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 详细处方信息以本药内容附件PDF文件（201032301020422.pdf）的“原文Priscribing Information”为准
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部分Habekacin  Injection 处方资料（仅供参考）

The pharmacokinetics of habekacin, a new semisynthetic aminoglycoside antibiotic, were investigated in six healthy subjects and 25 uremic patients (six of whom were on hemodialysis) after administration of a single 3-mg/kg dose. Six healthy subjects received the 3-mg/kg dose both intramuscularly (i.m.) and intravenously (i.v.) (1-h infusion). Uremic patients were given the 3-mg/kg dose as an i.m. injection, except for the hemodialysis patients, who received the dose as a 1-h i.v. infusion. After the i.m. injection, the peak concentrations in serum were higher and the times to peak levels were longer in patients with renal impairment than in healthy subjects. The elimination half-life in serum increased in relation to the degree of renal impairment, from 2 h in normal subjects to 32 h in patients with creatinine clearances of less than 10 ml/min. Renal impairment did not significantly modify the apparent volume of distribution. After the same 3-mg/kg dose as a 1-h i.v. infusion in six hemodialysis patients, the elimination half-life averaged 48 and 5 h off and on a 4- to 5-h hemodialysis session, respectively. The habekacin pharmacokinetic data appeared to be similar to those of the other available aminoglycoside antibiotics.

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Cellular uptake of habekacin, 1-N-(4-amino-2-hydroxybutyryl)dibekacin, was studied by incubating exponentially growing culture of Escherichia coli Q13 and its kanamycin-resistant mutants with [3H]habekacin. Kanamycin-resistant mutants, in which the resistance is due to alteration of ribosomes, were cross-resistant to habekacin, and showed a lower uptake of [3H]habekacin than the parental cells, suggesting that binding to ribosomes accelerates cellular uptake of habekacin. Cellular accumulation of [3H]habekacin by wild type cells was markedly inhibited by low temperature and by 2,4-dinitrophenol, suggesting that uptake of habekacin involves energy-dependent transport. The uptake of [3H]habekacin was reduced by various aminoglycoside antibiotics, suggesting common transport systems and/or common internal binding sites on the ribosome. Intracellular accumulation of [3H]dibekacin was reduced by habekacin, suggesting that both antibiotics possess a common transport system and/or common binding sites on the ribosome. Dibekacin was a better competitor than amikacin, suggesting that the dibekacin moiety of habekacin molecule, but not the 4-amino-2-hydroxybutyryl moiety, participates in the transport and/or binding to the ribosome. Binding of [3H]habekacin to E. coli ribosomes was reversed by various aminoglycosides and the degree of inhibition paralleled the one of cellular uptake, suggesting that competition by aminoglycosides for the habekacin uptake occurs at the ribosomal level.