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    | º¸°ü»ó ÁÖÀÇ | 
    
      
    	
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    | Á¶Á¦½Ã ÁÖÀÇ | 
    
      
    	
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                | ÇмúÁ¤º¸ | 
                             
	         
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    | Ç׸ñ | 
    ³»¿ë | 
   
  
    | 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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       [¿¬·É´ë±Ý±â»ó¼¼°Ë»ö]
       
       
        
        
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    | Mechanism of Action | 
    
       Alprostadil¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ Alprostadil causes vasodilation by means of a direct effect on vascular and ductus arteriosus (DA) smooth muscle, preventing or reversing the functional closure of the DA that occurs shortly after birth. This results in increased pulmonary or systemic blood flow in infants. In cyanotic congenital heart disease, alprostadil's actions result in an increased oxygen supply to the tissues. In infants with interrupted aortic arch or very severe aortic coarctation, alprostadil maintains distal aortic perfusion by permitting blood flow through the DA from the pulmonary artery to the aorta. In infants with aortic coarctation, alprostadil reduces aortic obstruction either by relaxing ductus tissue in the aortic wall or by increasing effective aortic diameter by dilating the DA. In infants with these aortic arch anomalies, systemic blood flow to the lower body is increased, improving tissue oxygen supply and renal perfusion. When administered by intracavernosal injection or as an intraurethral suppository, alprostadil acts locally to relax the trabecular smooth muscle of the corpora cavernosa and the cavernosal arteries. Swelling, elongation, and rigidity of the penis result when arterial blood rapidly flows into the corpus cavernosum to expand the lacunar spaces. The entrapped blood reduces the venous blood outflow as sinusoids compress against the tunica albuginea. 
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    | Pharmacology | 
     
       Alprostadil¿¡ ´ëÇÑ Pharmacology Á¤º¸ Alprostadil (prostaglandin E1) is produced endogenously to relax vascular smooth muscle and cause vasodilation. In adult males, the vasodilatory effects of alprostadil on the cavernosal arteries and the trabecular smooth muscle of the corpora cavernosa result in rapid arteriolar inflow and expansion of the lacunar spaces within the corpora. As the expanded corporal sinusoids are compressed against the tunica albuginea, venous outflow through the subtunical vessels is impeded and penile rigidity develops. This is referred to as the corporal veno-occlusive mechanism. In infants, the vasodilatory effects of alprostadil increase pulmonary or systemic blood flow. 
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    | Metabolism | 
    
       Alprostadil¿¡ ´ëÇÑ Metabolism Á¤º¸ # Phase_1_Metabolizing_Enzyme:Not Available 
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    | Protein Binding | 
    
       Alprostadil¿¡ ´ëÇÑ ´Ü¹é°áÇÕ Á¤º¸ Bound in plasma primarily to albumin (81% bound) and to a lesser extent alpha-globulin IV-4 fraction (55% bound). 
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    | Half-life | 
    
       Alprostadil¿¡ ´ëÇÑ ¹Ý°¨±â Á¤º¸ 5 to 10 minutes (after a single dose), in healthy adults and neonates. 
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    | Absorption | 
    
       Alprostadil¿¡ ´ëÇÑ Absorption Á¤º¸ The absolute bioavailability of alprostadil has not been determined. 
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    | Pharmacokinetics | 
    
       AlprostadilÀÇ ¾à¹°µ¿·ÂÇÐÀÚ·á 
	- ºÐÆ÷ : À½°æ ÁÖÀÔ ÈÄ À¯ÀÇÇÏÁö ¾ÊÀº ¾ç¸¸ÀÌ ¸»ÃÊ¿¡ ºÐÆ÷ÇÔ.
	
 - ´Ü¹é°áÇÕ : Ç÷Àå albumin¿¡ 81%
	
 - ´ë»ç : ¾à 75%±îÁö Æó ÃÊȸÅë°úÈ¿°ú¸¦ ¹Þ¾Æ »êÈ¿¡ ÀÇÇØ ´ë»çµÊ.
	
 - ¹Ý°¨±â : 5~10ºÐ
	
 - ¼Ò½Ç : ´ë»çü·Î ´¢¸¦ ÅëÇØ ¹è¼³µÊ. (24½Ã°£ À̳»¿¡´Â 90%)
  
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    | Biotransformation | 
    
       Alprostadil¿¡ ´ëÇÑ Biotransformation Á¤º¸ Alprostadil must be infused continuously because it is very rapidly metabolized. As much as 80% of the circulating alprostadil may be metabolized in one pass through the lungs, primarily by beta- and omega-oxidation. 
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    | Toxicity | 
    
       Alprostadil¿¡ ´ëÇÑ Toxicity Á¤º¸ Oral, mouse: LD50 = 186 mg/kg; Oral, rat: LD50 = 228 mg/kg. Apnea, bradycardia, pyrexia, hypotension, and flushing may be signs of drug overdosage. 
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    | Drug Interactions | 
    
       Alprostadil¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Not Available 
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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 | 
    
       Alprostadil¿¡ ´ëÇÑ Description Á¤º¸ Alprostadil is produced endogenously and causes vasodilation by means of a direct effect on vascular and ductus arteriosus (DA) smooth muscle, preventing or reversing the functional closure of the DA that occurs shortly after birth. This results in increased pulmonary or systemic blood flow in infants. In infants, it is used for palliative, not definitive, therapy to temporarily maintain the patency of the ductus arteriosus until corrective or palliative surgery can be performed in neonates who have congenital heart defects and who depend upon the patent ductus for survival. In adults, it is used for the treatment of erectile dysfunction due to neurogenic, vasculogenic, psychogenic, or mixed etiology. 
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    | Dosage Form | 
    
       Alprostadil¿¡ ´ëÇÑ Dosage_Form Á¤º¸ Liquid	IntravenousSolution	Intra-arterialSuppository	Urethral 
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    | Drug Category | 
    
       Alprostadil¿¡ ´ëÇÑ Drug_Category Á¤º¸ Fibrinolytic AgentsPlatelet Aggregation InhibitorsVasodilator Agents 
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    | Smiles String Canonical | 
    
       Alprostadil¿¡ ´ëÇÑ Smiles_String_canonical Á¤º¸ CCCCCC(O)C=CC1C(O)CC(=O)C1CCCCCCC(O)=O 
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    | Smiles String Isomeric | 
    
       Alprostadil¿¡ ´ëÇÑ Smiles_String_isomeric Á¤º¸ CCCCC[C@H](O)\C=C\[C@H]1[C@H](O)CC(=O)[C@@H]1CCCCCCC(O)=O 
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    | InChI Identifier | 
    
       Alprostadil¿¡ ´ëÇÑ InChI_Identifier Á¤º¸ InChI=1/C20H34O5/c1-2-3-6-9-15(21)12-13-17-16(18(22)14-19(17)23)10-7-4-5-8-11-20(24)25/h12-13,15-17,19,21,23H,2-11,14H2,1H3,(H,24,25)/t15-,16+,17+,19+/m0/s1/f/h24H 
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    | Chemical IUPAC Name | 
    
       Alprostadil¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ 7-[(1R,2R,3R)-3-hydroxy-2-[(3S)-3-hydroxyoct-1-enyl]-5-oxocyclopentyl]heptanoic 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. ALPROSTADIL[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[SGPT Increase](Activity Score)  I(Number of Rpts)  <4(Index value)  0[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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