneThe corticosteroid, fludrocortisone, may decrease the effect of the salicylate, salicylate-sodium.
GliclazideThe salicylate, salicylate-sodium, increases the effect of the sulfonylurea, gliclazide.
GlyburideThe salicylate, salicylate-sodium, increases the effect of the sulfonylurea, glibenclamide.
HydrocortisoneThe corticosteroid, hydrocortisone, may decrease the effect of the salicylate, salicylate-sodium.
MethazolamideThe salicylate, salicylate-sodium, at high dose increases the effect of the carbonic anhydrase inhibitor, methazolamide.
MethotrexateThe salicylate, salicylate-sodium, increases the effect and toxicity of methotrexate.
PrednisoloneThe corticosteroid, prednisolone, may decrease the effect of the salicylate, salicylate-sodium.
PrednisoneThe corticosteroid, prednisone, may decrease the effect of the salicylate, salicylate-sodium.
ProbenecidThe salicylate, salicylate-sodium, decreases the uricosuric effect of probenecid.
SulindacRisk 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.
TriamcinoloneThe corticosteroid, triamcinolone, may decrease the effect of the salicylate, salicylate-sodium.
WarfarinThe antiplatelet effects of sodium salicylate may increase the bleed risk associated with warfarin.
Food InteractionsNot Available

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. Wu KK: Aspirin and other cyclooxygenase inhibitors: new therapeutic insights. Semin Vasc Med. 2003 May;3(2):107-12. Pubmed
  2. Zheng L, Howell SJ, Hatala DA, Huang K, Kern TS: Salicylate-based anti-inflammatory drugs inhibit the early lesion of diabetic retinopathy. Diabetes. 2007 Feb;56(2):337-45. Pubmed
  3. Graham GG, Scott KF: Mechanisms of action of paracetamol and related analgesics. Inflammopharmacology. 2003;11(4):401-13. Pubmed
  4. Fiebich BL, Chrubasik S: Effects of an ethanolic salix extract on the release of selected inflammatory mediators in vitro. Phytomedicine. 2004 Feb;11(2-3):135-8. Pubmed
  5. Chae HJ, Chae SW, Reed JC, Kim HR: Salicylate regulates COX-2 expression through ERK and subsequent NF-kappaB activation in osteoblasts. Immunopharmacol Immunotoxicol. 2004 Feb;26(1):75-91. Pubmed

2. Prostaglandin G/H synthase 1

Kind: protein

Organism: Human

Pharmacological action: yes

Actions: inhibitor

Components

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

References:

  1. Moon C, Ahn M, Jee Y, Heo S, Kim S, Kim H, Sim KB, Koh CS, Shin YG, Shin T: Sodium salicylate-induced amelioration of experimental autoimmune encephalomyelitis in Lewis rats is associated with the suppression of inducible nitric oxide synthase and cyclooxygenases. Neurosci Lett. 2004 Feb 12;356(2):123-6. Pubmed
  2. Graham GG, Scott KF: Mechanisms of action of paracetamol and related analgesics. Inflammopharmacology. 2003;11(4):401-13. Pubmed
  3. Sun R, Carlson NG, Hemmert AC, Kishore BK: P2Y2 receptor-mediated release of prostaglandin E2 by IMCD is altered in hydrated and dehydrated rats: relevance to AVP-independent regulation of IMCD function. Am J Physiol Renal Physiol. 2005 Sep;289(3):F585-92. Epub 2005 Apr 19. Pubmed
  4. Celik G, Pasaoglu G, Bavbek S, Abadoglu O, Dursun B, Mungan D, Misirligil Z: Tolerability of selective cyclooxygenase inhibitor, celecoxib, in patients with analgesic intolerance. J Asthma. 2005 Mar;42(2):127-31. Pubmed
  5. Liu X, Lee TL, Wong PT: Cyclooxygenase-1 inhibition shortens the duration of diazepam-induced loss of righting reflex in mice. Anesth Analg. 2006 Jan;102(1):135-40. Pubmed
  6. Vane JR: Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs. Nat New Biol. 1971 Jun 23;231(25):232-5. Pubmed
  7. Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. Pubmed

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Drug created on July 08, 2007 11:05 / Updated on September 16, 2013 17:14