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Home / Drugs / Starting with N / Netilmicin

Netilmicin is a semisynthetic 1-N-ethyl derivative of sisomycin, an aminoglycoside antibiotic with action similar to gentamicin, but less ear and kidney toxicity. [PubChem] Netilmicin inhibits protein synthesis in susceptible organisms by binding to the bacterial 30S ribosomal subunit and interfering with mRNA binding and the acceptor tRNA site. The bactericidal effect of netilmiicin is not fully understood.
CategoriesAnti-Bacterial Agents
Protein Synthesis Inhibitors
ManufacturersSchering corp sub schering plough corp


For the treatment of bacteremia, septicaemia, respiratory tract infections, skin and soft-tissue infection, burns, wounds, and peri-operative infections caused by susceptible strains.


Netilmicin is a semisynthetic, water soluble antibiotic of the aminoglycoside group, produced by the fermentation of Micromonospora inyoensis, a species of actinomycete. Aminoglycosides are useful primarily in infections involving aerobic, Gram-negative bacteria, such as Pseudomonas, Acinetobacter, and Enterobacter. It is active at low concentrations against a wide variety of pathogenic bacteria including Escherichia coli, bacteria of the Klebsiella-Enterobacter-Serratia group, Citrobacter sp., Proteus sp. (indole-positive and indole-negative), including Proteus mirabilis, P. morganii, P. rettgrei, P. vulgaris, Pseudomonas aeruginosa and Neisseria gonorrhoea. Netilmicin is also active in vitro against isolates of Hemophilus influenzae, Salmonella sp., Shigella sp. and against penicillinase and non-penicillinase-producing Staphylococcus including methicillin-resistant strains. Some strains of Providencia sp., Acinetobacter sp. and Aeromonas sp. are also sensitive to netilmicin. Many strains of the above organisms which are found to be resistant to other aminoglycosides, such as kanamycin, gentamicin, tobramycin and sisomicin, are susceptible to netilmicin in vitro. Occasionally, strains have been identified which are resistant to amikacin but susceptible to netilmicin. The combination of netilmicin and penicillin G has a synergistic bactericidal effect against most strains of Streptococcus faecalis (enterococcus). The combined effect of netilmicin and carbenicillin or ticarcillin is synergistic for many strains of Pseudomonas aeruginosa. In addition, many isolates of Serratia, which are resistant to multiple antibiotics, are inhibited by synergistic combinations of netilmicin with carbenicillin, azlocillin, mezlocillin, cefamandole, cefotaxime or moxalactam. Aminoglycosides are mostly ineffective against anaerobic bacteria, fungi and viruses.

mechanism of action

Aminoglycosides like netilmicin "irreversibly" bind to specific 30S-subunit proteins and 16S rRNA. Specifically netilmicin 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, leaving the bacterium unable to synthesize proteins vital to its growth.


Netilmicin has nephrotoxic and ototoxic potential. Nephrotoxicity occurs via drug accumulation in renal proximal tubular cells resulting in cellular damage. Tubular cells may regenerate despite continued exposure and nephrotoxicity is usually mild and reversible. Netilmicin is less nephrotoxic than neomycin, gentamicin, tobramycin, and amikacin, likely due to a reduced number of cationic amino groups in its structure. Otoxicity occurs as a result of irreversible damage to hair cells of the cochlea and/or summit of the ampullar cristae in the vestibular complex caused drug accumulation in the endolymph and perilymph of the inner ear. Otoxicity appears to be correlated to total exposure and may be cumulative with further doses of aminoglycosides or other ototoxic drugs (e.g. cisplatin, furosemide). High frequency hearing loss is followed by low frequency hearing loss, which may be followed by retrograde degeneration of the auditory nerve. Vestibular toxicity may cause vertigo, nausea and vomiting, dizziness and loss of balance.


No evidence of metabolic transformation, typically 80% is recoverable in the urine within 24 hours


Rapidly and completely absorbed after IM administration, peak serum levels were achieved within 30-60 minutes. Aminoglycosides are poorly absorbed orally. Topical absorption is also poor unless severe skin damage is present.

half life

2.5 hours

drug interactions

Atracurium: The agent increases the effect of muscle relaxant

Bumetanide: Increased ototoxicity

Cefamandole: Increased risk of nephrotoxicity

Cefazolin: Increased risk of nephrotoxicity

Cefonicid: Increased risk of nephrotoxicity

Cefoperazone: Increased risk of nephrotoxicity

Ceforanide: Increased risk of nephrotoxicity

Cefotaxime: Increased risk of nephrotoxicity

Cefotetan: Increased risk of nephrotoxicity

Cefoxitin: Increased risk of nephrotoxicity

Cefradine: Increased risk of nephrotoxicity

Ceftazidime: Increased risk of nephrotoxicity

Ceftizoxime: Increased risk of nephrotoxicity

Ceftriaxone: Increased risk of nephrotoxicity

Cefuroxime: Increased risk of nephrotoxicity

Cephalothin Group: Increased risk of nephrotoxicity

Cephapirin: Increased risk of nephrotoxicity

Cisplatin: Increased risk of nephrotoxicity

Doxacurium chloride: The agent increases the effect of muscle relaxant

Ethacrynic acid: Increased ototoxicity

Furosemide: Increased ototoxicity

Metocurine: The agent increases the effect of muscle relaxant

Mivacurium: The agent increases the effect of muscle relaxant

Pancuronium: The agent increases the effect of muscle relaxant

Pipecuronium: The agent increases the effect of muscle relaxant

Rocuronium: The agent increases the effect of muscle relaxant

Succinylcholine: The agent increases the effect of muscle relaxant

Tacrolimus: Additive renal impairment may occur during concomitant therapy with aminoglycosides such as Netilmicin. Use caution during concomitant therapy.

Thalidomide: Thalidomide increases the renal toxicity of the aminoglycoside

Torasemide: Increased ototoxicity

Tubocurarine: The agent increases the effect of muscle relaxant

Vecuronium: The agent increases the effect of muscle relaxant