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 8) È£Èí±â°è : °£ÁúÆó·Å µå¹°°Ô ±â°üÁö°æ·Ã 
  
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 4) À§»êÀÇ pH¿¡ ÀÇÁ¸ÀûÀ¸·Î Èí¼öµÇ´Â ¾à¹°ÀÎ °æ¿ì¿¡ ÀÌ ¾à(¿À¸ÞÇÁ¶óÁ¹)À¸·Î Ä¡·áÇÏ´Â Áß¿¡ À§³» »êµµÀÇ °¨¼Ò·Î ÀÎÇØ ¾à¹° Èí¼ö°¡ Áõ°¡ÇÒ ¼öµµ ÀÖ°í °¨¼ÒÇÒ ¼öµµ ÀÖ´Ù.
  
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 6) °Ç°ÇÑ ÇÇÇèÀڵ鿡°Ô ¿À¸ÞÇÁ¶óÁ¹(1ÀÏ 20 mg)°ú µð°î½ÅÀ» ÇÔ²² º´¿ëÅõ¿©ÇÏ¸é µð°î½ÅÀÇ »ýüÀÌ¿ë·üÀÌ 10 % Áõ°¡Çß´Ù. µð°î½ÅÀÇ µ¶¼ºÀÌ µå¹°°Ô º¸°íµÇ¾ú´Ù. ±×·¯³ª ¿À¸ÞÇÁ¶óÁ¹ÀÌ °í·ÉÀÚ¿¡°Ô °í¿ë·®À¸·Î Åõ¿©µÉ ¶§ ÁÖÀÇÇØ¾ß ÇÑ´Ù. Ä¡·áÀûÀÎ ¾à¹°¸ð´ÏÅ͸µÀº °ÈµÇ¾î¾ß ÇÑ´Ù.
  
 7) Á¦»êÁ¦¿ÍÀÇ º´¿ëÅõ¿©½Ã »óÈ£ÀÛ¿ëÀº ¹ß°ßµÇÁö ¾Ê¾Ò´Ù.
  
 8) Ŭ·¡¸®Æ®·Î¸¶À̽Š¶Ç´Â ¿¡¸®Æ®·Î¸¶À̽Űú ¿À¸ÞÇÁ¶óÁ¹À» º´¿ë Åõ¿©ÇÏ¿´À» ¶§ ¿À¸ÞÇÁ¶óÁ¹ÀÇ Ç÷Àå ³óµµ°¡ Áõ°¡ÇÏ¿´´Ù. ¿À¸ÞÇÁ¶óÁ¹ÀÇ Ç÷Àå ³óµµ´Â ¾Æ¸ñ½Ã½Ç¸° ¶Ç´Â ¸ÞÆ®·Î´Ï´ÙÁ¹°úÀÇ º´¿ë Åõ¿©¿¡ ÀÇÇØ ¿µÇâÀ» ¹ÞÁö ¾Ê´Â´Ù.
  
 9) ¿À¸ÞÇÁ¶óÁ¹Àº ¸î °³ÀÇ Ç×¹ÙÀÌ·¯½ºÁ¦Á¦¿Í »óÈ£ÀÛ¿ëÀÌ ÀÖ´Â °ÍÀ¸·Î º¸°íµÇ¾ú´Ù. º¸°íµÈ »óÈ£ÀÛ¿ë ¿Ü ÀÓ»óÀû Á߿伺°ú ±âÀüÀº ¹àÇôÁöÁö ¾Ê¾Ò´Ù. ¿À¸ÞÇÁ¶óÁ¹ Åõ¿©½ÃÀÇ À§³» »êµµ °¨¼Ò´Â Ç×¹ÙÀÌ·¯½ºÁ¦Á¦ÀÇ Èí¼ö¸¦ º¯È½Ãų ¼ö ÀÖ´Ù. °¡´ÉÇÑ »óÈ£ÀÛ¿ëÀÇ ¶Ç ´Ù¸¥ ±âÀüÀº CYP2C19À̸ç, ¾ÆÅ¸ÀÚ³ªºñ¸£ ¹× ³ÚÇdzªºñ¸£¿Í °°Àº Ç×¹ÙÀÌ·¯½º Á¦Á¦¿¡¼´Â ¿À¸ÞÇÁ¶óÁ¹°ú º´¿ë Åõ¿©½Ã Ç÷û¼öÄ¡ °¨¼Ò°¡ º¸°íµÇ¾úÀ¸¸ç º´¿ëÅõ¿©Çؼ´Â ¾ÈµÈ´Ù. ±× ¿Ü »çÄû³ªºñ¸£¿Í °°Àº Ç×¹ÙÀÌ·¯½º Á¦Á¦¿¡¼´Â Ç÷û¼öÄ¡ Áõ°¡°¡ º¸°íµÇ¾ú´Ù. ¿À¸ÞÇÁ¶óÁ¹°ú º´¿ë Åõ¿©½Ã Ç÷û¼öÄ¡°¡ º¯ÇÏÁö ¾Ê´Â Ç×¹ÙÀÌ·¯½º Á¦Á¦ ¶ÇÇÑ Á¸ÀçÇÑ´Ù.
  
 10) ¿À¸ÞÇÁ¶óÁ¹°ú Ÿũ·Î¸®¹«½ºÀÇ º´¿ëÅõ¿©´Â Ÿũ·Î¸®¹«½ºÀÇ Ç÷û ³óµµ¸¦ ³ôÀÏ ¼ö ÀÖ´Ù. ÀÌ ¾àÀ» Åõ¿©Çϱ⠽ÃÀÛÇϰųª Áß´ÜÇÒ ¶§ Ÿũ·Î¸®¹«½ºÀÇ Ç÷Àå ³óµµ¸¦ ¸ð´ÏÅ͸µÇϵµ·Ï ÇÑ´Ù.
  
 11) ±³Â÷Àӻ󿬱¸¿¡¼ Ŭ·ÎÇǵµ±×·¼ ´Üµ¶(Ãʱâ¿ë·® 300 mg ÀÌÈÄ¿¡ 1ÀÏ ¿ë·® 75 mg)°ú ¿À¸ÞÇÁ¶óÁ¹°ú ÇÔ²²(Ŭ·ÎÇǵµ±×·¼°ú µ¿½Ã¿¡ 80 mg)Åõ¿©°¡ 5Àϵ¿¾È ½ÃÇàµÇ¾ú´Ù. Ŭ·ÎÇǵµ±×·¼ÀÇ È°¼º´ë»ç¹°·ÎÀÇ ³ëÃâÀº Ŭ·ÎÇǵµ±×·¼°ú ¿À¸ÞÇÁ¶óÁ¹ÀÌ ÇÔ²² Åõ¿©µÉ ¶§ ù³¯ 46 % °¨¼Ò, 5Àϰ 42 % °¨¼ÒÇß´Ù. 
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 12) ÀÌ»ó¹ÝÀÀ »ç·Ê º¸°í, Áý´Ü¾àµ¿ÇÐ ¿¬±¸(population pharmacokinetic studies) ¹× ÈÄÇâÀû ¿¬±¸ µî¿¡¼ ¸ÞÅ䯮·º¼¼ÀÌÆ®(ÁÖ·Î °í¿ë·®À» »ç¿ëÇÏ´Â °æ¿ì, ¸ÞÅ䯮·º¼¼ÀÌÆ®ÀÇ »ç¿ë»óÀÇ ÁÖÀÇ»çÇ× ÂüÁ¶)¿Í ÇÁ·ÎÅæÆßÇÁ¾ïÁ¦Á¦¸¦ º´¿ëÇÏ´Â °æ¿ì ¸ÞÅ䯮·º¼¼ÀÌÆ® ±×¸®°í/¶Ç´Â ±× ´ë»çüÀÎ È÷µå·Ï½Ã¸ÞÅ䯮·º¼¼ÀÌÆ®ÀÇ Ç÷û ³óµµ°¡ »ó½Â ¹× À¯ÁöµÇ¾î ¸ÞÅ䯮·º¼¼ÀÌÆ®ÀÇ µ¶¼ºÀÌ ³ªÅ¸³¯ ¼ö ÀÖ´Ù°í º¸°íµÇ¾ú´Ù. ±×·¯³ª °í¿ë·®ÀÇ ¸ÞÅ䯮·º¼¼ÀÌÆ®¿Í ÇÁ·ÎÅæÆßÇÁ¾ïÁ¦Á¦¿¡ ´ëÇÑ Á¤½Ä ¾à¹°»óÈ£Àۿ뿬±¸´Â ¼öÇàµÇÁö ¾Ê¾Ò´Ù(ÀϹÝÀû ÁÖÀÇÇ× ÂüÁ¶).
  
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    | Related FDA Approved Drug | 
    
      
      ±âÁØ ¼ººÐ: OMEPRAZOLE SODIUMNEXIUM IV (ESOMEPRAZOLE SODIUM) 
        
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    | Mechanism of Action | 
    
       Omeprazole¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ Omeprazole is a proton pump inhibitor that suppresses gastric acid secretion by specific inhibition of the H+/K+-ATPase in the gastric parietal cell. By acting specifically on the proton pump, omeprazole blocks the final step in acid production, thus reducing gastric acidity. 
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    | Pharmacology | 
     
       Omeprazole¿¡ ´ëÇÑ Pharmacology Á¤º¸ Omeprazole is a compound that inhibits gastric acid secretion and is indicated in the treatment of gastroesophageal reflux disease (GERD), the healing of erosive esophagitis, and H. pylori eradication to reduce the risk of duodenal ulcer recurrence. Omeprazole belongs to a new class of antisecretory compounds, the substituted benzimidazoles, that do not exhibit anticholinergic or H2 histamine antagonistic properties, but that suppress gastric acid secretion by specific inhibition of the H+/K+ ATPase enzyme system at the secretory surface of the gastric parietal cell. Because this enzyme system is regarded as the acid (proton) pump within the gastric mucosa, omeprazole has been characterized as a gastric acid-pump inhibitor, in that it blocks the final step of acid production. This effect is dose-related and leads to inhibition of both basal and stimulated acid secretion irrespective of the stimulus. 
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    | Metabolism | 
    
       Omeprazole¿¡ ´ëÇÑ Metabolism Á¤º¸ # Phase_1_Metabolizing_Enzyme:Cytochrome P450 2C19 (CYP2C19) 
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    | Protein Binding | 
    
       Omeprazole¿¡ ´ëÇÑ ´Ü¹é°áÇÕ Á¤º¸ 95% 
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    | Half-life | 
    
       Omeprazole¿¡ ´ëÇÑ ¹Ý°¨±â Á¤º¸ 0.5-1 hour 
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    | Absorption | 
    
       Omeprazole¿¡ ´ëÇÑ Absorption Á¤º¸ Absorption is rapid, absolute bioavailability (compared to intravenous administration) is about 30-40% at doses of 20-40 mg. 
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    | Biotransformation | 
    
       Omeprazole¿¡ ´ëÇÑ Biotransformation Á¤º¸ Hepatic. 
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    | Toxicity | 
    
       Omeprazole¿¡ ´ëÇÑ Toxicity Á¤º¸ Symptoms of overdose include confusion, drowsiness, blurred vision, tachycardia, nausea, diaphoresis, flushing, headache, and dry mouth. 
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    | Drug Interactions | 
    
       Omeprazole¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Alprazolam	Omeprazole increases the effect of benzodiazepineDiazepam	Omeprazole increases the effect of benzodiazepineClonazepam	Omeprazole increases the effect of benzodiazepineClorazepate	Omeprazole increases the effect of benzodiazepineChlordiazepoxide	Omeprazole increases the effect of benzodiazepineEstazolam	Omeprazole increases the effect of benzodiazepineFlurazepam	Omeprazole increases the effect of benzodiazepineHalazepam	Omeprazole increases the effect of benzodiazepineKetazolam	Omeprazole increases the effect of benzodiazepineMidazolam	Omeprazole increases the effect of benzodiazepinePrazepam	Omeprazole increases the effect of benzodiazepineQuazepam	Omeprazole increases the effect of benzodiazepineTriazolam	Omeprazole increases the effect of benzodiazepineMephenytoin	Omeprazole increases the effect of hydantoinPhenytoin	Omeprazole increases the effect of hydantoinFosphenytoin	Omeprazole increases the effect of hydantoinEthotoin	Omeprazole increases the effect of hydantoinVoriconazole	Voriconazole increases the effect and toxicity of omeprazoleSt. John's Wort	St. John's Wort decreases the levels/effects of omeprazole Methotrexate	Omeprazole increases the levels of methotrexateCilostazol	Omeprazole increases the effect of cilostazolAtazanavir	This gastric pH modifier decreases the levels/effects of atazanavirCyclosporine	Omeprazole increases the effect and toxicity of cyclosporineDasatinib	Possible decreased levels of dasatinibEnoxacin	The agent decreases the absorption of enoxacinIndinavir	Omeprazole decreases the absorption of indinavirItraconazole	The proton pump inhibitor decreases the absorption of the imidazoleKetoconazole	The proton pump inhibitor decreases the absorption of the imidazoleDisopyramide	The beta-blocker increases toxicity of disopyramide 
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    CYP450  Drug Interaction | 
    
      [CYP450 TableÁ÷Á¢Á¶È¸] Omeprazole¿¡ ´ëÇÑ P450 table
  SUBSTRATES 
CYP 2C19 
Proton Pump Inhibitors: 
**omeprazole** 
lansoprazole 
pantoprazole 
rabeprazole 
Anti-epileptics: 
diazepam 
phenytoin 
phenobarbitone 
amitriptyline 
clomipramine 
clopidogrel 
cyclophosphamide 
progesterone 
 INHIBITORS 
CYP 2C19 
fluoxetine 
fluvoxamine 
ketoconazole 
lansoprazole 
**omeprazole** 
ticlopidine 
 INDUCERS 
CYP 2C19 
N/A 
  SUBSTRATES 
CYP 2C19 
Proton Pump Inhibitors: 
**omeprazole** 
lansoprazole 
pantoprazole 
rabeprazole 
Anti-epileptics: 
diazepam 
phenytoin 
phenobarbitone 
amitriptyline 
clomipramine 
clopidogrel 
cyclophosphamide 
progesterone 
 INHIBITORS 
CYP 2C19 
fluoxetine 
fluvoxamine 
ketoconazole 
lansoprazole 
**omeprazole** 
ticlopidine 
 INDUCERS 
CYP 2C19 
N/A 
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    | Food Interaction | 
    
       Omeprazole¿¡ ´ëÇÑ Food Interaction Á¤º¸ Avoid alcohol.Take 30-60 minutes before meals. 
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    | Drug Target | 
    
      
      [Drug Target]
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    | SNP Á¤º¸ | 
    
      Name:Omeprazole (DB00338)
 Interacting Gene/Enzyme:Cytochrome P450 2C19 (Gene symbol = CYP2C19) Swissprot P33261
 SNP(s):CYP2C19*3 rs4986893 (A Allele, homozygote)
 Effect:Poor metabolizer, lower dose requirement, improved drug efficacy
 Reference(s):Furuta T, Ohashi K, Kamata T, Takashima M, Kosuge K, Kawasaki T, Hanai H, Kubota T, Ishizaki T, Kaneko E: Effect of genetic differences in omeprazole metabolism on cure rates for Helicobacter pylori infection and peptic ulcer. Ann Intern Med. 1998 Dec 15;129(12):1027-30. [PubMed] 
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    | Description | 
    
       Omeprazole¿¡ ´ëÇÑ Description Á¤º¸ A highly effective inhibitor of gastric acid secretion used in the therapy of stomach ulcers and zollinger-ellison syndrome. The drug inhibits the H(+)-K(+)-ATPase (H(+)-K(+)-exchanging ATPase) in the proton pump of gastric parietal cells. [PubChem] 
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    | Dosage Form | 
    
       Omeprazole¿¡ ´ëÇÑ Dosage_Form Á¤º¸ Capsule	OralCapsule, delayed release	OralTablet, delayed release	Oral 
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    | Drug Category | 
    
       Omeprazole¿¡ ´ëÇÑ Drug_Category Á¤º¸ Anti-Ulcer AgentsEnzyme InhibitorsProton-pump Inhibitors 
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    | Smiles String Canonical | 
    
       Omeprazole¿¡ ´ëÇÑ Smiles_String_canonical Á¤º¸ COC1=CC2=C(C=C1)N=C(N2)S(=O)CC1=NC=C(C)C(OC)=C1C 
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    | Smiles String Isomeric | 
    
       Omeprazole¿¡ ´ëÇÑ Smiles_String_isomeric Á¤º¸ COC1=CC2=C(C=C1)N=C(N2)[S@@](=O)CC1=NC=C(C)C(OC)=C1C 
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    | InChI Identifier | 
    
       Omeprazole¿¡ ´ëÇÑ InChI_Identifier Á¤º¸ InChI=1/C17H19N3O3S/c1-10-8-18-15(11(2)16(10)23-4)9-24(21)17-19-13-6-5-12(22-3)7-14(13)20-17/h5-8H,9H2,1-4H3,(H,19,20)/f/h20H 
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    | Chemical IUPAC Name | 
    
       Omeprazole¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ 6-methoxy-2-[(4-methoxy-3,5-dimethylpyridin-2-yl)methylsulfinyl]-1H-benzimidazole 
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    | Drug-Induced Toxicity Related Proteins | 
    
      OMEPRAZOLE ÀÇ Drug-Induced Toxicity Related ProteinÁ¤º¸ Replated Protein:Potassium-transporting ATPase Drug:omeprazole Toxicity:block gastric acid secretion.  [¹Ù·Î°¡±â] 
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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. OMEPRAZOLE[GGT Increase][Composite Activity](Score)  I(Marginal)  0(Active)  0[Alkaline Phosphatase Increase](Activity Score)  I(Number of Rpts)  ¡Ã4(Index value)  1.8[SGOT Increase](Activity Score)  I(Number of Rpts)  ¡Ã4(Index value)  1.2[SGPT Increase](Activity Score)  I(Number of Rpts)  ¡Ã4(Index value)  0.9[LDH Increase](Activity Score)  I(Number of Rpts)  ¡Ã4(Index value)  0.5[GGT Increase](Activity Score)  I(Number of Rpts)  ¡Ã4(Index value)  0.8
 
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