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    | º¸°ü»ó ÁÖÀÇ | 
    
      
    	
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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 | 
    
       Tacrolimus¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ The mechanism of action of tacrolimus in atopic dermatitis is not known. While the following have been observed, the clinical significance of these observations in atopic dermatitis is not known. It has been demonstrated that tacrolimus inhibits T-lymphocyte activation by first binding to an intracellular protein, FKBP-12. A complex of tacrolimus-FKBP-12, calcium, calmodulin, and calcineurin is then formed and the phosphatase activity of calcineurin is inhibited. This prevents the dephosphorylation and translocation of nuclear factor of activated T-cells (NF-AT), a nuclear component thought to initiate gene transcription for the formation of lymphokines. Tacrolimus also inhibits the transcription for genes which encode IL-3, IL-4, IL-5, GM-CSF, and TNF-, all of which are involved in the early stages of T-cell activation. Additionally, tacrolimus has been shown to inhibit the release of pre-formed mediators from skin mast cells and basophils, and to downregulate the expression of FceRI on Langerhans cells. 
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    | Pharmacology | 
     
       Tacrolimus¿¡ ´ëÇÑ Pharmacology Á¤º¸ Tacrolimus is a macrolide antibiotic. It acts by reducing peptidyl-prolyl isomerase activity by binding to the immunophilin FKBP-12 (FK506 binding protein) creating a new complex. This inhibits both T-lymphocyte signal transduction and IL-2 transcription. Although this activity is similar to cyclosporine studies have shown that the incidence of acute rejection is reduced by tacrolimus use over cyclosporine. Tacrolimus has also been shown to be effective in the topical treatment of eczema, particularly atopic eczema. It suppresses inflammation in a similar way to steroids, but is not as powerful. An important dermatological advantage of tacrolimus is that it can be used directly on the face; topical steroids cannot be used on the face, as they thin the skin dramatically there. On other parts of the body, topical steroid are generally a better treatment. 
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    | Metabolism | 
    
       Tacrolimus¿¡ ´ëÇÑ Metabolism Á¤º¸ # Phase_1_Metabolizing_Enzyme:Cytochrome P450 3A4 (CYP3A4)Cytochrome P450 3A5 (CYP3A5)Cytochrome P450 3A3 (CYP3A3) 
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    | Protein Binding | 
    
       Tacrolimus¿¡ ´ëÇÑ ´Ü¹é°áÇÕ Á¤º¸ 75-99% 
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    | Half-life | 
    
       Tacrolimus¿¡ ´ëÇÑ ¹Ý°¨±â Á¤º¸ 11.3 hours (range from 3.5 to 40.6 hours) 
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    | Absorption | 
    
       Tacrolimus¿¡ ´ëÇÑ Absorption Á¤º¸ 20% bioavailability; less after eating food rich in fat 
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    | Pharmacokinetics | 
    
       Tacrolimus hydrateÀÇ ¾à¹°µ¿·ÂÇÐÀÚ·á 
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    | Biotransformation | 
    
       Tacrolimus¿¡ ´ëÇÑ Biotransformation Á¤º¸ Hepatic, extensive, primarily by CYP3A4. The major metabolite identified in incubations with human liver microsomes is 13-demethyl tacrolimus. In in vitro studies, a 31-demethyl metabolite has been reported to have the same activity as tacrolimus. 
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    | Toxicity | 
    
       Tacrolimus¿¡ ´ëÇÑ Toxicity Á¤º¸ Side effects can be severe and include blurred vision, liver and kidney problems (it is nephrotoxic), seizures, tremors, hypertension, hypomagnesemia, diabetes mellitus, hyperkalemia, itching, insomnia, confusion. LD50=134-194 mg/kg (rat). 
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    | Drug Interactions | 
    
       Tacrolimus¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Not Available 
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    CYP450  Drug Interaction | 
    
      [CYP450 TableÁ÷Á¢Á¶È¸] 
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    | Food Interaction | 
    
       Tacrolimus¿¡ ´ëÇÑ Food Interaction Á¤º¸ Not Available 
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    | Drug Target | 
    
      
      [Drug Target]
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    | Description | 
    
       Tacrolimus¿¡ ´ëÇÑ Description Á¤º¸ Tacrolimus (also FK-506 or Fujimycin) is an immunosuppressive drug whose main use is after organ transplant to reduce the activity of the patient's immune system and so the risk of organ rejection. It is also used in a topical preparation in the treatment of severe atopic dermatitis, severe refractory uveitis after bone marrow transplants, and the skin condition vitiligo. It was discovered in 1984 from the fermentation broth of a Japanese soil sample that contained the bacteria Streptomyces tsukubaensis. Tacrolimus is chemically known as a macrolide. It reduces peptidyl-prolyl isomerase activity by binding to the immunophilin FKBP-12 (FK506 binding protein) creating a new complex. This FKBP12-FK506 complex interacts with and inhibits calcineurin thus inhibiting both T-lymphocyte signal transduction and IL-2 transcription. 
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    | Dosage Form | 
    
       Tacrolimus¿¡ ´ëÇÑ Dosage_Form Á¤º¸ Capsule	OralOintment	TopicalSolution	Intravenous 
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    | Drug Category | 
    
       Tacrolimus¿¡ ´ëÇÑ Drug_Category Á¤º¸ Immunosuppressive Agents 
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    | Smiles String Canonical | 
    
       Tacrolimus¿¡ ´ëÇÑ Smiles_String_canonical Á¤º¸ COC1CC(CCC1O)C=C(C)C1OC(=O)C2CCCCN2C(=O)C(=O)C2(O)OC(C(CC(C)CC(C)=CC(CC=C)C(=O)CC(O)C1C)OC)C(CC2C)OC 
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    | Smiles String Isomeric | 
    
       Tacrolimus¿¡ ´ëÇÑ Smiles_String_isomeric Á¤º¸ CO[C@@H]1C[C@@H](CC[C@H]1O)\C=C(\C)[C@H]1OC(=O)[C@@H]2CCCCN2C(=O)C(=O)[C@]2(O)O[C@H]([C@H](C[C@@H](C)C\C(C)=C\[C@@H](CC=C)C(=O)C[C@H](O)[C@H]1C)OC)[C@H](C[C@H]2C)OC 
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    | InChI Identifier | 
    
       Tacrolimus¿¡ ´ëÇÑ InChI_Identifier Á¤º¸ InChI=1/C44H69NO12/c1-10-13-31-19-25(2)18-26(3)20-37(54-8)40-38(55-9)22-28(5)44(52,57-40)41(49)42(50)45-17-12-11-14-32(45)43(51)56-39(29(6)34(47)24-35(31)48)27(4)21-30-15-16-33(46)36(23-30)53-7/h10,19,21,26,28-34,36-40,46-47,52H,1,11-18,20,22-24H2,2-9H3/t26-,28+,29+,30-,31+,32-,33+,34-,36+,37-,38-,39+,40+,44+/m0/s1 
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    | Chemical IUPAC Name | 
    
       Tacrolimus¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ [3S-[3R*[E(1S*,3S*,4S*)],4S*,5R*,8S*,9E,12R*,14R*,15S*,16R*,18S*,19S*,26aR*]]-5,6,8,11,12,13,14,15,16,17,18,19,24,25,26,26a-hexadecahydro-5, 19-dihydroxy-3- [2-(4-hydroxy-3-methoxycyclohexyl) -1-methylethenyl]-14, 16-dimethoxy-4,10,12,18-tetramethyl-8-(2-propenyl)-15, 19-epoxy-3H-pyrido[2,1-c][1,4] oxaazacyclotricosine-1,7,20, 21(4H,23H)-tetrone, monohydrate 
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