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トブラマイシン 化学構造式
トブラマイシン;O-[3-アミノ-3-デオキシ-α-D-グルコピラノシル-(1→6)]-O-[2,6-ジアミノ-2,3,6-トリデオキシ-α-D-リボ-ヘキソピラノシル-(1→4)]-2-デオキシ-D-ストレプタミン;トブラマイシン標準品;トブラマイシン, 遊離塩基;トブラマイシン DEUTERATED
MOL File:

トブラマイシン 物理性質

融点 :
178 °C
沸点 :
570.01°C (rough estimate)
比旋光度 :
D20 +129° (c = 1 in water)
比重(密度) :
1.3458 (rough estimate)
屈折率 :
143 ° (C=4, H2O)
貯蔵温度 :
H2O: 50 mg/mL, clear, faintly yellow
pKa 6.7 (Uncertain);8.3 (Uncertain);9.9 (Uncertain)
外見 :
White to off-white solid
white to off-white
水溶解度 :
Soluble in water
Merck :


主な危険性  Xi
Rフレーズ  36/37/38
Sフレーズ  26-37/39
WGK Germany  2
RTECS 番号 WK2100000
HSコード  29419090
有毒物質データの 32986-56-4(Hazardous Substances Data)
毒性 LD50 in mice, rats (mg/kg): 441, 969 s.c. (Welles)

トブラマイシン 価格 もっと(23)

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
富士フイルム和光純薬株式会社(wako) W01LKTT5604 トブラマイシン, 遊離塩基
Tobramycin, Free Base
32986-56-4 100mg ¥13700 2018-12-26 購入
富士フイルム和光純薬株式会社(wako) W01LKTT5604 トブラマイシン, 遊離塩基
Tobramycin, Free Base
32986-56-4 25mg ¥9100 2018-12-26 購入
東京化成工業 T2503 トブラマイシン >94.0%(T)
Tobramycin >94.0%(T)
32986-56-4 5g ¥10800 2018-12-04 購入
東京化成工業 T2503 トブラマイシン >94.0%(T)
Tobramycin >94.0%(T)
32986-56-4 25g ¥36100 2018-12-04 購入
関東化学株式会社(KANTO) 49838-95 トブラマイシン標準品
Tobramycin standard
32986-56-4 100mg ¥61000 2018-12-13 購入

トブラマイシン MSDS


トブラマイシン 化学特性,用途語,生産方法


White or almost white powder.


antibacterial, inhibits protein synthesis




Tobramycin is an aminoglycoside antibiotic.


Single factor antibiotic comprising about 10% of nebramycin, the aminoglycosidic antibiotic complex produced by Streptomyces tenebrarius. Antibacterial


ChEBI: A amino cyclitol glycoside that is kanamycin B lacking the 3-hydroxy substituent from the 2,6-diaminoglucose ring.


In-vitro activity against Ps. aeruginosa is usually somewhat greater than that of gentamicin; against other organisms activity is similar or a little lower. Other Pseudomonas species are generally resistant, as are streptococci and most anaerobic bacteria. Other organisms usually susceptible in vitro include Acinetobacter, Legionella and Yersinia spp. Alkaligenes, Flavobacterium spp. and Mycobacterium spp. are resistant. It exhibits bactericidal activity at concentrations close to the MIC and bactericidal synergy typical of aminoglycosides in combination with penicillins or cephalosporins.


It is inactivated by many aminoglycoside-modifying enzymes that inactivate gentamicin. However, AAC(3′)-I does not confer tobramycin resistance and AAC(3′)-II confers a lower degree of tobramycin resistance than of gentamicin resistance. Conversely, ANT(4′) confers tobramycin but not gentamicin resistance, as do some types of AAC(6′). Overproduction of APH(3′), conferring a low degree of resistance to tobramycin (MIC 8 mg/L), but not gentamicin (MIC 2 mg/L), was ascribed to ‘trapping’ rather than phosphorylation.
Resistance rates are generally similar to those of gentamicin, although they may vary locally because of the prevalence of particular enzyme types.


Cmax 80 mg intramuscular: 3–4 mg/L after 30 min
1 mg/kg intravenous: 6–7 mg/L after 30 min
5 mg/kg: >10 mg/L after 1 h
Plasma half-life: 1.5–3 h
Volume of distribution: c. 0.25 L/kg
Plasma protein binding: <30%
The pharmacokinetic behavior after systemic administration closely resembles that of gentamicin. In patients treated for prolonged periods with 2.5 mg/kg intravenously every 12 h, average peak steady-state values were 6.5 mg/L after 30 weeks and 7.1 mg/L after 40 weeks. Continuous intravenous infusion of 6.6 mg/h and 30 mg/h produced steady-state concentrations of 1 and 3.5–4.5 mg/L, respectively. Higher concentrations (10–12 mg/L) have been obtained by bolus injection over about 3 min. Peak concentrations of around 50 mg/L have been reported in cystic fibrosis patients given 9 mg/kg once daily. Ten minutes after a 300 mg dose of tobramycin solution for inhalation, mean concentration of drug in the sputum of cystic fibrosis patients was 1.2 mg/g and ranged from 0.04 to 1.4 mg/g. The systemic availability of nebulized drug is very variable (6–27%). In general, the concentration found in the sputum of cystic fibrosis patients is high when administered by inhalation, but varies widely depending on individual airway pathology and nebulizer efficiency.
In the neonate, peak plasma concentrations of 4–6 mg/L have been found 0.5–1 h after doses of 2 mg/kg. Mean plasma elimination half-lives of 4.6–8.7 h were inversely proportional to the birth weight and creatinine clearance. The half-life was found to be initially extremely variable (3–17 h) in infants weighing 2.5 kg at birth, but considerably more stable (4–8 h) at the end of therapy 6–9 days later.
β-Lactam inactivation
In common with other aminoglycosides, tobramycin interacts with certain β-lactam agents, but is said to be stable in the presence of ceftazidime, imipenem and aztreonam. Of the penicillins tested, piperacillin caused least inactivation in vitro.
The volume of distribution slightly exceeds the extracellular water volume; it increases in patients with ascites, and is relatively smaller in morbidly obese patients. In tracheostomized or intubated patients given a loading dose of 1 mg/kg and then intravenous infusions every 8 h of 2–3.5 mg/kg, average concentrations in the bronchial secretions were 0.7 mg/L with a mean secretion:serum ratio of 0.18. In patients with cystic fibrosis receiving 10 mg/kg of the drug per day, the bronchial secretions may contain 2 mg/L or more.
Concentrations are low in peritoneal fluid but can rise to 60% of the plasma concentration in peritonitis and in synovial fluid. Tobramycin crosses the placenta, and concentrations of 0.5 mg/L have been found in the fetal serum when the mother was receiving a dose of 2 mg/kg. Penetration into the CSF resembles that of gentamicin.
It is eliminated in the glomerular filtrate and is unaffected by probenecid. Renal clearance is 90 mL/min. About 60% of the administered dose is recovered from the urine over the first 10 h, producing urinary concentrations after a dose of 80 mg of 90–500 mg/L over the first 3 h. The nature of the extrarenal disposal of the remaining 40% of the drug has not been established. The total body clearance is increased in patients with cystic fibrosis and the plasma half-life is shorter, which may necessitate higher dosage (15 mg/kg per day) for optimum blood concentrations. Renal clearance is increased in younger burn patients. In patients with impaired renal function, urinary concentrations of the drug are depressed and the plasma half-life prolonged in proportion to the rise in serum creatinine, reaching 6–8 h at a creatinine concentration of 350 μmol/L. Dosage in patients with impaired renal function may be based on the procedures used for gentamicin since behavior of the two drugs is virtually identical. About 70% of the drug is removed by hemodialysis over 12 h, but the efficiency of different dialyzers varies markedly.


Severe infections caused by susceptible micro-organisms Ps. aeruginosa infections, including chronic pulmonary infections in cystic fibrosis (administration by injection or nebulizer)
For practical purposes use is identical to that of gentamicin, except possibly for Pseudomonas infection, where it has somewhat greater activity against gentamicin-susceptible and some gentamicin-resistant strains. Its value as a substitute for gentamicin in the speculative treatment of severe undiagnosed infection is offset by its lower activity against other organisms that may be implicated.
It has been used extensively to treat Ps. aeruginosa infections in patients with cystic fibrosis.


The effect is predominantly on the auditory branch of the eighth nerve; vestibular function is seldom affected. Experimental evidence suggests that comparable effects on cochlear electrophysiology and histology require doses about twice those of gentamicin. In patients, electrocochleography has shown an immediate and dramatic reduction of cochlear activity when the serum tobramycin concentration exceeded 8–10 mg/L, but there were no associated symptoms and function recovered fully as the drug was eliminated. Clinical ototoxicity is rare and most likely to be seen in patients with renal impairment, or treated concurrently or sequentially with other potentially ototoxic agents.
Renal impairment with proteinuria, excretion of granular casts, oliguria and rise of serum creatinine have been noted in 1–2% of patients. Some evidence of nephrotoxicity has been found in about 10% of patients, depending on the sensitivity of the tests employed. In patients treated with a 120 mg loading dose and 80 mg every 8 h, renal enzyme excretion increased and there was a small but significant reduction in chrome-EDTA clearance even when the clinical condition improved. It has been suggested that intermittent dosage with large but infrequent plasma peaks may be less toxic than, and as efficacious as, continuous dosing. Tobramycin appears to be less nephrotoxic than gentamicin in critically ill patients.
The likelihood of toxicity is thought to increase with preexisting renal impairment and higher or more prolonged dosage, but in a comparison of patients treated with 8 mg/kg per day for Pseudomonas endocarditis with those treated with 3 mg/kg per day for Gram-negative sepsis there was no evidence of renal impairment in either group. Although there was audiological evidence of high-frequency loss in some patients receiving the higher dosage, there was no sustained loss of conversational hearing. There seems to be no significant effect of age: in patients aged 20–39 years the mean elimination half-life of the drug at the end of treatment was 2.3 h while in those aged 60–79 years it was 2.4 h. Evidence of renal toxicity may be found in 20% of severely ill patients.
Other reactions
Other toxic manifestations are rare. Local reactions sometimes occur at the site of injection. Rashes and eosinophilia in the absence of other allergic manifestations are seen. Voice alterations and tinnitus were rare in cystic fibrosis patients receiving tobramycin by inhalation. Increased transaminase levels may occur in the absence of other evidence of hepatic derangement.

トブラマイシン 上流と下流の製品情報



トブラマイシン 生産企業

Global( 251)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
Shenzhen Sendi Biotechnology Co.Ltd.
0755-23311925 18102838259
0755-23311925 CHINA 3217 55
Henan DaKen Chemical CO.,LTD.
+86-371-55531817 CHINA 22043 58
Henan Tianfu Chemical Co.,Ltd.
0371-55170693 CHINA 20786 55
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Haihang Industry Co.,Ltd
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Jinan Tenglong Chemical Co.,Ltd
Whatsapp:+8615563263311 Skype:live:smions7080 CHINA 770 58
Dalian Meilun Biotech Co., Ltd. 0411-66771943;0411-66771942
0411-66771945 China 4143 58
Hubei widely chemical technology Co., Ltd. 027-83991130
027-83991130 1718093273@QQ.COM China 1026 58
Raw material medicin reagent co.,Ltd 025-57798860 China 4638 58
Shenzhen Enzan Biomedical Co., Ltd. 075525325458 CHINA 58 58


  • 32986-56-4
  • Tobramycin, Free Base - CAS 32986-56-4 - Calbiochem
  • 1-epitobramycin
  • 3’-deoxykanamycinb
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  • 6-trideoxy-alpha-d-ribo-hexopyranosyl-(1-4))-2-deoxy-
  • d-6-trideoxy-alpha-d-ribohexopyranosyl-(1-6))-2-deoxy
  • d-6-tyrideoxy-alpha-d-ribohexopyranosyl-(1-6))-2-deoxy
  • O-[3-Amino-3-deoxy-α-D-glucopyranosyl-(1→6)]-O-[2,6-diamino-2,3,6-trideoxy-α-D-ribohexopyranosyl-(1→4)]-2-deoxy-D-streptamine
  • Tobramycin Base
  • Tobramycin, Free Base
  • TobramycinSulphate49842-07-1/Base
  • O-3-Amino-3-deoxy-alpha-D-glucopyranosyl-(1-6)-O-(2,6-
  • Tobramycine
  • deoxykanamycinb
  • -d-glycopyranosyl]-2-deoxystreptamine
  • O-3-Amino-3-deoxy-a-D-glucopyranosyl-(1-6)-O-[2,6-diamino-2,3,6-trideoxy-a-D-ribo-hexopyranosyl-(1-4)]-2-deoxy-D-streptamine
  • >D-Streptamine, O-3-amino-3-deoxy-.alpha.-D-glucopyranosyl-(1?6)-O-2,6-diamino-2,3,6-trideoxy-.alpha.-D-ribo-hexopyranosyl-(1?4)-2-deoxy-
  • o-[3-amino-3-deoxy-α-d-glucopyranosyl-(1→6)]-o-[2,6-diamino-2,3,6-trideoxy-α-d-ribohexopyranosyl-(1→4)]-2-deoxy-d-streptamine
  • D-Streptamine, O-3-amino-3-deoxy-a-D-glucopyranosyl-(16)-O-[2,6-diamino-2,3,6-trideoxy-a-D-ribo-hexopyranosyl-(14)]-2-deoxy- (9CI)
  • NSC 180514
  • O-3-Amino-3-deoxy-a-D-glucopyranosyl-(14)-O-[2,6-diamino-2,3,6-trideoxy-a-D-ribo-hexopyranosyl-(16)]-2-deoxystreptamine
  • Streptamine, O-3-amino-3-deoxy-a-D-glucopyranosyl-(14)-O-[2,6-diamino-2,3,6-trideoxy-a-D-ribo-hexopyranosyl-(16)]-2-deoxy-, D- (8CI)
  • Tobracin
  • Tobramaxin
  • Tobramycetin
  • Tobramycin (base and/or unspecified salts)
  • O-[3-Amino-3-deoxy-alpha-D-glucopyranosyl-(1→6)]-O-[2,6-diamino-2,3,6-trideoxy-alpha-D-ribohexopyranosyl-(1→4)]-2-deoxy-D-streptamine
  • O-3-Amino-3-deoxy-α-D-glucopyranosyl-(1-6)-O-[2,6-diamino-2,3,6-trideoxy-a -D-ribo-hexopyranosyl-(1-4)]-2-deoxy-D-streptamine
  • Tobramax
  • トブラマイシン
  • O-[3-アミノ-3-デオキシ-α-D-グルコピラノシル-(1→6)]-O-[2,6-ジアミノ-2,3,6-トリデオキシ-α-D-リボ-ヘキソピラノシル-(1→4)]-2-デオキシ-D-ストレプタミン
  • トブラマイシン標準品
  • トブラマイシン, 遊離塩基
  • トブラマイシン DEUTERATED
  • 抗生物質
  • 生化学
  • 試験研究用抗菌剤
  • アミノグリコシド系 (試験研究用抗生物質)
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