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Home / Drugs / Starting with K / Ketorolac

A pyrrolizine carboxylic acid derivative structurally related to indomethacin. It is an NSAID and is used principally for its analgesic activity. (From Martindale The Extra Pharmacopoeia, 31st ed)
Acular LS
Acular Preservative Free
CategoriesCyclooxygenase Inhibitors
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Ketorolac Tromethamine
Ketorolaco [Spanish]
Ketorolacum [Latin]


For the short-term (~5 days) management of moderately severe acute pain that requires analgesia at the opioid level, usually in a postoperative setting.


Ketorolac, an antiinflammatory agent with analgesic and antipyretic properties, is used to treat osteoarthritis and control acute pain. It is a peripherally acting analgesic. The biological activity of ketorolac tromethamine is associated with the S-form. Ketorolac tromethamine possesses no sedative or anxiolytic properties.

mechanism of action

Ketorolac is a nonsteroidal anti-inflammatory drug (NSAID) chemically related to indomethacin and tolmetin. Ketorolac tromethamine is a racemic mixture of [-]S- and [+]R-enantiomeric forms, with the S-form having analgesic activity. Its antiinflammatory effects are believed to be due to inhibition of both cylooxygenase-1 (COX-1) and cylooxygenase-2 (COX-2) which leads to the inhibition of prostaglandin synthesis leading to decreased formation of precursors of prostaglandins and thromboxanes from arachidonic acid. The resultant reduction in prostaglandin synthesis and activity may be at least partially responsible for many of the adverse, as well as the therapeutic, effects of these medications. Analgesia is probably produced via a peripheral action in which blockade of pain impulse generation results from decreased prostaglandin activity. However, inhibition of the synthesis or actions of other substances that sensitize pain receptors to mechanical or chemical stimulation may also contribute to the analgesic effect. In terms of the ophthalmic applications of ketorolac - ocular administration of ketorolac reduces prostaglandin E2 levels in aqueous humor, secondary to inhibition of prostaglandin biosynthesis.


LD50 = 189 mg/kg (rat, oral).


Primarily hepatic. Less than 50% of a dose is metabolized. The major metabolites are a glucuronide conjugate, which may also be formed in the kidney, and p-hydroxy ketorolac. Neither metabolite has significant analgesic activity.


Rapidly and completely absorbed after oral administration

half life

2.5 hours for the S-enantiomer compared with 5 hours for the R-enantiomer

route of elimination

The principal route of elimination of ketorolac and its metabolites is renal. Approximately 6% of a dose is excreted in the feces.

drug interactions

Acenocoumarol: The NSAID, ketorolac, may increase the anticoagulant effect of acenocoumarol.

Acetylsalicylic acid: Acetylsalicylic acid may increase the adverse GI effects ketorolac.

Alendronate: Increased risk of gasrtic toxicity

Anisindione: The NSAID, ketorolac, 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.

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

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

Ketoprofen: Concomitant use of ketoprofen and ketorolac, two NSAIDs, is contraindicated due to the risk of additive or synergistic NSAID toxicities (e.g. GI bleeding, ulceration, renal dysfunction, etc).

Lithium: The NSAID, ketorolac, may decrease the renal excretion of lithium. Increased risk of lithium toxicity.

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

Probenecid: Probenecid increases toxicity of ketorolac

Sulindac: May cause additive or synergistic NSAID toxicities (e.g. GI bleeding, renal dysfunction, etc.). Concomitant therapy is contraindicated.

Telmisartan: Concomitant use of Telmisartan and Ketorolac may increase the risk of acute renal failure and hyperkalemia. Monitor renal function at the beginning and during treatment.

Tiaprofenic acid: Concomitant therapy is contraindicated due to the risk of synergistic NSAID toxicity.

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

Tolmetin: Risk of adverse NSAID toxic effects (e.g. GI bleeding, renal dysfunction). Concomitant therapy is contraindicated.

Trandolapril: The NSAID, Ketorolac, may reduce the antihypertensive effect of Trandolapril. Consider alternate therapy or monitor for changes in Trandolapril efficacy if Ketorolac is initiated, discontinued or dose changed.

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

Vilazodone: Increased risk of bleeding with concomitant use of vilazodone and ketorolac

Warfarin: The antiplatelet effects of ketorolac may increase the bleed risk associated with warfarin. Consider alternate therapy or monitor for signs and symptoms of bleeding during concomitant therapy.