Company InfoNewsInvestor InformationResearchDevelopmentCareersBusiness DevelopmentResourcesDrugs databaseBack to the home pageSearch  
Drugs database
Drugs A-Z

Brands A-Z

Drugs by categories

Drugs by manufacturer

Drugs by packager

Antibiotics for sale

Online Viagra bestellen in Nederland

Home / Drugs / Starting with E / Etodolac

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.
BrandsEtodolac [Usan:Ban:Inn]
Etodolacetodolic acid
Etodolaco [INN-Spanish]
Etodolacum [INN-Latin]
Etodolic Acid
Lodine XL
CategoriesAnti-inflammatory Agents
Cyclooxygenase Inhibitors
Analgesics, Non-Narcotic
Nonsteroidal Anti-inflammatory Agents (NSAIAs)
ManufacturersAaipharma 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
PackagersActavis Group
Apotex Inc.
Apotheca Inc.
A-S Medication Solutions LLC
Atlantic Biologicals Corporation
Bristol-Myers Squibb Co.
Bryant Ranch Prepack
Corepharma LLC
DHHS Program Support Center Supply Service Center
Direct Dispensing Inc.
Dispensing Solutions
Diversified Healthcare Services Inc.
Eon Labs
H.J. Harkins Co. Inc.
Innoviant Pharmacy Inc.
Ivax Pharmaceuticals
Kaiser Foundation Hospital
Keltman Pharmaceuticals Inc.
Lake Erie Medical and Surgical Supply
Letco Medical Inc.
Major Pharmaceuticals
Murfreesboro Pharmaceutical Nursing Supply
Novopharm Ltd.
Nucare Pharmaceuticals Inc.
Ohm Laboratories Inc.
Palmetto Pharmaceuticals Inc.
Par Pharmaceuticals
Patheon Inc.
PD-Rx Pharmaceuticals Inc.
Physicians Total Care Inc.
Preferred Pharmaceuticals Inc.
Prepak Systems Inc.
Prescript Pharmaceuticals
Ranbaxy Laboratories
Rebel Distributors Corp.
Redpharm Drug
Remedy Repack
Resource Optimization and Innovation LLC
Southwood Pharmaceuticals
St Mary's Medical Park Pharmacy
Stat Rx Usa
Taro Pharmaceuticals USA
Teva Pharmaceutical Industries Ltd.
Torpharm Inc.


For acute and long-term management of signs and symptoms of osteoarthritis and rheumatoid arthritis, as well as for the management of pain.


Etodolac 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 action

Similar 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.


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 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.


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.


Based on mass balance studies, the systemic bioavailability of etodolac from either the tablet or capsule formulation is at least 80%.

half life

Terminal t1/2, 7.3 ± 4.0 hours. Distribution t1/2, 0.71 ± 0.50 hours

route of elimination

It 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.

drug interactions

Acenocoumarol: The NSAID, etodolac, may increase the anticoagulant effect or acenocoumarol.

Alendronate: Increased risk of gastric toxicity

Anisindione: The NSAID, etodolac, may increase the anticoagulant effect of anisindione.

Colesevelam: Bile 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.

Cyclosporine: Monitor for nephrotoxicity

Dicumarol: The NSAID, etodolac, may increase the anticoagulant effect of dicumarol.

Ginkgo biloba: Additive anticoagulant/antiplatelet effects may increase bleed risk. Concomitant therapy should be avoided.

Methotrexate: The NSAID, etodolac, may decrease the renal excretion of methotrexate. Increased risk of methotrexate toxicity.

Timolol: The NSAID, Etodolac, may antagonize the antihypertensive effect of Timolol.

Trandolapril: The 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.

Treprostinil: The prostacyclin analogue, Treprostinil, may increase the risk of bleeding when combined with the NSAID, Etodolac. Monitor for increased bleeding during concomitant thearpy.

Warfarin: The 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.