アミカシン

危険有害性情報のコード(GHS)

• 絵表示(GHS)

  

• 注意喚起語

  Warning

• 危険有害性情報

  H317：アレルギー性皮膚反応を起こすおそれ

• 注意書き

  P280：保護手袋/保護衣/保護眼鏡/保護面を着用するこ と。

アミカシン 価格

アミカシン 化学特性,用途語,生産方法

• 解説

  アミカシン,白色の結晶性粉末．分解点203～204 ℃(1/2水和物)．[α]²³_D＋99°(水)．カナマイシン耐性菌にも有効．細菌のリボソームに作用し，タンパク質合成を阻害し，殺菌的に作用する．腸管からの吸収が悪く，筋肉注射または点滴静脈内投与をする．腎毒性，聴覚毒性がアミノ配糖体抗生物質のなかでもっとも低い．β-ラクタム系，ほかのアミノ配糖体抗生物質と交差耐性を示さない．
  森北出版「化学辞典（第2版）
  

• 用途

  アミカシンは多数の細菌感染症に使用される抗生物質である。アミカシンが用いられる細菌感染症には感染性関節炎、腹腔内感染症、髄膜炎、肺炎、敗血症、尿路感染症があげられる。また、多剤耐性結核の治療にも用いられる。

• 効能

  抗生物質, タンパク質合成阻害薬

• 製造

  アミカシン,カナマイシンAを出発材料として合成されたアミノ配糖体抗生物質．

• 毒性

  アミカシン,LD50 340(pH 6.6)，560(pH 7.4)mg/kg(マウス，静注)．

• 説明

  Amikacin is made semisynthetically from kanamycin A. Interestingly, the L-hydroxyaminobutyryl amide (HABA) moiety attached to N-3 inhibits adenylation and phosphorylation in the distant amino sugar ring (at C-2′and C-3′), even though the HABA substituent is not where the enzymatic reaction takes place. This effect is attributed to decreased binding to the R factor–mediated enzymes.

• 化学的特性

  white crystalline powder

• 使用

  Amikacin is a semi-synthetic derivative of kanamycin. It is much less sensitive to the enzymes that inactivate aminoglycoside antibiotics. The spectrum is similar to that of gentamicin. Amikacin principally finds use in the treatment of infections arising from bacteria that are resistant to gentamicin and/or tobramycin.

• 定義

  ChEBI: An amino cyclitol glycoside that is kanamycin A acylated at the N-1 position by a 4-amino-2-hydroxybutyryl group.

• 抗菌性

  Among other organisms, Acinetobacter, Alkaligenes, Campylobacter, Citrobacter, Hafnia, Legionella, Pasteurella, Providencia, Serratia and Yersinia spp. are usually susceptible in vitro. Stenotrophomonas maltophilia, many nonaeruginosa pseudomonads and Flavobacterium spp. are resistant. M. tuberculosis (including most streptomycin-resistant strains) and some other mycobacteria (including M. fortuitum and the M. avium complex) are susceptible; most other mycobacteria, including M. kansasii, are resistant. Nocardia asteroides is susceptible.
  It exhibits typical aminoglycoside characteristics, including an effect of divalent cations on its activity against Ps. aeruginosa analogous to that seen with gentamicin and synergy with β-lactam antibiotics.
  

• 獲得抵抗性

  Amikacin is unaffected by many of the modifying enzymes that inactivate gentamicin and tobramycin and is consequently active against staphylococci, enterobacteria and Pseudomonas that owe their resistance to the production of those enzymes. However, AAC(6′), ANT(4′) and some forms of APH(3′) can confer resistance; because these enzymes generally do not confer gentamicin resistance, amikacin-resistant strains can be missed in routine susceptibility tests when gentamicin is used as the representative aminoglycoside.
  There have been reports of resistance arising during treatment of infections due to Serratia spp. and Ps. aeruginosa. Outbreaks of infection with multiresistant strains of enterobacteria and Ps. aeruginosa have occurred after extensive use, particularly in burns units. Bacteria that owe their resistance to the expression of ANT(4′) have been described in Staph. aureus, coagulase-negative staphylococci, Esch. coli, Klebsiella spp. and Ps. aeruginosa. In E. faecalis, resistance to penicillin– aminoglycoside synergy has been associated with plasmidmediated APH(3′). Resistance in Gram-negative organisms is usually caused by either reduced accumulation of the drug or, more commonly, by the aminoglycoside-modifying enzymes AAC(6′) or AAC(3)-VI. The latter enzyme is usually found in Acinetobacter spp., but has also been found, encoded by a transposon, in Prov. stuartii. One type of AAC(6) is chromosomally encoded by Ser. marcescens, though not usually expressed.
  The prevalence of resistance to amikacin remains low (<5%) in many countries but can change rapidly with increased usage of the drug. However, the spread of extended spectrum β-lactamases belonging to the TEM and SHV families may result in an increase in amikacin resistance that is not associated with use, since most strains that produce such enzymes also produce AAC(6′).

• 一般的な説明

  Amikacin was synthesized by Kawaguchi et al. of the Bristol-Banyu Research Institute in 1970 starting with kanamycin and the acyl moiety of butirosin. Its design is based on knowledge of the mechanisms of bacterial resistance to kanamycin and related compounds in which the 3 -hydroxyl group of the antibiotic is phosphorylated enzymatically. The acyl moiety in butirosin prevents this enzymatic inactivation.

• 薬物動態学

  C_{max 7.5 mg/kg intramuscular： c. 30 mg/L after 1 h
  500 mg 30-min infusion： 35–50 mg/L end infusion
  15 mg/kg 30-min infusion： >50 mg/L after 1 h
  Plasma half-life： 2.2 h
  Volume of distribution： 0.25–0.3 L/kg
  Plasma protein binding： 3–11%
  It is readily absorbed after intramuscular administration. Rapid intravenous injection of 7.5 mg/kg produced concentrations in excess of 60 mg/L shortly after injection.
  Most pharmacokinetic parameters follow an almost linear correlation when the once-daily doses (15 mg/kg) are compared with the traditional 7.5 mg/kg twice daily. In patients on CAPD, there was no difference in mean peak plasma concentration or volume of distribution whether the drug was given intravenously or intraperitoneally. However, in patients with significant burn injuries, doses should be increased to 20 mg/kg.
  In infants receiving 7.5 mg/kg by intravenous injection, peak plasma concentrations were 17–20 mg/L. No accumulation occurred on 12 mg/kg per day for 5–7 days. There was little change in the plasma concentration or the half-life (1.7 and 1.9 h) on the third and seventh days of a period over which 150 mg/m2 was infused over 30 min every 6 h. When the dose was raised to 200 mg/m2 the concentration never fell below 8 mg/L. The plasma half-life was longer in babies of lower birth weight and was still 5–5.5 h in babies aged 1 week or older. The importance of dosage control in the neonate is emphasized by the findings that there is an inverse relationship between post-conception age and plasma elimination half-life, though in extremely premature babies the weight of the child is also a significant predictor of half-life.}

• 臨床応用

  Severe infection (including septicemia, neonatal sepsis, osteomyelitis, septic arthritis, respiratory tract, urinary tract, intra-abdominal, peritoneal and soft tissue infections) caused by susceptible micro-organisms Sepsis of unknown origin (combined with a β-lactam or anti-anaerobe agent as appropriate).
  Mycobacterial infection
  Amikacin is principally used for the treatment of infections caused by organisms resistant to other aminoglycosides because of their ability to degrade them. Peak concentrations on 15 mg/kg once daily administration should exceed 45 mg/L, and trough concentration of <5 mg/L should be maintained to achieve therapeutic effects.

• 安全性プロファイル

  Poison by intravenous,intraperitoneal, and intramuscular routes. Moderately toxicby intraperitoneal route. An experimental teratogen. Whenheated to decomposition it emits toxic fumes of NOx.

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アミカシン スペクトルデータ(¹HNMR)

37517-28-5, アミカシン キーワード