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10) È£Èí±â°è : È£Èí°ï¶õÀÌ ³ªÅ¸³¯ ¼ö ÀÖ´Ù.
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13) ¿ÍÆÄ¸° µî °æ±¸¿ë Ç×ÀÀÇ÷Á¦
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| DUR (ÀǾàǰ»ç¿ëÆò°¡) |
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°í½ÃµÈ º´¿ë±Ý±â ³»¿ëÀº ¾ø½À´Ï´Ù.
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| Mechanism of Action |
Diflunisal¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ The precise mechanism of the analgesic and anti-inflammatory actions of diflunisal is not known. Diflunisal is a prostaglandin synthetase inhibitor. In animals, prostaglandins sensitize afferent nerves and potentiate the action of bradykinin in inducing pain. Since prostaglandins are known to be among the mediators of pain and inflammation, the mode of action of diflunisal may be due to a decrease of prostaglandins in peripheral tissues.
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| Pharmacology |
Diflunisal¿¡ ´ëÇÑ Pharmacology Á¤º¸ Diflunisal is a nonsteroidal drug with analgesic, anti-inflammatory and antipyretic properties. It is a peripherally-acting non-narcotic analgesic drug. Habituation, tolerance and addiction have not been reported. Diflunisal is a difluorophenyl derivative of salicylic acid. Chemically, diflunisal differs from aspirin (acetylsalicylic acid) in two respects. The first of these two is the presence of a difluorophenyl substituent at carbon 1. The second difference is the removal of the 0-acetyl group from the carbon 4 position. Diflunisal is not metabolized to salicylic acid, and the fluorine atoms are not displaced from the difluorophenyl ring structure.
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| Absorption |
Diflunisal¿¡ ´ëÇÑ Absorption Á¤º¸ Rapidly and completely absorbed following oral administration, with a bioavailability of 80-90%.
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| Pharmacokinetics |
DiflunisalÀÇ ¾à¹°µ¿·ÂÇÐÀÚ·á
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- Èí¼ö : À§Àå°ü°è·ÎºÎÅÍ Àß Èí¼öµÊ
- ºÐÆ÷ : À¯Áó ºÐÆ÷
- ´ë»ç : °£´ë»ç Å
- ¹Ý°¨±â : 8-12 ½Ã°£. ½ÅÀå¾Ö½Ã ¿¬ÀåµÊ
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¾à 3%´Â ¹Ìº¯Èü·Î, 90%´Â glucuronide Æ÷ÇÕü·Î ½Å¹è¼³µÊ.
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| Toxicity |
Diflunisal¿¡ ´ëÇÑ Toxicity Á¤º¸ Oral LD50 in rat, mouse, and rabbit is 392 mg/kg, 439 mg/kg, and 603 mg/kg, respectively. Symptoms of overdose include coma, tachycardia, stupor, and vomiting. The lowest dose without the presence of other medicines which caused death was 15 grams.
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| Drug Interactions |
Diflunisal¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Alendronate Increased risk of gastric toxicityAnisindione The NSAID increases the anticoagulant effectDicumarol The NSAID increases the anticoagulant effectWarfarin The NSAID increases the anticoagulant effectIndomethacin Increases the effect and toxicity of indomethacinProbenecid Probenecid increases toxicity of diflunisalAcenocoumarol The NSAID increases the anticoagulant effect
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CYP450 Drug Interaction |
[CYP450 TableÁ÷Á¢Á¶È¸]
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| Drug Target |
[Drug Target]
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| Description |
Diflunisal¿¡ ´ëÇÑ Description Á¤º¸ A salicylate derivative and anti-inflammatory analgesic with actions and side effects similar to those of aspirin. [PubChem]
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| Drug Category |
Diflunisal¿¡ ´ëÇÑ Drug_Category Á¤º¸ Anti-Inflammatory Agents, Non-SteroidalCyclooxygenase Inhibitors
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| Smiles String Canonical |
Diflunisal¿¡ ´ëÇÑ Smiles_String_canonical Á¤º¸ OC(=O)C1=C(O)C=CC(=C1)C1=C(F)C=C(F)C=C1
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| Smiles String Isomeric |
Diflunisal¿¡ ´ëÇÑ Smiles_String_isomeric Á¤º¸ OC(=O)C1=C(O)C=CC(=C1)C1=C(F)C=C(F)C=C1
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| InChI Identifier |
Diflunisal¿¡ ´ëÇÑ InChI_Identifier Á¤º¸ InChI=1/C13H8F2O3/c14-8-2-3-9(11(15)6-8)7-1-4-12(16)10(5-7)13(17)18/h1-6,16H,(H,17,18)/f/h17H
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| Chemical IUPAC Name |
Diflunisal¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ 5-(2,4-difluorophenyl)-2-hydroxybenzoic acid
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µå·°ÀÎÆ÷ ÀǾàÇмúÁ¤º¸´Â ½ÄǰÀǾàǰ¾ÈÀüóÀÇ Á¦Ç°Çã°¡»çÇ×, Çмú¹®Çå, Á¦¾àȸ»ç Á¦°øÁ¤º¸ µîÀ» ±Ù°Å·Î ÀÛ¼ºµÈ Âü°í Á¤º¸ÀÔ´Ï´Ù.
Á¤º¸ÀÇ Á¤È®¼ºÀ» À§ÇØ ³ë·ÂÇϰí ÀÖÀ¸³ª ÆíÁý»óÀÇ ¿À·ù, Çã°¡»çÇ× º¯°æ, Ãß°¡ÀûÀÎ Çмú¿¬±¸ ¶Ç´Â Àӻ󿬱¸ ¹ßÇ¥ µîÀ¸·Î ÀÎÇØ ¹ß»ýÇÏ´Â ¹®Á¦¿¡ ´ëÇØ µå·°ÀÎÆ÷´Â
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ÀüÈ: 02-3486-1061 ¤Ó À̸ÞÀÏ: webmaster@druginfo.co.kr
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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. DIFLUNISAL[GGT Increase][Composite Activity](Score) I(Marginal) 0(Active) 0[Alkaline Phosphatase Increase](Activity Score) I(Number of Rpts) <4(Index value) 0[SGOT Increase](Activity Score) I(Number of Rpts) <4(Index value) 0.3[SGPT Increase](Activity Score) I(Number of Rpts) <4(Index value) 0.5[LDH Increase](Activity Score) I(Number of Rpts) <4(Index value) 0[GGT Increase](Activity Score) I(Number of Rpts) <4(Index value) 0
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