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Indapamide¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ Indapamide blocks the slow component of delayed rectifier potassium current (IKs) without altering the rapid component (IKr) or the inward rectifier current. Specifically it blocks or antagonizes the action the proteins KCNQ1 and KCNE1. Indapamide is also thought to stimulate the synthesis of the vasodilatory hypotensive prostaglandin PGE2.
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Indapamide¿¡ ´ëÇÑ Pharmacology Á¤º¸ Indapamide is an antihypertensive and a diuretic. It contains both a polar sulfamoyl chlorobenzamide moiety and a lipid- soluble methylindoline moiety. Indapamide bears a structural similarity to the triazide diuretics which are known to decrease vascular smooth muscle reactivity. However, it differs chemically from the thiazides in that it does not possess the thiazide ring system and contains only one sulfonamide group. Indapamide appears to cause vasodilation, probably by inhibiting the passage of calcium and other ions (sodium, potassium) across membranes. This same effect may cause hypokalcemia in susceptible individuals. Indapamide has also been shown to cause uterine myometrial relaxation in experimental animals. Overall, indapamide has an extra-renal antihypertensive action resulting in a decrease in vascular hyperreactivity and a reduction in total peripheral and arteriolar resistance.
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Indapamide¿¡ ´ëÇÑ ´Ü¹é°áÇÕ Á¤º¸ 71-79%
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Indapamide¿¡ ´ëÇÑ ¹Ý°¨±â Á¤º¸ 14 hours (biphasic)
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| Absorption |
Indapamide¿¡ ´ëÇÑ Absorption Á¤º¸ Rapidly absorbed from gastrointestinal tract.
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| Pharmacokinetics |
IndapamideÀÇ ¾à¹°µ¿·ÂÇÐÀÚ·á
- Èí¼ö : À§Àå°ü¿¡¼ ¿ÏÀüÈ÷ Èí¼öµÈ´Ù.
- ´Ü¹é°áÇÕ : 71-79%
- ´ë»ç : ´ëºÎºÐ °£¿¡¼ ´ë»çµÈ´Ù.
- ¹Ý°¨±â : 14-18½Ã°£
- Ç÷ÁßÃÖ°í³óµµ µµ´Þ½Ã°£ : 2-2.5½Ã°£
- ¼Ò½Ç : 48½Ã°£ À̳»¿¡ 60%±îÁö ´¢·Î ¹è¼³µÈ´Ù. 16-23%´Â ´ãÁóÀ» ÅëÇØ º¯À¸·Î ¹è¼³µÈ´Ù.
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| Biotransformation |
Indapamide¿¡ ´ëÇÑ Biotransformation Á¤º¸ Primarily hepatic. Indapamide is an extensively metabolized drug with only about 7+ACU- of the total dose administered, recovered in the urine as unchanged drug during the first 48 hours after administration.
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| Toxicity |
Indapamide¿¡ ´ëÇÑ Toxicity Á¤º¸ Side effects include electrolyte imbalance (potassium or salt depletion due to too much fluid loss), nausea, stomach disorders, vomiting, weakness
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| Drug Interactions |
Indapamide¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Amantadine The diuretic increases the adverse effect of amantadineDeslanoside Possible electrolyte variations and arrhythmiasDiazoxide Significant hyperglycemic effectDigitoxin Possible electrolyte variations and arrhythmiasDigoxin Possible electrolyte variations and arrhythmiasDofetilide Increased risk of cardiotoxicity and arrhythmiasLithium The thiazide diuretic increases serum levels of lithium
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CYP450 Drug Interaction |
[CYP450 TableÁ÷Á¢Á¶È¸]
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| Food Interaction |
Indapamide¿¡ ´ëÇÑ Food Interaction Á¤º¸ Take without regard to meals. Magnesium, potassium and zinc needs increased.
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| Drug Target |
[Drug Target]
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| Description |
Indapamide¿¡ ´ëÇÑ Description Á¤º¸ A benzamide-sulfonamide-indole. It is called a thiazide-like diuretic but structure is different enough (lacking the thiazo-ring) so it is not clear that the mechanism is comparable. [PubChem]
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| Drug Category |
Indapamide¿¡ ´ëÇÑ Drug_Category Á¤º¸ Antihypertensive AgentsDiuretics
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| Smiles String Canonical |
Indapamide¿¡ ´ëÇÑ Smiles_String_canonical Á¤º¸ CC1CC2=CC=CC=C2N1NC(=O)C1=CC(=C(Cl)C=C1)S(N)(=O)=O
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| Smiles String Isomeric |
Indapamide¿¡ ´ëÇÑ Smiles_String_isomeric Á¤º¸ C[C@H]1CC2=CC=CC=C2N1NC(=O)C1=CC(=C(Cl)C=C1)S(N)(=O)=O
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| InChI Identifier |
Indapamide¿¡ ´ëÇÑ InChI_Identifier Á¤º¸ InChI=1/C16H16ClN3O3S/c1-10-8-11-4-2-3-5-14(11)20(10)19-16(21)12-6-7-13(17)15(9-12)24(18,22)23/h2-7,9-10H,8H2,1H3,(H,19,21)(H2,18,22,23)/f/h19H,18H2
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| Chemical IUPAC Name |
Indapamide¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ 4-chloro-N-(2-methyl-2,3-dihydroindol-1-yl)-3-sulfamoylbenzamide
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| Drug-Induced Toxicity Related Proteins |
INDAPAMIDE ÀÇ Drug-Induced Toxicity Related ProteinÁ¤º¸ Replated Protein:Elastin Drug:indapamide Toxicity:reduce arterial rigidity. [¹Ù·Î°¡±â]
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ÀüÈ: 02-3486-1061 ¤Ó À̸ÞÀÏ: webmaster@druginfo.co.kr
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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. INDAPAMIDE[GGT Increase][Composite Activity](Score) I(Marginal) 0(Active) 0[Alkaline Phosphatase Increase](Activity Score) I(Number of Rpts) <4(Index value) 0.5[SGOT Increase](Activity Score) I(Number of Rpts) <4(Index value) 1[SGPT Increase](Activity Score) I(Number of Rpts) <4(Index value) 0.5[LDH Increase](Activity Score) I(Number of Rpts) <4(Index value) 0.5[GGT Increase](Activity Score) I(Number of Rpts) <4(Index value) 0
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