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| Mechanism of Action |
Glipizide¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ Sulfonylureas likely bind to ATP-sensitive potassium-channel receptors on the pancreatic cell surface, reducing potassium conductance and causing depolarization of the membrane. Depolarization stimulates calcium ion influx through voltage-sensitive calcium channels, raising intracellular concentrations of calcium ions, which induces the secretion, or exocytosis, of insulin.
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| Pharmacology |
Glipizide¿¡ ´ëÇÑ Pharmacology Á¤º¸ Glipizide, a second-generation sulfonylurea, is used with diet to lower blood glucose in patients with diabetes mellitus type II. The primary mode of action of glipizide in experimental animals appears to be the stimulation of insulin secretion from the beta cells of pancreatic islet tissue and is thus dependent on functioning beta cells in the pancreatic islets. In humans glipizide appears to lower the blood glucose acutely by stimulating the release of insulin from the pancreas, an effect dependent upon functioning beta cells in the pancreatic islets. In man, stimulation of insulin secretion by glipizide in response to a meal is undoubtedly of major importance. Fasting insulin levels are not elevated even on long-term glipizide administration, but the postprandial insulin response continues to be enhanced after at least 6 months of treatment. Some patients fail to respond initially, or gradually lose their responsiveness to sulfonylurea drugs, including glipizide.
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| Metabolism |
Glipizide¿¡ ´ëÇÑ Metabolism Á¤º¸ # Phase_1_Metabolizing_Enzyme:Cytochrome P450 2C9 (CYP2C9)
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| Protein Binding |
Glipizide¿¡ ´ëÇÑ ´Ü¹é°áÇÕ Á¤º¸ 98-99%, primarily to albumin.
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| Half-life |
Glipizide¿¡ ´ëÇÑ ¹Ý°¨±â Á¤º¸ 2-5 hours
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| Absorption |
Glipizide¿¡ ´ëÇÑ Absorption Á¤º¸ Gastrointestinal absorption is uniform, rapid, and essentially complete.
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| Pharmacokinetics |
GlipizideÀÇ ¾à¹°µ¿·ÂÇÐÀÚ·á
- ÀÛ¿ë ¹ßÇö ½Ã°£ : 1-1.5 ½Ã°£
- ÀÛ¿ë Áö¼Ó ½Ã°£ : 12-24 ½Ã°£
- ÃÖ´ëÈ¿°ú ¹ßÇö½Ã°£ : 1.5-2 ½Ã°£ À̳»
- Èí¼ö : À½½Ä¹° Á¸Àç½Ã Áö¿¬µÈ´Ù.
- ´Ü¹é°áÇÕ : 92-99%
- ´ë»ç : 91-97%°¡ °£¿¡¼ ´ë»çµÈ´Ù.
- ¹Ý°¨±â : 2-4 ½Ã°£
- ¼Ò½Ç : ´ë»çüÀÇ 60-80%°¡ ½Å¹è¼³µÇ°í 11%°¡ º¯¹è¼³µÈ´Ù.
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| Biotransformation |
Glipizide¿¡ ´ëÇÑ Biotransformation Á¤º¸ Hepatic. The major metabolites of glipizide are products of aromatic hydroxylation and have no hypoglycemic activity. A minor metabolite which accounts for less than 2% of a dose, an acetylaminoethyl benzine derivatives, is reported to have 1/10 to 1/3 as much hypoglycemic activity as the parent compound.
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| Toxicity |
Glipizide¿¡ ´ëÇÑ Toxicity Á¤º¸ The acute oral toxicity was extremely low in all species tested (LD50 greater than 4 g/kg). Overdosage of sulfonylureas including glipizide can produce hypoglycemia.
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| Drug Interactions |
Glipizide¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Not Available
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CYP450 Drug Interaction |
[CYP450 TableÁ÷Á¢Á¶È¸] Glipizide¿¡ ´ëÇÑ P450 table
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 |
Glipizide¿¡ ´ëÇÑ Food Interaction Á¤º¸ Avoid alcohol.Avoid sugar and sugary food.Take 30-60 minutes before breakfast.
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| Drug Target |
[Drug Target]
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| SNP Á¤º¸ |
Name:Glipizide (DB01067)
Interacting Gene/Enzyme:Cytochrome P450 2C9 (Gene symbol = CYP2C9) Swissprot P11712
SNP(s):CYP2C9*1 rs1057910 (C Allele)
Effect:Poor drug metabolizer, lower dose requirements
Reference(s):Kidd RS, Straughn AB, Meyer MC, Blaisdell J, Goldstein JA, Dalton JT: Pharmacokinetics of chlorpheniramine, phenytoin, glipizide and nifedipine in an individual homozygous for the CYP2C9*3 allele. Pharmacogenetics. 1999 Feb;9(1):71-80. [PubMed]
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| Description |
Glipizide¿¡ ´ëÇÑ Description Á¤º¸ An oral hypoglycemic agent which is rapidly absorbed and completely metabolized. [PubChem]
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| Drug Category |
Glipizide¿¡ ´ëÇÑ Drug_Category Á¤º¸ Hypoglycemic Agents
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| Smiles String Canonical |
Glipizide¿¡ ´ëÇÑ Smiles_String_canonical Á¤º¸ CC1=CN=C(C=N1)C(=O)NCCC1=CC=C(C=C1)S(=O)(=O)NC(=O)NC1CCCCC1
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| Smiles String Isomeric |
Glipizide¿¡ ´ëÇÑ Smiles_String_isomeric Á¤º¸ CC1=CN=C(C=N1)C(=O)NCCC1=CC=C(C=C1)S(=O)(=O)NC(=O)NC1CCCCC1
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| InChI Identifier |
Glipizide¿¡ ´ëÇÑ InChI_Identifier Á¤º¸ InChI=1/C21H27N5O4S/c1-15-13-24-19(14-23-15)20(27)22-12-11-16-7-9-18(10-8-16)31(29,30)26-21(28)25-17-5-3-2-4-6-17/h7-10,13-14,17H,2-6,11-12H2,1H3,(H,22,27)(H2,25,26,28)/f/h22,25-26H
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| Chemical IUPAC Name |
Glipizide¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ N-[2-[4-(cyclohexylcarbamoylsulfamoyl)phenyl]ethyl]-5-methylpyrazine-2-carboxamide
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| Drug-Induced Toxicity Related Proteins |
GLIPIZIDE ÀÇ Drug-Induced Toxicity Related ProteinÁ¤º¸ Replated Protein:Cytochrome P450 2C9 Drug:Glipizide Toxicity:Hypoglycaemia. [¹Ù·Î°¡±â] Replated Protein:Glucose transporter (GLUT 4) Drug:glipizide Toxicity:suppression of hepatic glucose production. [¹Ù·Î°¡±â]
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µå·°ÀÎÆ÷ ÀǾàÇмúÁ¤º¸´Â ½ÄǰÀǾàǰ¾ÈÀüóÀÇ Á¦Ç°Çã°¡»çÇ×, Çмú¹®Çå, Á¦¾àȸ»ç Á¦°øÁ¤º¸ µîÀ» ±Ù°Å·Î ÀÛ¼ºµÈ Âü°í Á¤º¸ÀÔ´Ï´Ù.
Á¤º¸ÀÇ Á¤È®¼ºÀ» À§ÇØ ³ë·ÂÇϰí ÀÖÀ¸³ª ÆíÁý»óÀÇ ¿À·ù, Çã°¡»çÇ× º¯°æ, Ãß°¡ÀûÀÎ Çмú¿¬±¸ ¶Ç´Â Àӻ󿬱¸ ¹ßÇ¥ µîÀ¸·Î ÀÎÇØ ¹ß»ýÇÏ´Â ¹®Á¦¿¡ ´ëÇØ µå·°ÀÎÆ÷´Â
Ã¥ÀÓÀ» ÁöÁö ¾Ê½À´Ï´Ù. ÀÚ¼¼ÇÑ ³»¿ëÀº ¡°Ã¥ÀÓÀÇ ÇÑ°è ¹× ¹ýÀû°íÁö¡±¸¦ ÂüÁ¶ÇØ ÁֽʽÿÀ.
¹Ýµå½Ã Á¦Á¶¡¤¼öÀÔ»ç, ÆÇ¸Å»ç, ÀÇ»ç, ¾à»ç¿¡°Ô ÃÖÁ¾ÀûÀ¸·Î È®ÀÎÇϽñ⠹ٶø´Ï´Ù.
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. GLIPIZIDE[GGT Increase][Composite Activity](Score) I(Marginal) 0(Active) 0[Alkaline Phosphatase Increase](Activity Score) I(Number of Rpts) ¡Ã4(Index value) 0.8[SGOT Increase](Activity Score) I(Number of Rpts) ¡Ã4(Index value) 0.7[SGPT Increase](Activity Score) I(Number of Rpts) ¡Ã4(Index value) 0.6[LDH Increase](Activity Score) I(Number of Rpts) <4(Index value) 0.4[GGT Increase](Activity Score) I(Number of Rpts) <4(Index value) 0
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