QuickView for amikacin (compound)

Summary
General Info

PubChem

PubChem Compound 2142

Name:	Amikacin
PubChem Compound ID:	2142
Description:	A broad-spectrum antibiotic derived from KANAMYCIN. It is reno- and oto-toxic like the other aminoglycoside antibiotics.
Molecular formula:	C₂₂H₄₃N₅O₁₃
Molecular weight:	585.603 g/mol
Synonyms:	Amikacin; NSC177001; ANTIBIOTIC BB-K8; BB-K8; Novamin; Briclin

DrugBank

Identification

Name:	Amikacin
Name (isomeric):	DB00479
Drug Type:	small molecule
Description:	A broad-spectrum antibiotic derived from KANAMYCIN. It is reno- and oto-toxic like the other aminoglycoside antibiotics.
Synonyms:	Amikacin Base; Amikacinum [INN-Latin]; Amikacin Sulfate; Amikacine [INN-French]; Amikacina [INN-Spanish]; ANTIBIOTIC BB-K8; BB-K8; Amikacin Dihydrate
Brand:	Amikavet, Amicacin, Amiglyde-V, Briclin, Amikin
Category:	Anti-Bacterial Agents, Aminoglycosides
CAS number:	37517-28-5

Pharmacology

Indication:	For short-term treatment of serious infections due to susceptible strains of Gram-negative bacteria, including Pseudomonas species, Escherichia coli, species of indole-positive and indole-negative Proteus, Providencia species, Klebsiella-Enterobacter-Serratia species, and Acinetobacter (Mima-Herellea) species. Amikacin may also be used to treat Mycobacterium avium and Mycobacterium tuberculosis infections.
Pharmacology:	Amikacin is an aminoglycoside antibiotic. Aminoglycosides work by binding to the bacterial 30S ribosomal subunit, causing misreading of t-RNA, leaving the bacterium unable to synthesize proteins vital to its growth. Aminoglycosides are useful primarily in infections involving aerobic, Gram-negative bacteria, such as Pseudomonas, Acinetobacter, and ... show more » Amikacin is an aminoglycoside antibiotic. Aminoglycosides work by binding to the bacterial 30S ribosomal subunit, causing misreading of t-RNA, leaving the bacterium unable to synthesize proteins vital to its growth. Aminoglycosides are useful primarily in infections involving aerobic, Gram-negative bacteria, such as Pseudomonas, Acinetobacter, and Enterobacter. In addition, some mycobacteria, including the bacteria that cause tuberculosis, are susceptible to aminoglycosides. Infections caused by Gram-positive bacteria can also be treated with aminoglycosides, but other types of antibiotics are more potent and less damaging to the host. In the past the aminoglycosides have been used in conjunction with penicillin-related antibiotics in streptococcal infections for their synergistic effects, particularly in endocarditis. Aminoglycosides are mostly ineffective against anaerobic bacteria, fungi and viruses. show less «
Mechanism of Action:	Aminoglycosides like Amikacin "irreversibly" bind to specific 30S-subunit proteins and 16S rRNA. Amikacin inhibits protein synthesis by binding to the 30S ribosomal subunit to prevent the formation of an initiation complex with messenger RNA. Specifically Amikacin binds to four nucleotides of 16S rRNA and a single amino acid of protein S12. This in... show more » Aminoglycosides like Amikacin "irreversibly" bind to specific 30S-subunit proteins and 16S rRNA. Amikacin inhibits protein synthesis by binding to the 30S ribosomal subunit to prevent the formation of an initiation complex with messenger RNA. Specifically Amikacin 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. show less «
Absorption:	Rapidly absorbed after intramuscular administration. Rapid absorption occurs from the peritoneum and pleura. Poor oral and topical absorption. Poorly absorbed from bladder irrigations and intrathecal administration.
Protein binding:	0-11%
Route of elimination:	Amikacin is excreted primarily by glomerular filtration.
Half Life:	2-3 hours
Clearance:	100 mL/min
Toxicity:	Mild and reversible nephrotoxicity may be observed in 5 - 25% of patients. Amikacin accumulates in proximal renal tubular cells. Tubular cell regeneration occurs despite continued drug exposure. Toxicity usually occurs several days following initiation of therapy. May cause irreversible ototoxicity. Otoxocity appears to be correlated to cumulative lifetime exposure. Drug accumulation in the endolymph and perilymph of the inner ear causes irreversible damage to hair cells of the cochlea or summit of ampullar cristae in the vestibular complex. High frequency hearing is lost first with progression leading to loss of low frequency hearing. Further toxicity may lead to retrograde degeneration of the 8th cranial (vestibulocochlear) nerve. Vestibular toxicity may cause vertigo, nausea, vomiting, dizziness and loss of balance.
Affected organisms:	Enteric bacteria and other eubacteria

Interactions

Drug interaction:

Cefalotin	Increased risk of nephrotoxicity
Pancuronium	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
Furosemide	Increased ototoxicity

Cefalotin	Increased risk of nephrotoxicity
Pancuronium	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
Furosemide	Increased ototoxicity
Colistimethate	Aminoglycosides may enhance the nephrotoxic effect of Colistimethate. Aminoglycosides may enhance the neuromuscular-blocking effect of Colistimethate. Due to the potential for additive or synergistic toxicities (including both nephrotoxicity and neuromuscular blockade) between colistimethate and the aminoglycoside antibiotics, this combination should be avoided whenever possible. If these agents must be used together, patients' renal and neuromuscular function should be monitored closely.
Cephapirin	Increased risk of nephrotoxicity
Cisplatin	Increased risk of nephrotoxicity
Doxacurium chloride	The agent increases the effect of muscle relaxant
Mivacurium	The agent increases the effect of muscle relaxant
Ceftizoxime	Increased risk of nephrotoxicity
Metocurine	The agent increases the effect of muscle relaxant
Cefoxitin	Increased risk of nephrotoxicity
Cefamandole	Increased risk of nephrotoxicity
Ceforanide	Increased risk of nephrotoxicity
Tubocurarine	The agent increases the effect of muscle relaxant
Ethacrynic acid	Increased ototoxicity
Ceftazidime	Increased risk of nephrotoxicity
Thalidomide	Thalidomide increases the renal toxicity of the aminoglycoside
Torasemide	Increased ototoxicity
Cefotetan	Increased risk of nephrotoxicity
Cefuroxime	Increased risk of nephrotoxicity
Cefonicid	Increased risk of nephrotoxicity
Ticarcillin	Ticarcillin may reduce the serum concentration of Amikacin. Ticarcillin may inactivate Amikacin in vitro and the two agents should not be administered simultaneously through the same IV line.
Cefoperazone	Increased risk of nephrotoxicity
Vecuronium	The agent increases the effect of muscle relaxant
Pipecuronium	The agent increases the effect of muscle relaxant
Cefradine	Increased risk of nephrotoxicity
Tacrolimus	Additive renal impairment may occur during concomitant therapy with aminoglycosides such as Amikacin. Use caution during concomitant therapy.
Cefotaxime	Increased risk of nephrotoxicity
Bumetanide	Increased ototoxicity
Cefazolin	Increased risk of nephrotoxicity
Ceftriaxone	Increased risk of nephrotoxicity
Atracurium	The agent increases the effect of muscle relaxant

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Targets

30S ribosomal protein S12

16S rRNA