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| Mechanism of Action |
Gentamicin¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ Aminoglycosides like gentamicin "irreversibly" bind to specific 30S-subunit proteins and 16S rRNA. Specifically gentamicin binds to four nucleotides of 16S rRNA and a single amino acid of protein S12. This interferes with decoding site in the vicinity of nucleotide 1400 in 16S rRNA of 30S subunit. This region interacts with the wobble base in the anticodon of tRNA. This leads to interference with the initiation complex, misreading of mRNA so incorrect amino acids are inserted into the polypeptide leading to nonfunctional or toxic peptides and the breakup of polysomes into nonfunctional monosomes.
Prednisolone¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ Glucocorticoids such as Prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.
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| Pharmacology |
Gentamicin¿¡ ´ëÇÑ Pharmacology Á¤º¸ Gentamicin is a broad spectrum aminoglycoside antibiotic. Aminoglycosides work by binding to the bacterial 30S ribosomal subunit, causing misreading of t-RNA, leaving the bacterium unable to synthesize proteins vital to its growth. Aminoglycosides are useful primarily in infections involving aerobic, Gram-negative bacteria, such as Pseudomonas, Acinetobacter, and Enterobacter. In addition, some mycobacteria, including the bacteria that cause tuberculosis, are susceptible to aminoglycosides. Infections caused by Gram-positive bacteria can also be treated with aminoglycosides, but other types of antibiotics are more potent and less damaging to the host. In the past the aminoglycosides have been used in conjunction with penicillin-related antibiotics in streptococcal infections for their synergistic effects, particularly in endocarditis. Aminoglycosides are mostly ineffective against anaerobic bacteria, fungi and viruses.
Prednisolone¿¡ ´ëÇÑ Pharmacology Á¤º¸ Prednisolone is a synthetic glucocorticoid used as antiinflammatory or immunosuppressive agent. Prednisolone is indicated in the treatment of various conditions, including congenital adrenal hyperplasia, psoriatic arthritis, systemic lupus erythematosus, bullous dermatitis herpetiformis, seasonal or perennial allergic rhinitis, allergic corneal marginal ulcers, symptomatic sarcoidosis, idiopathic thrombocytopenic purpura in adults, leukemias and lymphomas in adults, and ulcerative colitis. Glucocorticoids are adrenocortical steroids and cause profound and varied metabolic effects. In addition, they modify the body's immune responses to diverse stimuli.
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| Metabolism |
Prednisolone¿¡ ´ëÇÑ Metabolism Á¤º¸ # Phase_1_Metabolizing_Enzyme:Cytochrome P450 3A4 (CYP3A4)
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| Protein Binding |
Gentamicin¿¡ ´ëÇÑ ´Ü¹é°áÇÕ Á¤º¸ Low (between 0 and 30%)
Prednisolone¿¡ ´ëÇÑ ´Ü¹é°áÇÕ Á¤º¸ Very high (>90%)
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| Half-life |
Gentamicin¿¡ ´ëÇÑ ¹Ý°¨±â Á¤º¸ 3-3¨ö hours in infants one week to six months of age; this increases to 5¨ö hours in full-term and large premature infants less than one week old.
Prednisolone¿¡ ´ëÇÑ ¹Ý°¨±â Á¤º¸ 2-3 hours
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| Absorption |
Gentamicin¿¡ ´ëÇÑ Absorption Á¤º¸ Injections lead to peak serum concentrations in 30-60 minutes. Topical gentamicin is readily absorbed from large burned, denuded, or granulating areas but not through intact skin. Absorption of gentamicin is faster and greater with the cream compared to the ointment. Gentamicin is absorbed in small quantities following topical application to the eye. Gentamicin is also absorbed in small amounts following topical application to the ear (especially if the eardrum is perforated or if tissue damage is present).
Prednisolone¿¡ ´ëÇÑ Absorption Á¤º¸ Readily absorbed by gastrointestinal tract, peak plasma concentration is reached 1-2 hours after administration.
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| Pharmacokinetics |
Gentamicin SulfateÀÇ ¾à¹°µ¿·ÂÇÐÀÚ·á
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| Biotransformation |
Prednisolone¿¡ ´ëÇÑ Biotransformation Á¤º¸ Excreted in the urine as either free or glucoconjugate.
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| Toxicity |
Gentamicin¿¡ ´ëÇÑ Toxicity Á¤º¸ Mouse, intravenous LD50: 52 mg/kg; rat, intravenous LD50: 96 mg/kg.
Prednisolone¿¡ ´ëÇÑ Toxicity Á¤º¸ LD50=500 mg/kg (oral, rat), short-term side effects include high blood glucose levels and fluid retention. Long term side effects include Cushing's syndrome, weight gain, osteoporosis, glaucoma, type II diabetes and adrenal suppression.
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| Drug Interactions |
Gentamicin¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Atracurium The agent increases the effect of muscle relaxantDoxacurium The agent increases the effect of muscle relaxantGallamine Triethiodide The agent increases the effect of muscle relaxantMetocurine The agent increases the effect of muscle relaxantMivacurium The agent increases the effect of muscle relaxantPancuronium The agent increases the effect of muscle relaxantPipecuronium The agent increases the effect of muscle relaxantRocuronium The agent increases the effect of muscle relaxantSuccinylcholine The agent increases the effect of muscle relaxantTubocurarine The agent increases the effect of muscle relaxantVecuronium The agent increases the effect of muscle relaxantBumetanide Increased ototoxicityEthacrynic acid Increased ototoxicityFurosemide Increased ototoxicityTorasemide Increased ototoxicityThalidomide Thalidomide increases the renal toxicity of the aminoglycosideCisplatin Increased risk of nephrotoxicityCefradine Increased risk of nephrotoxicityCephapirin Increased risk of nephrotoxicityCefamandole Increased risk of nephrotoxicityCefazolin Increased risk of nephrotoxicityCefonicid Increased risk of nephrotoxicityCefoperazone Increased risk of nephrotoxicityCeforanide Increased risk of nephrotoxicityCefotaxime Increased risk of nephrotoxicityCefotetan Increased risk of nephrotoxicityCefoxitin Increased risk of nephrotoxicityCeftazidime Increased risk of nephrotoxicityCeftizoxime Increased risk of nephrotoxicityCeftriaxone Increased risk of nephrotoxicityCefuroxime Increased risk of nephrotoxicityCephalothin Group Increased risk of nephrotoxicity
Prednisolone¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Ambenonium The corticosteroid decreases the effect of anticholinesterasesEdrophonium The corticosteroid decreases the effect of anticholinesterasesNeostigmine The corticosteroid decreases the effect of anticholinesterasesPyridostigmine The corticosteroid decreases the effect of anticholinesterasesWarfarin The corticosteroid alters the anticoagulant effectAcenocoumarol The corticosteroid alters the anticoagulant effectDicumarol The corticosteroid alters the anticoagulant effectAnisindione The corticosteroid alters the anticoagulant effectMidodrine Increased arterial pressureAspirin The corticosteroid decreases the effect of salicylatesBismuth Subsalicylate The corticosteroid decreases the effect of salicylatesSalicylate-magnesium The corticosteroid decreases the effect of salicylatesSalicylate-sodium The corticosteroid decreases the effect of salicylatesSalsalate The corticosteroid decreases the effect of salicylatesTrisalicylate-choline The corticosteroid decreases the effect of salicylatesTalbutal The barbiturate decreases the effect of the corticosteroidSecobarbital The barbiturate decreases the effect of the corticosteroidQuinidine barbiturate The barbiturate decreases the effect of the corticosteroidPrimidone The barbiturate decreases the effect of the corticosteroidPhenobarbital The barbiturate decreases the effect of the corticosteroidPentobarbital The barbiturate decreases the effect of the corticosteroidMethylphenobarbital The barbiturate decreases the effect of the corticosteroidMethohexital The barbiturate decreases the effect of the corticosteroidHexobarbital The barbiturate decreases the effect of the corticosteroidHeptabarbital The barbiturate decreases the effect of the corticosteroidDihydroquinidine barbiturate The barbiturate decreases the effect of the corticosteroidButethal The barbiturate decreases the effect of the corticosteroidButalbital The barbiturate decreases the effect of the corticosteroidButabarbital The barbiturate decreases the effect of the corticosteroidAprobarbital The barbiturate decreases the effect of the corticosteroidAmobarbital The barbiturate decreases the effect of the corticosteroidChlorotrianisene The estrogenic agent increases the effect of the corticosteroidClomifene The estrogenic agent increases the effect of the corticosteroidDiethylstilbestrol The estrogenic agent increases the effect of the corticosteroidEstradiol The estrogenic agent increases the effect of the corticosteroidEstriol The estrogenic agent increases the effect of the corticosteroidConjugated Estrogens The estrogenic agent increases the effect of the corticosteroidEstrone The estrogenic agent increases the effect of the corticosteroidEstropipate The estrogenic agent increases the effect of the corticosteroidEthinyl Estradiol The estrogenic agent increases the effect of the corticosteroidMestranol The estrogenic agent increases the effect of the corticosteroidQuinestrol The estrogenic agent increases the effect of the corticosteroidEthotoin The enzyme inducer decreases the effect of the corticosteroidFosphenytoin The enzyme inducer decreases the effect of the corticosteroidMephenytoin The enzyme inducer decreases the effect of the corticosteroidPhenytoin The enzyme inducer decreases the effect of the corticosteroidRifampin The enzyme inducer decreases the effect of the corticosteroidItraconazole The imidazole increases the effect and toxicity of the corticosteroidKetoconazole The imidazole increases the effect and toxicity of the corticosteroid
|
CYP450 Drug Interaction |
[CYP450 TableÁ÷Á¢Á¶È¸]
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| Food Interaction |
Prednisolone¿¡ ´ëÇÑ Food Interaction Á¤º¸ Take with food to reduce gastric irritation.Avoid alcohol. Avoid caffeine.
|
| Drug Target |
[Drug Target]
|
| Description |
Gentamicin¿¡ ´ëÇÑ Description Á¤º¸ A complex of three different closely related aminoglycoside sulfates, Gentamicins C1, C2, and C1(subA), obtained from Micromonospora purpurea and related species. They are broad-spectrum antibiotics, but may cause ear and kidney damage. They act to inhibit protein synthesis (genetic translation). [PubChem]
Prednisolone¿¡ ´ëÇÑ Description Á¤º¸ A glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [PubChem]
|
| Dosage Form |
Gentamicin¿¡ ´ëÇÑ Dosage_Form Á¤º¸ Cream TopicalLiquid OphthalmicOintment OphthalmicOintment TopicalSolution Auricular (otic)Solution IntravenousSolution OphthalmicSolution / drops Auricular (otic)Solution / drops Ophthalmic
Prednisolone¿¡ ´ëÇÑ Dosage_Form Á¤º¸ Liquid OralSolution OralSolution / drops OphthalmicSuspension OphthalmicTablet Oral
|
| Drug Category |
Gentamicin¿¡ ´ëÇÑ Drug_Category Á¤º¸ Anti-Bacterial AgentsProtein Synthesis Inhibitors
Prednisolone¿¡ ´ëÇÑ Drug_Category Á¤º¸ Adrenergic AgentsAnti-inflammatory AgentsAntineoplastic AgentsAntineoplastic Agents, HormonalGlucocorticoids
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| Smiles String Canonical |
Gentamicin¿¡ ´ëÇÑ Smiles_String_canonical Á¤º¸ CNC(C)C1CCC(N)C(O1)OC1C(N)CC(N)C(OC2OCC(C)(O)C(NC)C2O)C1O
Prednisolone¿¡ ´ëÇÑ Smiles_String_canonical Á¤º¸ CC12CC(O)C3C(CCC4=CC(=O)C=CC34C)C1CCC2(O)C(=O)CO
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| Smiles String Isomeric |
Gentamicin¿¡ ´ëÇÑ Smiles_String_isomeric Á¤º¸ CN[C@H](C)[C@@H]1CC[C@@H](N)[C@@H](O1)O[C@H]1[C@H](N)C[C@H](N)[C@@H](O[C@@H]2OC[C@@](C)(O)[C@H](NC)[C@H]2O)[C@@H]1O
Prednisolone¿¡ ´ëÇÑ Smiles_String_isomeric Á¤º¸ C[C@]12C[C@H](O)[C@H]3[C@@H](CCC4=CC(=O)C=C[C@]34C)[C@@H]1CC[C@]2(O)C(=O)CO
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| InChI Identifier |
Gentamicin¿¡ ´ëÇÑ InChI_Identifier Á¤º¸ InChI=1/C21H43N5O7/c1-9(25-3)13-6-5-10(22)19(31-13)32-16-11(23)7-12(24)17(14(16)27)33-20-15(28)18(26-4)21(2,29)8-30-20/h9-20,25-29H,5-8,22-24H2,1-4H3
Prednisolone¿¡ ´ëÇÑ InChI_Identifier Á¤º¸ InChI=1/C21H28O5/c1-19-7-5-13(23)9-12(19)3-4-14-15-6-8-21(26,17(25)11-22)20(15,2)10-16(24)18(14)19/h5,7,9,14-16,18,22,24,26H,3-4,6,8,10-11H2,1-2H3/t14-,15-,16-,18+,19-,20-,21-/m0/s1
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| Chemical IUPAC Name |
Gentamicin¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ 2-[4,6-diamino-3-[3-amino-6-(1-methylaminoethyl)oxan-2-yl]oxy-2-hydroxycyclohexyl]oxy-5-methyl-4-methylaminooxane-3,5-diol
Prednisolone¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ (8S,9S,10R,11S,13S,14S,17R)-11,17-dihydroxy-17-(2-hydroxyacetyl)-10,13-dimethyl-7,8,9,11,12,14,15,16-octahydro-6H-cyclopenta[a]phenanthren-3-one
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| Drug-Induced Toxicity Related Proteins |
GENTAMICIN ÀÇ Drug-Induced Toxicity Related ProteinÁ¤º¸ Replated Protein:Phospholipase A Drug:gentamicin Toxicity:aminoglycoside toxicity. [¹Ù·Î°¡±â] Replated Protein:phospholipases C Drug:gentamicin Toxicity:aminoglycoside toxicity. [¹Ù·Î°¡±â] Replated Protein:Angiotensinase A Drug:gentamicin Toxicity:important consequences upon renal function and metabolism. [¹Ù·Î°¡±â] Replated Protein:Dipeptidylpeptidase IV Drug:gentamicin Toxicity:important consequences upon renal function and metabolism. [¹Ù·Î°¡±â] Replated Protein:Sodium/potassium-transporting ATPase Drug:Gentamicin Toxicity:necrosis. [¹Ù·Î°¡±â] PREDNISOLONE ÀÇ Drug-Induced Toxicity Related ProteinÁ¤º¸ Replated Protein:DNA topoisomerase 1 Drug:prednisolone Toxicity:appearance of apoptotic cells. [¹Ù·Î°¡±â]
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ÃÖ±ÙÁ¤º¸¼öÁ¤ÀÏ 2020-05-27
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º» ¼öÁ¤ÀÏ Á¤º¸´Â Çã°¡Á¤º¸ ÀÌ¿ÜÀÇ ±âŸÁ¤º¸ ¼öÁ¤ÀÏÀ» ÀǹÌÇϹǷÎ, Çã°¡Á¤º¸¼öÁ¤ÀÏÀº º»¹®¿¡ Ç¥±âµÈ ³¯Â¥¸¦ ÂüÁ¶ÇϽñ⠹ٶø´Ï´Ù.
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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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