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| Mechanism of Action |
Ketorolac¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ 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.
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| Pharmacology |
Ketorolac¿¡ ´ëÇÑ Pharmacology Á¤º¸ 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.
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| Protein Binding |
Ketorolac¿¡ ´ëÇÑ ´Ü¹é°áÇÕ Á¤º¸ 99%
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| Half-life |
Ketorolac¿¡ ´ëÇÑ ¹Ý°¨±â Á¤º¸ 2.5 hours for the S-enantiomer compared with 5 hours for the R-enantiomer
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| Absorption |
Ketorolac¿¡ ´ëÇÑ Absorption Á¤º¸ Rapidly and completely absorbed after oral administration
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| Pharmacokinetics |
Ketorolac TromethamineÀÇ ¾à¹°µ¿·ÂÇÐÀÚ·á
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| Biotransformation |
Ketorolac¿¡ ´ëÇÑ Biotransformation Á¤º¸ 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.
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| Toxicity |
Ketorolac¿¡ ´ëÇÑ Toxicity Á¤º¸ LD50 = 189 mg/kg (rat, oral).
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| Drug Interactions |
Ketorolac¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Alendronate Increased risk of gasrtic toxicityMethotrexate The NSAID increases the effect and toxicity of methotrexateAnisindione The NSAID increases the anticoagulant effectAcenocoumarol The NSAID increases the anticoagulant effectDicumarol The NSAID increases the anticoagulant effectWarfarin The NSAID increases the anticoagulant effectLithium The NSAID increases serum levels of lithiumAspirin ASA increases toxicity of ketorolacProbenecid Probenecid increases toxicity of ketorolac
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CYP450 Drug Interaction |
[CYP450 TableÁ÷Á¢Á¶È¸]
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| Food Interaction |
Ketorolac¿¡ ´ëÇÑ Food Interaction Á¤º¸ Take with food to reduce GI irritation
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| Drug Target |
[Drug Target]
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| Description |
Ketorolac¿¡ ´ëÇÑ Description Á¤º¸ 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)
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| Dosage Form |
Ketorolac¿¡ ´ëÇÑ Dosage_Form Á¤º¸ Liquid IntramuscularSolution IntramuscularSolution OphthalmicTablet Oral
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| Drug Category |
Ketorolac¿¡ ´ëÇÑ Drug_Category Á¤º¸ Anti-Inflammatory Agents, Non-SteroidalCyclooxygenase Inhibitors
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| Smiles String Canonical |
Ketorolac¿¡ ´ëÇÑ Smiles_String_canonical Á¤º¸ OC(=O)C1CCN2C1=CC=C2C(=O)C1=CC=CC=C1
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| Smiles String Isomeric |
Ketorolac¿¡ ´ëÇÑ Smiles_String_isomeric Á¤º¸ OC(=O)[C@@H]1CCN2C1=CC=C2C(=O)C1=CC=CC=C1
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| InChI Identifier |
Ketorolac¿¡ ´ëÇÑ InChI_Identifier Á¤º¸ InChI=1/C15H13NO3/c17-14(10-4-2-1-3-5-10)13-7-6-12-11(15(18)19)8-9-16(12)13/h1-7,11H,8-9H2,(H,18,19)/f/h18H
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| Chemical IUPAC Name |
Ketorolac¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ 5-(benzoyl)-2,3-dihydro-1H-pyrrolizine-1-carboxylic acid
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The database contains the following fields: The generic name of each chemical For module A10 (liver enzyme composite module): Overall activity category for each compound (A for active, M for marginally active, or I for inactive) based on the number of active and marginally active scores for each compound at the five individual endpoints (see research article for full description of method) Number of endpoints at which each compound is marginally active (M) Number of endpoints at which each compound is active (A) For modules A11 to A15 (alkaline phosphatase increased, SGOT increased, SGPT increased, LDH increased, and GGT increased, respectively): Overall activity category for each compound (A for active, M for marginally active, or I for inactive) based on the RI and ADR values (see the research article for full description of method) Number of ADR reports for each compound, given as <4 or ¡Ã4 Reporting Index value for each compound, except where no shipping units were available (NSU) Group 1 comprises of compounds for which ADR data were available for the first five years of marketing, so when no ADR reports were listed during this period the compounds were evaluated as inactive. Group 2 comprises of compounds for which a 'steady state' period of ADR data were available (1992-1996). In cases where no ADR reports were filed during this period, the compounds were scored as 'NA' (data not available) since they may have had one or more ADR reports during their first five years of marketing which should not be negated by a lack of ADR reports during the steady-state period. KETOROLAC[GGT Increase][Composite Activity](Score) I(Marginal) 0(Active) 0[Alkaline Phosphatase Increase](Activity Score) I(Number of Rpts) ¡Ã4(Index value) 1.4[SGOT Increase](Activity Score) I(Number of Rpts) ¡Ã4(Index value) 0.9[SGPT Increase](Activity Score) I(Number of Rpts) ¡Ã4(Index value) 0.6[LDH Increase](Activity Score) I(Number of Rpts) ¡Ã4(Index value) 0.5[GGT Increase](Activity Score) I(Number of Rpts) <4(Index value) 0.5
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