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(4) ¸ÞÅ䯮·º¼¼ÀÌÆ®(½Å¼¼´¢°ü¿¡¼ ¸ÞÅ䯮·º¼¼ÀÌÆ®ÀÇ ¹è¼³ÀÌ Áö¿¬µÇ¾î Ä¡¸íÀûÀÎ ¸ÞÅ䯮·º¼¼ÀÌÆ®ÀÇ Ç÷¾×ÇÐÀû µ¶¼ºÀÌ Áõ°¡µÉ ¼ö ÀÖÀ¸¹Ç·Î, Ç׾Ͽä¹ýÀ¸·Î »ç¿ëÇÏ´Â °í¿ë·®ÀÇ ¸ÞÅ䯮·º¼¼ÀÌÆ®¿Í´Â º´¿ëÅõ¿©ÇÏÁö ¾ÊÀ¸¸ç, Àú¿ë·®ÀÇ ¸ÞÅ䯮·º¼¼ÀÌÆ®¿Í º´¿ëÅõ¿© ½Ã ½ÅÁßÈ÷ Åõ¿©ÇØ¾ß ÇÑ´Ù.) 
(5) Äí¸¶¸°°è Ç×ÀÀÇ÷Á¦(¿ÍÆÄ¸° µî)(Äí¸¶¸°°è Ç׿ì¿ïÁ¦¿Í º´¿ëÅõ¿© ½Ã ±× ÀÛ¿ëÀ» Áõ°½Ãų ¼ö ÀÖ°í, ÁßÁõÀÇ À§Àå°ü°è ÃâÇ÷ÀÇ À§ÇèÀÌ ³ô¾ÆÁú ¼ö ÀÖ´Ù.) 
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    | DUR (ÀǾàǰ»ç¿ëÆò°¡) | 
    º´¿ë±Ý±â :
     
	 °í½ÃµÈ º´¿ë±Ý±â ³»¿ëÀº ¾ø½À´Ï´Ù.
	 
	  [»óÈ£ÀÛ¿ë/º´¿ë±Ý±â°Ë»ö]										
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      °í½ÃµÈ ¿¬·É±Ý±â ³»¿ëÀº ¾ø½À´Ï´Ù.
      
       [¿¬·É´ë±Ý±â»ó¼¼°Ë»ö]
       
       
        
        
     | 
   
  
   
    | µ¶¼ºÁ¤º¸ | 
    Acetaminophen¿¡ ´ëÇÑ µ¶¼ºÁ¤º¸ : Á¤º¸º¸±â 
Codeine¿¡ ´ëÇÑ µ¶¼ºÁ¤º¸ : Á¤º¸º¸±â 
Ibuprofen¿¡ ´ëÇÑ µ¶¼ºÁ¤º¸ : Á¤º¸º¸±â 
  Ãâó: ±¹¸³µ¶¼º°úÇпø µ¶¼º¹°ÁúÁ¤º¸DB : http://www.nitr.go.kr/nitr/contents/m134200/view.do  | 
   
  
   
    | Mechanism of Action | 
    
       Acetaminophen¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ Acetaminophen is thought to act primarily in the CNS, increasing the pain threshold by inhibiting both isoforms of cyclooxygenase, COX-1 and COX-2, enzymes involved in prostaglandin (PG) synthesis. Unlike NSAIDs, acetaminophen does not inhibit cyclooxygenase in peripheral tissues and, thus, has no peripheral anti-inflammatory affects. While aspirin acts as an irreversible inhibitor of COX and directly blocks the enzyme's active site, studies have found that acetaminophen indirectly blocks COX, and that this blockade is ineffective in the presence of peroxides. This might explain why acetaminophen is effective in the central nervous system and in endothelial cells but not in platelets and immune cells which have high levels of peroxides. Studies also report data suggesting that acetaminophen selectively blocks a variant of the COX enzyme that is different from the known variants COX-1 and COX-2. This enzyme is now referred to as COX-3. Its exact mechanism of action is still poorly understood, but future research may provide further insight into how it works.
  Codeine¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ Opiate receptors are coupled with G-protein receptors and function as both positive and negative regulators of synaptic transmission via G-proteins that activate effector proteins. Binding of the opiate stimulates the exchange of GTP for GDP on the G-protein complex. As the effector system is adenylate cyclase and cAMP located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as substance P, GABA, dopamine, acetylcholine and noradrenaline is inhibited. Opioids also inhibit the release of vasopressin, somatostatin, insulin and glucagon. Codeine's analgesic activity is, most likely, due to its conversion to morphine. Opioids close N-type voltage-operated calcium channels (OP2-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (OP3 and OP1 receptor agonist). This results in hyperpolarization and reduced neuronal excitability.
  Ibuprofen¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ The exact mechanisms of action of Ibuprofen is unknown. 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, and results in the inhibition of prostaglandin synthesis. Antipyretic effects may be due to action on the hypothalamus, resulting in an increased peripheral blood flow, vasodilation, and subsequent heat dissipation. 
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    | Pharmacology | 
     
       Acetaminophen¿¡ ´ëÇÑ Pharmacology Á¤º¸ Acetaminophen (USAN) or Paracetamol (INN) is a popular analgesic and antipyretic drug that is used for the relief of fever, headaches, and other minor aches and pains. It is a major ingredient in numerous cold and flu medications and many prescription analgesics. It is extremely safe in standard doses, but because of its wide availability, deliberate or accidental overdoses are not uncommon. Acetaminophen, unlike other common analgesics such as aspirin and ibuprofen, has no anti-inflammatory properties or effects on platelet function, and so it is not a member of the class of drugs known as non-steroidal anti-inflammatory drugs or NSAIDs. In normal doses acetaminophen does not irritate the lining of the stomach nor affect blood coagulation, the kidneys, or the fetal ductus arteriosus (as NSAIDs can). Like NSAIDs and unlike opioid analgesics, acetaminophen does not cause euphoria or alter mood in any way. Acetaminophen and NSAIDs have the benefit of being completely free of problems with addiction, dependence, tolerance and withdrawal. Acetaminophen is used on its own or in combination with pseudoephedrine, dextromethorphan, chlorpheniramine, diphenhydramine, doxylamine, codeine, hydrocodone, or oxycodone.
  Codeine¿¡ ´ëÇÑ Pharmacology Á¤º¸ Codeine, an opiate agonist in the CNS, is similar to other phenanthrene derivatives such as morphine. Codeine, in combination with guaifenesin or iodinated glycerol, is used as a cough suppressant and, as a single agent or in combination with acetaminophen or other products, is used for pain control and as an antidiarrheal agent.
  Ibuprofen¿¡ ´ëÇÑ Pharmacology Á¤º¸ Ibuprofen is a nonsteroidal antiinflammatory drug (NSAID) with analgesic and antipyretic properties. Ibuprofen has pharmacologic actions similar to those of other prototypical NSAIAs, that is thought to be associated with the inhibition of prostaglandin synthesis. Ibuprofen is used to treat rheumatoid arthritis, osteoarthritis, dysmenorrhea, and to alleviate moderate pain. 
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    | Metabolism | 
    
       Acetaminophen¿¡ ´ëÇÑ Metabolism Á¤º¸ # Phase_1_Metabolizing_Enzyme:Cytochrome P450 1A2 (CYP1A2)Cytochrome P450 2E1 (CYP2E1)
  Codeine¿¡ ´ëÇÑ Metabolism Á¤º¸ # Phase_1_Metabolizing_Enzyme:Cytochrome P450 2D6 (CYP2D6)
  Ibuprofen¿¡ ´ëÇÑ Metabolism Á¤º¸ # Phase_1_Metabolizing_Enzyme:Cytochrome P450 2C9 (CYP2C9)Monoamine oxidase type B (MAO-B) 
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    | Protein Binding | 
    
       Codeine¿¡ ´ëÇÑ ´Ü¹é°áÇÕ Á¤º¸ 7-25%
  Ibuprofen¿¡ ´ëÇÑ ´Ü¹é°áÇÕ Á¤º¸ 99% 
     | 
   
  
   
    | Half-life | 
    
       Acetaminophen¿¡ ´ëÇÑ ¹Ý°¨±â Á¤º¸ 1 to 4 hours
  Codeine¿¡ ´ëÇÑ ¹Ý°¨±â Á¤º¸ 2-4 hours
  Ibuprofen¿¡ ´ëÇÑ ¹Ý°¨±â Á¤º¸ 1.8-2.0 hours 
     | 
   
  
   
    | Absorption | 
    
       Acetaminophen¿¡ ´ëÇÑ Absorption Á¤º¸ Rapid and almost complete
  Codeine¿¡ ´ëÇÑ Absorption Á¤º¸ Well absorbed following oral administration with a bioavailability of approximately 90%.
  Ibuprofen¿¡ ´ëÇÑ Absorption Á¤º¸ rapidly absorbed 
     | 
   
  
   
    | Pharmacokinetics | 
    
       AcetaminophenÀÇ ¾à¹°µ¿·ÂÇÐÀÚ·á 
	- ´Ü¹é°áÇÕ : 20-50%
	
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		- °æ±¸ : »ó¿ë·® º¹¿ë½Ã 10-60ºÐ, ±Þ¼º Áßµ¶·® º¹¿ë½Ã Áö¿¬µÉ ¼ö ÀÖ´Ù.
	
  
   Codeine phosphateÀÇ ¾à¹°µ¿·ÂÇÐÀÚ·á 
	- ÀÛ¿ë¹ßÇö½Ã°£ 
	
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	 - ÀÛ¿ëÁö¼Ó½Ã°£ : 4-6 ½Ã°£
	
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 - ºÐÆ÷ : ÅÂ¹Ý Åë°ú, À¯Áó ºÐÆ÷
	
 - ´Ü¹é°áÇÕ : 7%
	
 - ´ë»ç : °£¿¡¼ morphine(Ȱ¼ºÇü)À¸·Î ´ë»ç
	
 - ¹Ý°¨±â : 2.5-3.5 ½Ã°£
	
 - ¼Ò½Ç : 3-16%°¡ ¹Ìº¯Èü, norcodeine, À¯¸®Çü ¹× Æ÷ÇÕÇü morphineÀ¸·Î¼ ´¢¸¦ ÅëÇØ ¹è¼³µÊ.
  
 IbuprofenÀÇ ¾à¹°µ¿·ÂÇÐÀÚ·á 
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 - ÀÛ¿ëÁö¼Ó½Ã°£ : 4-6 ½Ã°£
 
 - Ç׿°È¿°ú ¹ßÇö½Ã°£ : 7ÀϱîÁö
 
 - ÃÖ´ë Ç׿°È¿°ú ¹ßÇö½Ã°£ : 1-2ÁÖ
 
 - Èí¼ö : °æ±¸ : ½Å¼ÓÇÏ°Ô Èí¼öµÊ (85%)
 
 - ´Ü¹é°áÇÕ : 90-99%
 
 - ´ë»ç : °£¿¡¼ »êÈ´ë»ç
 
 - ¹Ý°¨±â : 2-4 ½Ã°£  (¸»±â ½ÅÁúȯ¿¡¼µµ ¹Ý°¨±â´Â º¯ÈÇÏÁö ¾ÊÀ½)
 
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     | 
   
  
   
    | Biotransformation | 
    
       Acetaminophen¿¡ ´ëÇÑ Biotransformation Á¤º¸ Approximately 90 to 95% of a dose is metabolized in the liver via the cytochrome P450 enzyme pathways (primarily by conjugation with glucuronic acid, sulfuric acid, and cysteine). An intermediate metabolite is hepatotoxic and most likely nephrotoxic and can accumulate after the primary metabolic pathways have been saturated.
  Codeine¿¡ ´ëÇÑ Biotransformation Á¤º¸ Hepatic. Codeine is a prodrug, itself inactive, but demethylated to the active morphine by the liver enzyme CYP2D6.
  Ibuprofen¿¡ ´ëÇÑ Biotransformation Á¤º¸ Hepatic 
     | 
   
  
   
    | Toxicity | 
    
       Acetaminophen¿¡ ´ëÇÑ Toxicity Á¤º¸ Oral, mouse: LD50 = 338 mg/kg; Oral, rat: LD50 = 1944 mg/kg. Acetaminophen is metabolized primarily in the liver, where most of it is converted to inactive compounds by conjugation with sulfate and glucuronide, and then excreted by the kidneys. Only a small portion is metabolized via the hepatic cytochrome P450 enzyme system. The toxic effects of acetaminophen are due to a minor alkylating metabolite (N-acetyl-p-benzo-quinone imine), not acetaminophen itself nor any of the major metabolites. This toxic metabolite reacts with sulfhydryl groups. At usual doses, it is quickly detoxified by combining irreversibly with the sulfhydryl group of glutathione to produce a non-toxic conjugate that is eventually excreted by the kidneys. The toxic dose of paracetamol is highly variable. In adults, single doses above 10 grams or 140 mg/kg have a reasonable likelihood of causing toxicity. In adults, single doses of more than 25 grams have a high risk of lethality.
  Codeine¿¡ ´ëÇÑ Toxicity Á¤º¸ Respiratory depression, sedation and miosis and common symptoms of overdose. Other symptoms include nausea, vomiting, skeletal muscle flaccidity, bradycardia, hypotension, and cool, clammy skin. Apnea and death may ensue.
  Ibuprofen¿¡ ´ëÇÑ Toxicity Á¤º¸ Abdominal pain, breathing difficulties, coma, drowsiness, headache, irregular heartbeat, kidney failure, low blood pressure, nausea, ringing in the ears, seizures, sluggishness, vomiting; LD50=1255mg/kg(orally in mice) 
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    | Drug Interactions | 
    
       Acetaminophen¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Anisindione	Acetaminophen  increases the anticoagulant effectWarfarin	Acetaminophen increases the anticoagulant effectImatinib	Increased hepatic toxicity of both agentsIsoniazid	Risk of hepatotoxicityDicumarol	Acetaminophen increases the anticoagulant effectDicumarol	Increases the anticoagulant effectAcenocoumarol	Increases the anticoagulant effect
  Codeine¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Cimetidine	Cimetidine increases the effect of the narcoticDihydroquinidine barbiturate	Quinidine decreases the analgesic effect of codeineNaltrexone	Naltrexone may precipitate a withdrawal syndrome in opioid-dependent individualQuinidine	Quinidine decreases the analgesic effect of codeineQuinidine barbiturate	Quinidine decreases the analgesic effect of codeine
  Ibuprofen¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Acebutolol	Risk of inhibition of renal prostaglandinsAtenolol	Risk of inhibition of renal prostaglandinsBetaxolol	Risk of inhibition of renal prostaglandinsBevantolol	Risk of inhibition of renal prostaglandinsBisoprolol	Risk of inhibition of renal prostaglandinsCarteolol	Risk of inhibition of renal prostaglandinsCarvedilol	Risk of inhibition of renal prostaglandinsEsmolol	Risk of inhibition of renal prostaglandinsLabetalol	Risk of inhibition of renal prostaglandinsNadolol	Risk of inhibition of renal prostaglandinsMetoprolol	Risk of inhibition of renal prostaglandinsOxprenolol	Risk of inhibition of renal prostaglandinsPenbutolol	Risk of inhibition of renal prostaglandinsPindolol	Risk of inhibition of renal prostaglandinsPractolol	Risk of inhibition of renal prostaglandinsPropranolol	Risk of inhibition of renal prostaglandinsSotalol	Risk of inhibition of renal prostaglandinsTimolol	Risk of inhibition of renal prostaglandinsWarfarin	The NSAID increases the anticoagulant effectAcenocoumarol	The NSAID increases the anticoagulant effectDicumarol	The NSAID increases the anticoagulant effectAnisindione	The NSAID increases the anticoagulant effectEthacrynic acid	The NSAID decreases the diuretic and antihypertensive effect of the loop diureticFurosemide	The NSAID decreases the diuretic and antihypertensive effect of the loop diureticTorasemide	The NSAID decreases the diuretic and antihypertensive effect of the loop diureticBumetanide	The NSAID decreases the diuretic and antihypertensive effect of the loop diureticAspirin	Ibuprofen reduces ASA cardioprotective effectsMethotrexate	The NSAID increases the effect and toxicity of methotrexateAlendronate	Increased risk of gastric toxicityCyclosporine	Monitor for nephrotoxicityLithium	The NSAID increases serum levels of lithium 
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    CYP450  Drug Interaction | 
    
      [CYP450 TableÁ÷Á¢Á¶È¸] Ibuprofen¿¡ ´ëÇÑ P450 table Codeine¿¡ ´ëÇÑ P450 table Acetaminophen¿¡ ´ëÇÑ P450 table
  SUBSTRATES 
CYP 2E1 
**acetaminophen** 
chlorzoxazone 
ethanol 
 INHIBITORS 
CYP 2E1 
disulfiram 
 INDUCERS 
CYP 2E1 
ethanol 
isoniazid 
  SUBSTRATES 
CYP 2D6 
Beta Blockers: 
S-metoprolol 
propafenone 
timolol 
Antidepressants: 
amitriptyline 
clomipramine 
desipramine 
imipramine 
paroxetine 
Antipsychotics: 
haloperidol 
risperidone 
thioridazine 
aripiprazole 
**codeine** 
dextromethorphan 
duloxetine 
flecainide 
mexiletine 
ondansetron 
tamoxifen 
tramadol 
venlafaxine 
 INHIBITORS 
CYP 2D6 
amiodarone 
buproprion 
chlorpheniramine 
cimetidine 
clomipramine 
duloxetine 
fluoxetine 
haloperidol 
methadone 
mibefradil 
paroxetine 
quinidine 
ritonavir 
 INDUCERS 
CYP 2D6 
N/A 
  SUBSTRATES 
CYP 2C9 
NSAIDs: 
diclofenac 
**ibuprofen** 
piroxicam 
Oral Hypoglycemic Agents: 
tolbutamide 
glipizide 
Angiotensin II Blockers: 
NOT candesartan 
irbesartan 
losartan 
NOT valsartan 
celecoxib 
fluvastatin naproxen 
phenytoin 
sulfamethoxazole 
tamoxifen 
tolbutamide 
torsemide 
warfarin 
 INHIBITORS 
CYP 2C9 
amiodarone 
fluconazole 
isoniazid 
 INDUCERS 
CYP 2C9 
rifampin 
secobarbital 
 
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    | Food Interaction | 
    
       Acetaminophen¿¡ ´ëÇÑ Food Interaction Á¤º¸ Take without regard to meals.Avoid alcohol (may increase risk of hepatotoxicity).
  Codeine¿¡ ´ëÇÑ Food Interaction Á¤º¸ Avoid alcohol.Take with food, food reduces irritation.To avoid constipation: increase your daily intake of fiber (beans, whole grains, vegetables).
  Ibuprofen¿¡ ´ëÇÑ Food Interaction Á¤º¸ Avoid alcohol.Take with food to reduce irritation. 
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    | Drug Target | 
    
      
      [Drug Target]
     | 
   
  
   
    | SNP Á¤º¸ | 
    
      Name:Codeine (DB00318)
 Interacting Gene/Enzyme:Cytochrome P450 2D6 (Gene symbol = CYP2D6) Swissprot P10635
 SNP(s):CYP2D6*5 (Deletion, homozygote)
 Effect:Poor drug metabolizer, lower dose requirements
 Reference(s):Desmeules J, Gascon MP, Dayer P, Magistris M: Impact of environmental and genetic factors on codeine analgesia. Eur J Clin Pharmacol. 1991;41(1):23-6. [PubMed] 
     | 
   
  
   
    | Description | 
    
       Acetaminophen¿¡ ´ëÇÑ Description Á¤º¸ Analgesic antipyretic derivative of acetanilide. It has weak anti-inflammatory properties and is used as a common analgesic, but may cause liver, blood cell, and kidney damage. [PubChem]
  Codeine¿¡ ´ëÇÑ Description Á¤º¸ An opioid analgesic related to morphine but with less potent analgesic properties and mild sedative effects. It also acts centrally to suppress cough. [PubChem]
  Ibuprofen¿¡ ´ëÇÑ Description Á¤º¸ A nonsteroidal anti-inflammatory agent with analgesic properties used in the therapy of rheumatism and arthritis. [PubChem] 
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    | Dosage Form | 
    
       Acetaminophen¿¡ ´ëÇÑ Dosage_Form Á¤º¸ Capsule	OralElixir	OralLiquid	OralSolution	OralSolution / drops	OralSuppository	RectalSuspension	OralSyrup	OralTablet	OralTablet, effervescent	OralTablet, extended release	Oral
  Codeine¿¡ ´ëÇÑ Dosage_Form Á¤º¸ Liquid	IntramuscularLiquid	OralSolution	IntramuscularSyrup	OralTablet	Oral
  Ibuprofen¿¡ ´ëÇÑ Dosage_Form Á¤º¸ Capsule	OralSuspension	OralTablet	OralTablet, chewable	Oral 
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    | Drug Category | 
    
       Acetaminophen¿¡ ´ëÇÑ Drug_Category Á¤º¸ Analgesics, Non-NarcoticAntipyretics
  Codeine¿¡ ´ëÇÑ Drug_Category Á¤º¸ AnalgesicsAnalgesics, OpioidAntitussive AgentsAntitussivesNarcoticsOpiate Agonists
  Ibuprofen¿¡ ´ëÇÑ Drug_Category Á¤º¸ AnalgesicsAnalgesics, Non-NarcoticAnti-Inflammatory Agents, Non-SteroidalAnti-inflammatory AgentsCyclooxygenase InhibitorsNonsteroidal Antiinflammatory Agents (NSAIDs) 
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    | Smiles String Canonical | 
    
       Acetaminophen¿¡ ´ëÇÑ Smiles_String_canonical Á¤º¸ CC(=O)NC1=CC=C(O)C=C1
  Codeine¿¡ ´ëÇÑ Smiles_String_canonical Á¤º¸ COC1=C2OC3C(O)C=CC4C5CC(C=C1)=C2C34CCN5C
  Ibuprofen¿¡ ´ëÇÑ Smiles_String_canonical Á¤º¸ CC(C)CC1=CC=C(C=C1)C(C)C(O)=O 
     | 
   
  
   
    | Smiles String Isomeric | 
    
       Acetaminophen¿¡ ´ëÇÑ Smiles_String_isomeric Á¤º¸ CC(=O)NC1=CC=C(O)C=C1
  Codeine¿¡ ´ëÇÑ Smiles_String_isomeric Á¤º¸ COC1=C2O[C@H]3[C@@H](O)C=C[C@H]4[C@H]5CC(C=C1)=C2[C@@]34CCN5C
  Ibuprofen¿¡ ´ëÇÑ Smiles_String_isomeric Á¤º¸ CC(C)CC1=CC=C(C=C1)[C@@H](C)C(O)=O 
     | 
   
  
   
    | InChI Identifier | 
    
       Acetaminophen¿¡ ´ëÇÑ InChI_Identifier Á¤º¸ InChI=1/C8H9NO2/c1-6(10)9-7-2-4-8(11)5-3-7/h2-5,11H,1H3,(H,9,10)/f/h9H
  Codeine¿¡ ´ëÇÑ InChI_Identifier Á¤º¸ InChI=1/C18H21NO3/c1-19-8-7-18-11-4-5-13(20)17(18)22-16-14(21-2)6-3-10(15(16)18)9-12(11)19/h3-6,11-13,17,20H,7-9H2,1-2H3/t11-,12+,13-,17-,18-/m0/s1
  Ibuprofen¿¡ ´ëÇÑ InChI_Identifier Á¤º¸ InChI=1/C13H18O2/c1-9(2)8-11-4-6-12(7-5-11)10(3)13(14)15/h4-7,9-10H,8H2,1-3H3,(H,14,15)/f/h14H 
     | 
   
  
   
    | Chemical IUPAC Name | 
    
       Acetaminophen¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ N-(4-hydroxyphenyl)acetamide
  Codeine¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ (5(,6()-7,8-didehydro-4,5-epoxy-3-methoxy-17-methylmorphinan-6-ol
  Ibuprofen¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ 2-[4-(2-methylpropyl)phenyl]propanoic acid 
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    | Drug-Induced Toxicity Related Proteins | 
    
      ACETAMINOPHEN ÀÇ Drug-Induced Toxicity Related ProteinÁ¤º¸ Replated Protein:Alpha-2A adrenergic receptor  Drug:acetaminophen Toxicity:hepatic injury .  [¹Ù·Î°¡±â] Replated Protein:Myeloperoxidase  Drug:acetaminophen Toxicity:respiratory burst.  [¹Ù·Î°¡±â] Replated Protein:Glucose-6-phosphate 1-dehydrogenase Drug:acetaminophen Toxicity:drug-induced hemolysis.  [¹Ù·Î°¡±â] Replated Protein:Ornithine decarboxylase Drug:acetaminophen Toxicity:hepatotoxicity.  [¹Ù·Î°¡±â] Replated Protein:Lactate dehydrogenase Drug:acetaminophen Toxicity:hepatotoxicity.  [¹Ù·Î°¡±â] Replated Protein:Transcription factor AP-1(JUN) Drug:acetaminophen Toxicity:hepatotoxicity.  [¹Ù·Î°¡±â] Replated Protein:Haptoglobin  Drug:acetaminophen Toxicity:drug-induced hemolysis.  [¹Ù·Î°¡±â] Replated Protein:Alanine aminotransferase Drug:acetaminophen Toxicity:hepatotoxicity.  [¹Ù·Î°¡±â] Replated Protein:Beta-glucuronidase  Drug:acetaminophen Toxicity:hepatotoxin-induced effects.  [¹Ù·Î°¡±â] Replated Protein:CYP2E1 Drug:Acetaminophen Toxicity:idiosyncratic hepatotoxicity.  [¹Ù·Î°¡±â] Replated Protein:Cytochrome P450 2E1  Drug:acetaminophen  Toxicity:hepatotoxicity.  [¹Ù·Î°¡±â] Replated Protein:Sulfotransferase family cytosolic Drug:acetaminophen  Toxicity:chronic hypoxia.  [¹Ù·Î°¡±â] Replated Protein:Cytochrome P450 3A4  Drug:acetaminophen  Toxicity:hepatotoxicity.  [¹Ù·Î°¡±â] Replated Protein:Caspase recruitment domain-containing protein  Drug:acetaminophen  Toxicity:hepatotoxicity.  [¹Ù·Î°¡±â] Replated Protein:Cytochrome P450 1A2  Drug:acetaminophen  Toxicity:hepatotoxicity.  [¹Ù·Î°¡±â] ACETAMINOPHEN (APAP) ÀÇ Drug-Induced Toxicity Related ProteinÁ¤º¸ Replated Protein:Cytochrome P450 Drug:acetaminophen (APAP) Toxicity:renal functional changes, strain-dependent histopathological changes.  [¹Ù·Î°¡±â] IBUPROFEN ÀÇ Drug-Induced Toxicity Related ProteinÁ¤º¸ Replated Protein:Myeloperoxidase  Drug:ibuprofen Toxicity:increase the incidence of ventricular fibrillation.  [¹Ù·Î°¡±â] Replated Protein:Myeloperoxidase  Drug:ibuprofen Toxicity:increase the incidence of haemorrhagic infarction.  [¹Ù·Î°¡±â] Replated Protein:Arylamine N-acetyltransferase 2 Drug:ibuprofen  Toxicity:ibuprofen inhibition.  [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. ACETAMINOPHEN[Composite Activity](Score)  A(Marginal)  3(Active)  2[Alkaline Phosphatase Increase](Activity Score)  M(Number of Rpts)  ¡Ã4(Index value)  NSU[SGOT Increase](Activity Score)  A(Number of Rpts)  ¡Ã4(Index value)  NSU[SGPT Increase](Activity Score)  A(Number of Rpts)  ¡Ã4(Index value)  NSU[LDH Increase](Activity Score)  M(Number of Rpts)  ¡Ã4(Index value)  NSU[GGT Increase](Activity Score)  M(Number of Rpts)  ¡Ã4(Index value)  NSUIBUPROFEN[GGT Increase][Composite Activity](Score)  NA(Marginal)  3(Active)  0[Alkaline Phosphatase Increase](Activity Score)  M(Number of Rpts)  ¡Ã4(Index value)  NSU[SGOT Increase](Activity Score)  M(Number of Rpts)  ¡Ã4(Index value)  NSU[SGPT Increase](Activity Score)  M(Number of Rpts)  ¡Ã4(Index value)  NSU[LDH Increase](Activity Score)  NA(Number of Rpts)  NA(Index value)  NA[GGT Increase](Activity Score)  NA(Number of Rpts)  NA(Index value)  NA
 
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