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| Mechanism of Action |
Minoxidil¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ Minoxidil is thought to promote the survival of human dermal papillary cells (DPCs) or hair cells by activating both extracellular signal-regulated kinase (ERK) and Akt and by preventing cell death by increasing the ratio of BCl-2/Bax. Minoxidil may stimulate the growth of human hairs by prolonging anagen through these proliferative and anti-apoptotic effects on DPCs. Minoxidil, when used as a vasodilator, acts by opening adenosine triphosphate-sensitive potassium channels in vascular smooth muscle cells. This vasodilation may also improve the viability of hair cells or hair follicles.
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| Pharmacology |
Minoxidil¿¡ ´ëÇÑ Pharmacology Á¤º¸ Minoxidil is an orally effective direct acting peripheral vasodilator that reduces elevated systolic and diastolic blood pressure by decreasing peripheral vascular resistance. Minoxidil is also used topically to treat androgenetic alopecia. Microcirculatory blood flow in animals is enhanced or maintained in all systemic vascular beds. In man, forearm and renal vascular resistance decline; forearm blood flow increases while renal blood flow and glomerular filtration rate are preserved. The predominant site of minoxidil action is arterial. Venodilation does not occur with minoxidil; thus, postural hypotension is unusual with its administration. The antihypertensive activity of minoxidil is due to its sulphate metabolite, minoxidil sulfate.
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| Metabolism |
Minoxidil¿¡ ´ëÇÑ Metabolism Á¤º¸ # Phase_1_Metabolizing_Enzyme:Not Available
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| Protein Binding |
Minoxidil¿¡ ´ëÇÑ ´Ü¹é°áÇÕ Á¤º¸ Minoxidil does not bind to plasma proteins.
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| Half-life |
Minoxidil¿¡ ´ëÇÑ ¹Ý°¨±â Á¤º¸ 4.2 hours
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| Absorption |
Minoxidil¿¡ ´ëÇÑ Absorption Á¤º¸ Minoxidil is at least 90% absorbed from the GI tract in experimental animals and man.
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| Pharmacokinetics |
MinoxidilÀÇ ¾à¹°µ¿·ÂÇÐÀÚ·á
- Ç÷¾Ð°ÇÏÈ¿°ú ¹ßÇö½Ã°£ : °æ±¸ : 30ºÐ À̳»
- ÃÖ´ëÈ¿°ú ¹ßÇö½Ã°£ : 2-8½Ã°£ À̳»
- ÀÛ¿ëÁö¼Ó½Ã°£ : 2-5ÀϱîÁö
- ´Ü¹é°áÇÕ : ¾ø½¿
- ´ë»ç : 88%°¡ ÀÏÂ÷ÀûÀ¸·Î glucuronidationÀ¸·Î ´ë»ç
- »ýü³»ÀÌ¿ë·ü : °æ±¸ : 90%
- ¹Ý°¨±â : ¼ºÀÎ : 3.5-4.2½Ã°£
- ¼Ò½Ç : 12%°¡ ¹Ìº¯Èü·Î ½Å ¹è¼³µÊ
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| Biotransformation |
Minoxidil¿¡ ´ëÇÑ Biotransformation Á¤º¸ Approximately 90% of the administered drug is metabolized, predominantly by conjugation with glucuronic acid at the N-oxide position in the pyrimidine ring, but also by conversion to more polar products. Known metabolites exert much less pharmacologic effect than minoxidil itself.
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| Toxicity |
Minoxidil¿¡ ´ëÇÑ Toxicity Á¤º¸ Oral LD50 in rats has ranged from 1321-3492 mg/kg; in mice, 2456-2648 mg/kg. Side effects include cardiovascular effects associated with hypotension such as sudden weight gain, rapid heart beat, faintness or dizziness.
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| Drug Interactions |
Minoxidil¿¡ ´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 |
Minoxidil¿¡ ´ëÇÑ Food Interaction Á¤º¸ Take without regard to meals.
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| Drug Target |
[Drug Target]
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| Description |
Minoxidil¿¡ ´ëÇÑ Description Á¤º¸ A potent direct-acting peripheral vasodilator (vasodilator agents) that reduces peripheral resistance and produces a fall in blood pressure. (From Martindale, The Extra Pharmacopoeia, 30th ed, p371)
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| Dosage Form |
Minoxidil¿¡ ´ëÇÑ Dosage_Form Á¤º¸ Liquid TopicalSolution TopicalTablet Oral
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| Drug Category |
Minoxidil¿¡ ´ëÇÑ Drug_Category Á¤º¸ Antihypertensive AgentsVasodilator Agents
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| Smiles String Canonical |
Minoxidil¿¡ ´ëÇÑ Smiles_String_canonical Á¤º¸ [H]N=C1N=C(C=C(N)N1O)N1CCCCC1
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| Smiles String Isomeric |
Minoxidil¿¡ ´ëÇÑ Smiles_String_isomeric Á¤º¸ [H]\N=C1/N=C(C=C(N)N1O)N1CCCCC1
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| InChI Identifier |
Minoxidil¿¡ ´ëÇÑ InChI_Identifier Á¤º¸ InChI=1/C9H15N5O/c10-7-6-8(12-9(11)14(7)15)13-4-2-1-3-5-13/h6,11,15H,1-5,10H2/b11-9+
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| Chemical IUPAC Name |
Minoxidil¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ 3-hydroxy-2-imino-6-piperidin-1-ylpyrimidin-4-amine
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ÀüÈ: 02-3486-1061 ¤Ó À̸ÞÀÏ: webmaster@druginfo.co.kr
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