Chinese english Germany Korea


ゲンタミシン 化学構造式
Gentavet;Uromycine;Lyramycin;GENTAMYCIN;GENTAMICIN;Gentacycol;GENTAMYCINE;Refobacin tm;GENTAMICINUM;GentamysinsolutionforBiochemistry
MOL File:

ゲンタミシン 物理性質

融点 :
比旋光度 :
D25 +146°
pKa 8.2(66% DMF) (Uncertain);7.9(H2O) (Uncertain)
CAS データベース:
1403-66-3(CAS DataBase Reference)


有毒物質データの 1403-66-3(Hazardous Substances Data)

ゲンタミシン 価格

メーカー 製品番号 製品説明 CAS番号 包装 価格 更新時間 購入

ゲンタミシン 化学特性,用途語,生産方法


抗生物質, タンパク質合成阻害薬


Amorphous solid. Freely soluble in water, pyridine, acid solutions; moderately soluble in methanol, ethanol, and acetone; practically insoluble in benzene and halogenated hydrocarbons.



brand name

Apogen (King); Garamycin (Schering); Genoptic (Allergan); Gentacidin (Novartis); Gentafair (Pharmafair); Gentak (Akorn); U-Gencin (Pharmacia & Upjohn).


Gentamicin has been used inin situ preparations for the treatment of minor infections. Antibiotics that are also available for systemic use are not considered acceptable for topical use because of the risk of development of resistance. Neomycin is the topical aminoglycoside listed in the WHO Model List of Essential Drugs.


It is active against staphylococci, but streptococci are at least moderately resistant. Gram-positive bacilli, including Actinomyces and Listeria spp., are moderately susceptible, but clostridia and other obligate anaerobes are resistant. There is no clinically useful activity against mycobacteria. It is active against most enterobacteria, including Citrobacter, Enterobacter, Proteus, Serratia and Yersinia spp., and against some other aerobic Gram-negative bacilli including Acinetobacter, Brucella, Francisella and Legionella spp., although its in-vitro activity against intracellular parasites such as Brucella spp. is of doubtful usefulness. It is active against Ps. aeruginosa and other members of the fluorescens group, but other pseudomonads are often resistant and Flavobacterium spp. are always resistant.
The MIC for susceptible strains of Ps. aeruginosa can vary more than 300-fold with the Mg2+ content of the medium. Activity against Ps. aeruginosa is also significantly lower in serum or sputum than in ion-depleted broth, as a result both of binding (more in sputum than in serum) and antagonism by ions.
The action is bactericidal and increases with pH, but to different degrees against different bacterial species. Marked bactericidal synergy is commonly demonstrable with β-lactam antibiotics, notably with ampicillin or benzylpenicillin against E. faecalis, and with vancomycin against streptococci and staphylococci. Bactericidal synergy with β-lactam antibiotics can also be demonstrated in vitro against many Gram-negative rods, including Ps. aeruginosa. Antagonism with chloramphenicol occurs in vitro, but this is of doubtful clinical significance. Like other aminoglycosides, gentamicin is degraded in the presence of high concentrations of some β-lactam agents.


Resistant strains of staphylococci, enterobacteria, Pseudomonas and Acinetobacter spp. have been reported from many centers, often from burns and intensive care units where the agent has been used extensively. Overall prevalence rates of resistance in various countries range from 3% to around 50% for Gramnegative organisms. Countries in which control of the prescription of antibiotics is lax often have very high rates.
Acquired resistance in Gram-negative organisms is usually caused by aminoglycoside-modifying enzymes. The prevalence of the different enzymes varies geographically. ANT(2″) is most common in the USA, but in Europe various forms of AAC(3), particularly AAC(3)-II, are common. ANT(2″) is also common in the Far East, usually accompanied by AAC(6′). Strains that owe their resistance to a non-specific decrease in uptake of aminoglycosides have been involved in outbreaks of hospital-acquired infection, and are cross- resistant to all aminoglycosides.
Resistance in staphylococci and high-level resistance in enterococci is usually caused by the bifunctional APH(2″)- AAC(6′) enzyme. Other aminoglycoside-modifying enzymes do not contribute greatly to gentamicin resistance. Gentamicinresistant staphylococci began to emerge in the mid-1970s. Rates of resistance in the UK are around 2.5% in methicillin-sensitive Staph. aureus, 9% in MRSA and 23–73% in coagulase-negative staphylococci depending on methicillin susceptibility.
High-level resistance to gentamicin (MIC >2000 mg/L) in E. faecalis is widespread, accounting for around one-third of blood culture isolates in some places. Penicillin does not exert synergistic bactericidal activity against such strains, although the combination of penicillin with streptomycin may remain active. High-level gentamicin resistance in E. faecium is much less common, but has been reported in the UK, the USA and Asia.


Cmax 1 mg/kg intramuscular: 4–7.6 mg/L after 0.5–1 h
80 mg intramuscular: 4–12 mg/L after 0.5–2 h
5 mg/kg infusion: >10 mg/L after 1 h
Plasma half-life (mean): 2 h
Volume of distribution: 0.25 L/kg
Plasma protein binding: <10%
Gentamicin is almost unabsorbed from the alimentary tract, but well absorbed after intramuscular injection.
Wide variations are observed in the peak plasma concentrations and half-lives of the drug after similar doses, but individual patients tend to behave consistently. Some patients with normal renal function develop unexpectedly high, or unexpectedly low, peak values on conventional doses. Severe sepsis appears to be a significant factor in reducing the peak concentration, and anemia is a significant factor in raising it. The mechanisms involved in these effects seem to be principally related to volume of distribution changes.
Intravenous infusion over 20–30 min achieves concentrations similar to those after intramuscular injection. The peak plasma concentration increases proportionally with dose and there is dose linearity in the AUC. Despite the very high bronchial concentrations achieved, nebulised administration does not give rise to detectable plasma concentrations.
There is a marked effect of age: in children up to 5 years the peak plasma concentration is about half, and for children between 5 and 10 years about two-thirds, of the concentration produced by the same dose per kg in adults. This difference can be eliminated to a large extent by calculating dosage not on the basis of weight but on surface area, which is more closely related to the volume of the extracellular fluid in which gentamicin is distributed.
Some febrile neutropenic patients do not differ from normal subjects in their pharmacokinetics, but in others, as in patients with cystic fibrosis, gentamicin clearance is enhanced and dosage adjustment is necessary.
Absorption of around half the dose is achieved by addition to the dialysate in patients on continuous ambulatory peritoneal dialysis (CAPD).
Gentamicin does not enter cells so intracellular organisms are protected from its action. Fat contains less extracellular fluid than other tissues and pharmacokinetic comparisons indicate that the volume of distribution in obese patients approximates to the lean body mass plus 40% of the adipose mass.
Access to the lower respiratory tract is limited. Rapid intravenous infusion produces high but short-lived intrabronchial concentrations, while intramuscular injection produces lower but more sustained concentrations.
It does not reach the CSF in useful concentrations after systemic administration. In patients receiving 3.5 mg/kg per day plus 4 mg intrathecally, CSF concentrations of 20–25 mg/L have been found. Formulations specifically designed for intrathecal use should be used, owing to issues with the excipients present.
Serous fluids and exudates
Concentrations in pleural, pericardial and synovial fluids are less than half the simultaneous plasma concentrations but may rise in the presence of inflammation. In cirrhotic patients with bacterial peritonitis treated with 3–5 mg/kg per day, concentrations of 4.2 mg/L were found in the peritoneal fluid with a fluid to serum ratio of 0.68. The maximum concentration in inflammatory exudate is less than that in the plasma, partly because it is reversibly bound in purulent exudates, but it persists much longer.
Other tissues
Concentrations in skin and muscle, as judged from assay of decubitus ulcers excised 150 min after patients had received 80 mg intramuscularly, were 5.8 and 6.5 mg/kg, respectively, the serum concentrations at that time being 5.1 and 5.4 mg/L.
Peak concentrations in bone exceed 5 mg/L and closely mirror the pharmacokinetic profile in blood. Penetration varies from 28% to 47% depending on the method used.
Concentrations in fetal blood are about one-third of that in the maternal blood.
The initial plasma half-life is about 2 h, but a significant proportion is eliminated much more slowly, the terminal halflife being of the order of 12 days. There is much individual variation.
Gentamicin accumulates in the renal cortical cells, and over the first day or two of treatment only about 40% of the dose is recovered. The renal clearance is around 60 mL/ min. Subsequently it is excreted virtually unchanged in the urine, principally by glomerular filtration. In severely oliguric patients some extrarenal elimination by unidentified routes evidently occurs. Urinary concentrations of 16–125 mg/L are found in patients with normal renal function receiving 1.5 mg/kg per day. In the presence of severe renal impairment, urinary concentrations as high as 1000 mg/L may be found. The clearance of the drug is linearly related to that of creatinine, and this relationship is used as the basis of the modified dosage schedules that are required in patients with impaired renal function in order to avoid accumulation of the drug. Concentrations in bile are less than half the simultaneous plasma concentration.
Hemodialysis can remove the drug at about 60% of the rate at which creatinine is cleared, but the efficiency of different dialyzers varies markedly. Peritoneal dialysis removes about 20% of the administered dose over 36h–a rate that does not add materially to normal elimination.


In severe sepsis of unknown origin, gentamicin has been traditionally combined with other agents. However, monotherapy has been shown to be as effective as combination therapy. In systemic Ps. aeruginosa infections it is advisable to combine gentamicin with an antipseudomonal penicillin or cephalosporin, owing to likelihood of gentamicin resistance.
Suspected or documented Gram-negative septicemia, particularly when shock or hypotension is present
Enterococcal endocarditis (with a penicillin)
Respiratory tract infection caused by Gram-negative bacilli
Urinary tract infection
Bone and soft-tissue infections, including peritonitis, burns complicated by sepsis and infected surgical and traumatic wounds
Serious staphylococcal infection when other conventional antimicrobial therapy is inappropriate
Gentamicin drops are used for conjunctival infections and for infections of the external ear. The drug is also used in orthopedic surgery in bone cements. In these applications systemic concentrations achieved are negligible and toxicities are restricted to local effects.
In the elderly and those with renal impairment the dosage must be suitably modified.


Vestibular function is usually affected, but labyrinthine damage has been reported in about 2% of patients, usually in those with peak plasma concentrations in excess of 8 mg/L. Symptoms range from acute Meniere’s disease to tinnitus and are usually permanent. Deafness is unusual but may occur in patients treated with other potentially ototoxic agents. In an extensive study, the overall incidence of ototoxicity was 2%. Vestibular damage accounted for twothirds of this and impaired renal function was the main determinant.
Some degree of renal toxicity has been observed in 5–10% of patients. Among 97 patients receiving 102 courses of the drug in dosages adjusted in relation to renal function, nephrotoxicity was described as definite in 9.8% and possible in 7.8%. In patients treated for 39–48 days, serum creatinine increased initially, but renal function recovered after 3–4 weeks despite continuing treatment. However, many patients are treated for severe sepsis associated with shock or disseminated intravascular coagulopathy, or from other disorders that are themselves associated with renal failure. In critically ill patients with severe sepsis, treatment has been complicated by nephrotoxicity in 23–37%.
Autoradiographic localization indicates that gentamicin is very selectively localized in the proximal convoluted tubules, and a specific effect on potassium excretion may both indicate the site of toxicity and provide an early indication of renal damage. Accumulation of the drug and excretion of proximal tubular enzymes may precede any rise in the serum creatinine.
Alanine aminopeptidase excretion is an unreliable predictor of renal damage. β2-Microglobulin excretion may indicate decreased tubular function both before and during treatment. Excretion of the protein has also been shown to parallel increases in elimination half-life in patients on well-controlled therapy in whom reduction of creatinine clearance occurred, although the serum creatinine concentration remained within normal limits.
Other effects.
Neuromuscular blockade is possible but unlikely in view of the small amounts of the drug administered. Intrathecal injection may result in radiculitis, fever and persistent pleocytosis. Significant hypomagnesemia may occur, particularly in patients also receiving cytotoxic agents.


Poison by intravenous, intraperitoneal, intramuscular, and subcuta neous routes. Mildly toxic by ingestion. Ex perimental teratogenic and reproductive effects. Mutation data reported. Human systemic effects: change in motor activity, changes in vestibular functions, dlstorted perceptions, eye hemorrhage, hallucinations, hdney changes, motor activity changes, trigeminal nerve sensory changes, vestibular function changes, visual field changes. Af fects the peripheral nervous system by intra venous route. An antibiotic. When heated to decomposition it emits acrid smoke and irritating fumes. See also other gentamycin entries.

ゲンタミシン 上流と下流の製品情報



ゲンタミシン 生産企業

Global( 50)Suppliers
名前 電話番号 ファックス番号 電子メール 国籍 製品カタログ 優位度
Capot Chemical Co.,Ltd.
+86 (0)571-855 867 18
+86 (0)571-858 647 95 China 19918 60
Mainchem Co., Ltd.
+86-0592-6210733 CHINA 32457 55
Chemwill Asia Co.,Ltd.
86-21-51861608;;; CHINA 24001 58
Beijing dtftchem Technology Co., Ltd. 13651141086; 86(10)60275028、60275820
86 (10) 60270825 China 3395 62
BeiJing Hwrk Chemicals Limted 4006990298;010-57411839;0757-86311057;021-51691807
010-87653215;0757-86311057;021-55236763 China 14611 55
Pure Chemistry Scientific Inc. 001-857-928-2050 or 1-888-588-9418
001-617-206-9595 United States 9922 62
Nanjing Chemlin Chemical Co., Ltd 025-83697070
+86-25-83453306 China 19982 64
Hangzhou Yuhao Chemical Technology Co., Ltd 0571-82693216
+86-571-82880190 China 9409 52
Jinan Haohua Industry Co., Ltd 0531-58773082 ;58773060
0531-58773099 China 5587 58
86-029-85456576-808 China 294 55


  • 1403-66-3
  • GentamysinsolutionforBiochemistry
  • Gentacycol
  • Gentavet
  • Refobacin tm
  • Uromycine
  • Gentamicin (base and/or unspecified salts)
  • 2-[4,6-Diamino-3-[3-amino-6-(1-methylaminoethyl)oxan-2-yl]oxy-2-hydroxycyclohexyl]oxy-5-methyl-4-methylaminooxane-3,5-diol
  • Lyramycin
  • ゲンタシコール
  • ゲンタマイシン
  • GM【ゲンタマイシン】
  • リラマイシン
  • ゲンタベット
  • オキシトセラニム
  • セプチゲン
  • ゲンタルリン
  • ゲンタミシン
Copyright 2017 © ChemicalBook. All rights reserved