You are using an unsupported browser. Please upgrade your browser to a newer version to get the best experience on DrugBank.
Identification
NameEtodolac
Accession NumberDB00749  (APRD00067)
Typesmall molecule
Groupsapproved, investigational
Description

Etodolac is a non-steroidal anti-inflammatory drug (NSAID) with anti-inflammatory, analgesic and antipyretic properties. Its therapeutic effects are due to its ability to inhibit prostaglandin synthesis. It is indicated for relief of signs and symptoms of rheumatoid arthritis and osteoarthritis.

Structure
Thumb
Synonyms
SynonymLanguageCode
(+-)-1,8-Diethyl-1,3,4,9-tetrahydropyrano(3,4-b)indole-1-acetic acidNot AvailableNot Available
(1,8-Diethyl-1,3,4,9-tetrahydro-pyrano[3,4-b]indol-1-yl)-acetic acidNot AvailableNot Available
1,3,4,9-Tetrahydro-1,8-diethylpyrano(3,4-b)indole-1-acetic acidNot AvailableNot Available
1,8-Diethyl-1,3,4,9-tetrahydropyrano(3,4-b)indole-1-acetic acidNot AvailableNot Available
1,8-Diethyl-1,3,4,9-tetrahydropyrano[3,4-b]indol-1-ylacetic acidNot AvailableNot Available
ÉtodolacFrenchNot Available
EtodolacNot AvailableINN, BAN, USAN
EtodolacoSpanishINN
EtodolacumLatinINN
Etodolic acidNot AvailableIS
EtodolsäureNot AvailableIS
SaltsNot Available
Brand names
NameCompany
BodopineYuan Chou
DolaritDrogsan
DolchisKorea United Pharm
DolocUnifarma
DualganITF
EccoxolacMeda
Edolar FortPfizer
EdopainIncepta
Edopain ERIncepta
ElacRoyal
ElderinLek
EricU.C. Pharma
EsodaxMünir Sahin
ETLSenton
EtodinNobel
Etodin FortUlkar
EtodolYuhan
EtodonShinlon
EtoflamStandard Chem
Etol FortNobel
EtolacAlkaloid
EtomaxIpca
Etomax-ERIpca
EtonoxCharoen Bhaesaj
EtopanWinthrop Pharmaceuticals
EtopinU-Liang
LodineWyeth
Lodine XLWyeth
Brand mixtures
Brand NameIngredients
Etomax-PEtodolac and Paracetamol
Categories
CAS number41340-25-4
WeightAverage: 287.3535
Monoisotopic: 287.152143543
Chemical FormulaC17H21NO3
InChI KeyNNYBQONXHNTVIJ-UHFFFAOYSA-N
InChI
InChI=1S/C17H21NO3/c1-3-11-6-5-7-12-13-8-9-21-17(4-2,10-14(19)20)16(13)18-15(11)12/h5-7,18H,3-4,8-10H2,1-2H3,(H,19,20)
IUPAC Name
2-{1,8-diethyl-1H,3H,4H,9H-pyrano[3,4-b]indol-1-yl}acetic acid
SMILES
CCC1=C2NC3=C(CCOC3(CC)CC(O)=O)C2=CC=C1
Mass SpecNot Available
Taxonomy
KingdomOrganic Compounds
SuperclassHeterocyclic Compounds
ClassIndoles and Derivatives
SubclassIndolyl Carboxylic Acids and Derivatives
Direct parentIndolyl Carboxylic Acids and Derivatives
Alternative parentsIndoles; Benzene and Substituted Derivatives; Pyrroles; Polyamines; Dialkyl Ethers; Carboxylic Acids; Enolates
Substituentsindole; benzene; pyrrole; carboxylic acid derivative; carboxylic acid; enolate; ether; dialkyl ether; polyamine; organonitrogen compound
Classification descriptionThis compound belongs to the indolyl carboxylic acids and derivatives. These are compounds containing a carboxylic acid chain (of at least 2 carbon atoms) linked to an indole ring.
Pharmacology
IndicationFor acute and long-term management of signs and symptoms of osteoarthritis and rheumatoid arthritis, as well as for the management of pain.
PharmacodynamicsEtodolac is an anti-inflammatory agent with analgesic and antipyretic properties. It is used to treat osteoarthritis, rheumatoid arthritis and control acute pain. The therapeutic effects of etodolac are achieved via inhibition of the synthesis of prostaglandins involved in fever, pain, swelling and inflammation. Etodolac is administered as a racemate. As with other NSAIDs, the S-form has been shown to be active while the R-form is inactive. Both enantiomers are stable and there is no evidence of R- to S- conversion in vivo.
Mechanism of actionSimilar to other NSAIDs, the anti-inflammatory effects of etodolac result from inhibition of the enzyme cycooxygenase (COX). This decreases the synthesis of peripheral prostaglandins involved in mediating inflammation. Etodolac binds to the upper portion of the COX enzyme active site and prevents its substrate, arachidonic acid, from entering the active site. Etodolac was previously thought to be a non-selective COX inhibitor, but it is now known to be 5 – 50 times more selective for COX-2 than COX-1. Antipyresis may occur by central action on the hypothalamus, resulting in peripheral dilation, increased cutaneous blood flow, and subsequent heat loss.
AbsorptionBased on mass balance studies, the systemic bioavailability of etodolac from either the tablet or capsule formulation is at least 80%.
Volume of distribution
  • 390 mL/kg
Protein binding> 99% bound, primarily to albumin
Metabolism

Etodolac is extensively metabolized in the liver. Renal elimination of etodolac and its metabolites is the primary route of excretion (72%). Metabolites found in urine (with percents of the administered dose) are: unchanged etodolac (1%), etodolac glucuronide (13%), hydroxylated metabolites (6-, 7-, and 8-OH; 5%), hydroxylated metabolite glucuronides (20%), and unidentified metabolites (33%). Fecal excretion accounts for 16% of its elimination.

SubstrateEnzymesProduct
Etodolac
6-HydroxyetodolacDetails
Etodolac
7-HydroxyetodolacDetails
Etodolac
Etodolac acyl glucuronideDetails
Route of eliminationIt is not known whether etodolac is excreted in human milk; however, based on its physical-chemical properties, excretion into breast milk is expected. Etodolac is extensively metabolized in the liver. The hydroxylated-etodolac metabolites undergo further glucuronidation followed by renal excretion and partial elimination in the feces (16% of dose). Approximately 1% of a etodolac dose is excreted unchanged in the urine with 72% of the dose excreted into urine as parent drug plus metabolite.
Half lifeTerminal t1/2, 7.3 ± 4.0 hours. Distribution t1/2, 0.71 ± 0.50 hours
Clearance
  • Oral cl=49.1 mL/h/kg [Normal healthy adults]
  • Oral cl=49.4 mL/h/kg [Healthy males (18-65 years)]
  • Oral cl=35.7 mL/h/kg [Healthy females (27-65 years)]
  • Oral cl=45.7 mL/h/kg [Eldery (>65 years)]
  • Oral cl=58.3 mL/h/kg [Renal impairement (46-73 years)]
  • Oral cl=42.0 mL/h/kg [Hepatic impairement (34-60 years)]
ToxicitySelective 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 etodolac. Etodolac may increase blood pressure and/or cause fluid retention and edema. Risk of GI toxicity including bleeding, ulceration and perforation. Risk of direct renal injury, including renal papillary necrosis. Anaphylactoid and serious skin reactions (e.g. exfoliative dermatitis, Stevens-Johnson syndrome, toxic epidermal necrolysis) have been reported. Common adverse events include abdominal pain, constipation, diarrhea, dyspepsia, flatulence, GI bleeding, GI perforation, nausea, peptic ulcer, vomiting, renal function abnormalities, anemia, dizziness, edema, liver function test abnormalities, headache, prolonged bleeding time, pruritus, rash, tinnitus. Symptoms of overdose include lethargy, drowsiness, nausea, vomiting, and epigastric pain.
Affected organisms
  • Humans and other mammals
Pathways
PathwayCategorySMPDB ID
Etodolac Action PathwayDrug actionSMP00084
SNP Mediated EffectsNot Available
SNP Mediated Adverse Drug ReactionsNot Available
ADMET
Predicted ADMET features
Property Value Probability
Human Intestinal Absorption + 0.9971
Blood Brain Barrier + 0.9065
Caco-2 permeable + 0.5726
P-glycoprotein substrate Substrate 0.7462
P-glycoprotein inhibitor I Non-inhibitor 0.9242
P-glycoprotein inhibitor II Non-inhibitor 0.8988
Renal organic cation transporter Non-inhibitor 0.8178
CYP450 2C9 substrate Non-substrate 0.8545
CYP450 2D6 substrate Non-substrate 0.7567
CYP450 3A4 substrate Non-substrate 0.5
CYP450 1A2 substrate Non-inhibitor 0.9045
CYP450 2C9 substrate Non-inhibitor 0.907
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 0.6904
Ames test Non AMES toxic 0.9132
Carcinogenicity Non-carcinogens 0.9453
Biodegradation Not ready biodegradable 0.9835
Rat acute toxicity 3.4536 LD50, mol/kg Not applicable
hERG inhibition (predictor I) Weak inhibitor 0.9808
hERG inhibition (predictor II) Non-inhibitor 0.7763
Pharmacoeconomics
Manufacturers
  • Aaipharma llc
  • Apotex inc
  • Endo pharmaceuticals inc
  • Genpharm inc
  • Ivax pharmaceuticals inc sub teva pharmaceuticals usa
  • Mylan pharmaceuticals inc
  • Sandoz inc
  • Taro pharmaceutical industries ltd
  • Teva pharmaceuticals usa inc
  • Watson laboratories inc
  • Wyeth pharmaceuticals inc
  • Point holdings inc
  • Watson laboratories inc florida
  • Actavis elizabeth llc
  • Apotex inc etobicoke site
  • Mylan laboratories inc
  • Ranbaxy laboratories ltd
Packagers
Dosage forms
FormRouteStrength
CapsuleOral200 mg
CapsuleOral300 mg
TabletOral400 mg
TabletOral500 mg
Tablet, extended releaseOral400 mg
Tablet, extended releaseOral500 mg
Tablet, extended releaseOral600 mg
Prices
Unit descriptionCostUnit
Etodolac CR 600 mg 24 Hour tablet2.76USDtablet
Lodine 400 mg tablet2.65USDtablet
Lodine 500 mg tablet1.8USDtablet
Etodolac CR 500 mg 24 Hour tablet1.6USDtablet
Etodolac 500 mg tablet1.52USDtablet
Etodolac 400 mg tablet1.5USDtablet
Etodolac CR 400 mg 24 Hour tablet1.46USDtablet
Etodolac 300 mg capsule1.31USDcapsule
Apo-Etodolac 200 mg Capsule0.8USDcapsule
Apo-Etodolac 300 mg Capsule0.8USDcapsule
DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.
PatentsNot Available
Properties
Statesolid
Experimental Properties
PropertyValueSource
melting point146.5 °CPhysProp
water solubility16 mg/LNot Available
logP2.5Not Available
pKa4.65Not Available
Predicted Properties
PropertyValueSource
water solubility3.92e-02 g/lALOGPS
logP3.39ALOGPS
logP3.44ChemAxon
logS-3.9ALOGPS
pKa (strongest acidic)4.73ChemAxon
pKa (strongest basic)-4.2ChemAxon
physiological charge-1ChemAxon
hydrogen acceptor count3ChemAxon
hydrogen donor count2ChemAxon
polar surface area62.32ChemAxon
rotatable bond count4ChemAxon
refractivity81.16ChemAxon
polarizability31.94ChemAxon
number of rings3ChemAxon
bioavailability1ChemAxon
rule of fiveYesChemAxon
Ghose filterYesChemAxon
Veber's ruleNoChemAxon
MDDR-like ruleNoChemAxon
Spectra
SpectraNot Available
References
Synthesis Reference

Christopher A. Demerson, Leslie G. Humber, “Process for preparing 1,8-diethyl-1,3,4,9-tetrahydropyrano(3,4-b)-indole-1-acetic acid, etodolac.” U.S. Patent US4585877, issued May, 1977.

US4585877
General ReferenceNot Available
External Links
ResourceLink
KEGG DrugD00315
PubChem Compound3308
PubChem Substance46505184
ChemSpider3192
BindingDB50016799
ChEBI4909
ChEMBLCHEMBL622
Therapeutic Targets DatabaseDAP000778
PharmGKBPA449550
Drug Product Database2242915
RxListhttp://www.rxlist.com/cgi/generic/etodolac.htm
Drugs.comhttp://www.drugs.com/etodolac.html
WikipediaEtodolac
ATC CodesM01AB08
AHFS Codes
  • 28:08.04.92
PDB EntriesNot Available
FDA labelshow(290 KB)
MSDSNot Available
Interactions
Drug Interactions
Drug
AcenocoumarolThe NSAID, etodolac, may increase the anticoagulant effect or acenocoumarol.
AlendronateIncreased risk of gastric toxicity
AnisindioneThe NSAID, etodolac, 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.
CyclosporineMonitor for nephrotoxicity
DicoumarolThe NSAID, etodolac, may increase the anticoagulant effect of dicumarol.
EltrombopagIncreases levels of Etodolac via metabolism decrease. UDP-glucuronosyltransferase inhibition.
Ginkgo bilobaAdditive anticoagulant/antiplatelet effects may increase bleed risk. Concomitant therapy should be avoided.
MethotrexateThe NSAID, etodolac, may decrease the renal excretion of methotrexate. Increased risk of methotrexate toxicity.
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.
TimololThe NSAID, Etodolac, may antagonize the antihypertensive effect of Timolol.
TrandolaprilThe NSAID, Etodolac, may reduce the antihypertensive effect of Trandolapril. Consider alternate therapy or monitor for changes in Trandolapril efficacy if Etodolac is initiated, discontinued or dose changed.
TreprostinilThe prostacyclin analogue, Treprostinil, may increase the risk of bleeding when combined with the NSAID, Etodolac. Monitor for increased bleeding during concomitant thearpy.
WarfarinThe antiplatelet effects of etodolac may increase the bleed risk associated with warfarin. Consider alternate therapy or monitor for signs and symptoms of bleeding during concomitant therapy.
Food Interactions
  • Avoid alcohol.
  • Food increases the peak plasma concentration of extended-release tablets with no effect on extent of absorption.
  • Food increases the time to peak concentration of regular release oral formulations by 1.4 to 3.8 hours 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. Chen WS, Liu JH, Wei SJ, Liu JM, Hong CY, Yang WK: Colon cancer cells with high invasive potential are susceptible to induction of apoptosis by a selective COX-2 inhibitor. Cancer Sci. 2003 Mar;94(3):253-8. Pubmed
  2. Chen WS, Wei SJ, Liu JM, Hsiao M, Kou-Lin J, Yang WK: Tumor invasiveness and liver metastasis of colon cancer cells correlated with cyclooxygenase-2 (COX-2) expression and inhibited by a COX-2-selective inhibitor, etodolac. Int J Cancer. 2001 Mar 15;91(6):894-9. Pubmed
  3. Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. Pubmed
  4. Kusuhara H, Komatsu H, Sumichika H, Sugahara K: Reactive oxygen species are involved in the apoptosis induced by nonsteroidal anti-inflammatory drugs in cultured gastric cells. Eur J Pharmacol. 1999 Nov 3;383(3):331-7. Pubmed
  5. Svendsen KB, Bech JN, Sorensen TB, Pedersen EB: A comparison of the effects of etodolac and ibuprofen on renal haemodynamics, tubular function, renin, vasopressin and urinary excretion of albumin and alpha-glutathione-S-transferase in healthy subjects: a placebo-controlled cross-over study. Eur J Clin Pharmacol. 2000 Aug;56(5):383-8. Pubmed
  6. Wilson JE, Chandrasekharan NV, Westover KD, Eager KB, Simmons DL: Determination of expression of cyclooxygenase-1 and -2 isozymes in canine tissues and their differential sensitivity to nonsteroidal anti-inflammatory drugs. Am J Vet Res. 2004 Jun;65(6):810-8. 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. Campbell NB, Jones SL, Blikslager AT: The effects of cyclo-oxygenase inhibitors on bile-injured and normal equine colon. Equine Vet J. 2002 Jul;34(5):493-8. Pubmed
  2. Glaser K, Sung ML, O’Neill K, Belfast M, Hartman D, Carlson R, Kreft A, Kubrak D, Hsiao CL, Weichman B: Etodolac selectively inhibits human prostaglandin G/H synthase 2 (PGHS-2) versus human PGHS-1. Eur J Pharmacol. 1995 Jul 25;281(1):107-11. Pubmed
  3. Hirate K, Uchida A, Ogawa Y, Arai T, Yoda K: Zaltoprofen, a non-steroidal anti-inflammatory drug, inhibits bradykinin-induced pain responses without blocking bradykinin receptors. Neurosci Res. 2006 Apr;54(4):288-94. Epub 2006 Feb 13. Pubmed
  4. Riendeau D, Percival MD, Boyce S, Brideau C, Charleson S, Cromlish W, Ethier D, Evans J, Falgueyret JP, Ford-Hutchinson AW, Gordon R, Greig G, Gresser M, Guay J, Kargman S, Leger S, Mancini JA, O’Neill G, Ouellet M, Rodger IW, Therien M, Wang Z, Webb JK, Wong E, Chan CC, et al.: Biochemical and pharmacological profile of a tetrasubstituted furanone as a highly selective COX-2 inhibitor. Br J Pharmacol. 1997 May;121(1):105-17. PubmedAPRIL 26, 2010
  5. Wilson JE, Chandrasekharan NV, Westover KD, Eager KB, Simmons DL: Determination of expression of cyclooxygenase-1 and -2 isozymes in canine tissues and their differential sensitivity to nonsteroidal anti-inflammatory drugs. Am J Vet Res. 2004 Jun;65(6):810-8. Pubmed

3. Retinoic acid receptor RXR-alpha

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: other

Components

Name UniProt ID Details
Retinoic acid receptor RXR-alpha P19793 Details

References:

  1. Kolluri SK, Corr M, James SY, Bernasconi M, Lu D, Liu W, Cottam HB, Leoni LM, Carson DA, Zhang XK: The R-enantiomer of the nonsteroidal antiinflammatory drug etodolac binds retinoid X receptor and induces tumor-selective apoptosis. Proc Natl Acad Sci U S A. 2005 Feb 15;102(7):2525-30. Epub 2005 Feb 7. Pubmed

Enzymes

1. Cytochrome P450 2C9

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: substrate inhibitor

Components

Name UniProt ID Details
Cytochrome P450 2C9 P11712 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

2. UDP-glucuronosyltransferase 1-9

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: substrate

Components

Name UniProt ID Details
UDP-glucuronosyltransferase 1-9 O60656 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

3. UDP-glucuronosyltransferase 1-3

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: substrate

Components

Name UniProt ID Details
UDP-glucuronosyltransferase 1-3 P35503 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

4. UDP-glucuronosyltransferase 1-10

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: substrate

Components

Name UniProt ID Details
UDP-glucuronosyltransferase 1-10 Q9HAW8 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

5. UDP-glucuronosyltransferase 2B7

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: substrate

Components

Name UniProt ID Details
UDP-glucuronosyltransferase 2B7 P16662 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

Carriers

1. Serum albumin

Kind: protein

Organism: Human

Pharmacological action: unknown

Components

Name UniProt ID Details
Serum albumin P02768 Details

References:

  1. Mignot I, Presle N, Lapicque F, Monot C, Dropsy R, Netter P: Albumin binding sites for etodolac enantiomers. Chirality. 1996;8(3):271-80. Pubmed
  2. Muller N, Lapicque F, Monot C, Payan E, Dropsy R, Netter P: Stereoselective binding of etodolac to human serum albumin. Chirality. 1992;4(4):240-6. Pubmed
  3. Smith PC, Song WQ, Rodriguez RJ: Covalent binding of etodolac acyl glucuronide to albumin in vitro. Drug Metab Dispos. 1992 Nov-Dec;20(6):962-5. 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

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