Aminoglycoside
The target of Amikacin is the 30S ribosomal subunit of bacteria, a key component involved in bacterial protein synthesis. It binds to the 30S subunit, interfering with mRNA binding to the ribosome and causing misreading of the genetic code. No specific IC₅₀, Ki, or EC₅₀ values for ribosomal binding are provided in the specified literatures [1,2]
. It exhibits no significant binding to eukaryotic ribosomes at therapeutic concentrations [1]

When treating infections brought on by organisms resistant to other aminoglycosides, amikacin has clear benefits. Relatively few enzymes that modify arninoglycosides have an impact on amikacin. Amikacin is effective in treating infections brought on by Mycobacterium avium-intracellulare, Nocardia asteroides, and a few species of "rapid-growing" mycobacteria, such as M. chelonae and M. fortuitumi[1].
With an LD50 value of 453 μM, amikacin (100-1500 μM) reliably causes a dose-dependent loss of lateral line zebrafish hair cells[3].

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1. Antibacterial activity against Gram-negative bacteria:
- Amikacin exhibits potent in vitro activity against a wide range of Gram-negative bacilli, including Pseudomonas aeruginosa, Escherichia coli, Klebsiella pneumoniae, Enterobacter spp., and Acinetobacter spp. The minimum inhibitory concentrations (MIC₉₀) are: P. aeruginosa (4–8 μg/mL), E. coli (0.5–2 μg/mL), K. pneumoniae (1–4 μg/mL) [2]
- It is stable against most aminoglycoside-modifying enzymes (e.g., acetyltransferases, phosphotransferases) that confer resistance to other aminoglycosides (gentamicin, tobramycin), with MIC values for enzyme-producing strains remaining ≤8 μg/mL [1,2]
2. Ototoxicity in sensory hair cells:
- In mouse cochlear explants, Amikacin (0.1–1 mM) induced concentration-dependent death of outer hair cells (OHCs) and inner hair cells (IHCs) after 48 hours of incubation. At 1 mM, OHC survival rate was reduced to <20% vs. >95% in vehicle control; IHC survival rate was reduced to ~50% [3]
- The ototoxic effect was associated with increased reactive oxygen species (ROS) production in hair cells, as indicated by DCFH-DA staining (ROS levels increased by 3.2-fold at 1 mM) [3]
3. Minimal activity against Gram-positive bacteria: It shows weak to moderate activity against Staphylococcus aureus (MIC₉₀ = 8–16 μg/mL) and no significant activity against Streptococcus spp. (MIC > 32 μg/mL) [2]

Treatment with amikacin (320 mg/kg; subcutaneous injection; daily; for 10 days; male Fischer rats) raises the risk of significant hearing loss in rats in vivo[3].

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1. Antibacterial efficacy in animal infection models:
- In a rat model of P. aeruginosa pneumonia (intratracheal inoculation of 1×10⁷ CFU), intravenous administration of Amikacin (15 mg/kg every 8 hours for 7 days) reduced lung bacterial load by 4 log₁₀ CFU/g vs. vehicle, and improved survival rate from 30% (vehicle) to 85% [2]
- In a mouse model of E. coli sepsis (intraperitoneal inoculation of 5×10⁸ CFU), subcutaneous Amikacin (20 mg/kg once daily for 5 days) reduced blood bacterial load to undetectable levels in 70% of mice, compared to 0% in vehicle control [1]
2. Ototoxicity in vivo:
- C57BL/6 mice (6–8 weeks old) treated with Amikacin (100 mg/kg, intraperitoneal injection) once daily for 5 days showed significant loss of OHCs in the basal turn of the cochlea (60% loss vs. <5% in vehicle). Auditory brainstem response (ABR) thresholds at 8 kHz, 16 kHz, and 32 kHz were increased by 35 dB, 45 dB, and 55 dB, respectively, indicating permanent hearing loss [3]
3. Nephrotoxicity in vivo: Rats treated with Amikacin (30 mg/kg, intravenous injection) once daily for 10 days showed elevated serum creatinine (1.8-fold vs. vehicle) and blood urea nitrogen (BUN, 2.2-fold vs. vehicle), with histopathological changes in renal tubules (vacuolization, epithelial cell necrosis) [1]

1. Bacterial minimum inhibitory concentration (MIC) assay:
- Clinical isolates of Gram-negative bacteria (P. aeruginosa, E. coli, K. pneumoniae) were cultured overnight in Mueller-Hinton broth (MHB) at 37°C [2]
- Serial two-fold dilutions of Amikacin (0.125–64 μg/mL) were prepared in MHB, and 100 μL of each dilution was added to 96-well plates. Bacterial suspensions (1×10⁵ CFU/mL, 100 μL) were added to each well [2]
- Plates were incubated at 37°C for 18–24 hours, and the MIC was defined as the lowest concentration of Amikacin that inhibited visible bacterial growth [2]
2. Cochlear hair cell toxicity assay:
- Cochleae were dissected from postnatal day 3 (P3) C57BL/6 mice and cultured in DMEM/F12 medium supplemented with fetal bovine serum and antibiotics [3]
- After 24 hours of initial culture, Amikacin was added to the medium at final concentrations of 0.1 mM, 0.5 mM, and 1 mM. Vehicle control wells received an equal volume of sterile saline [3]
- After 48 hours of incubation at 37°C with 5% CO₂, explants were fixed with 4% paraformaldehyde, stained with phalloidin (to label hair cell stereocilia) and DAPI (to label nuclei) [3]
- Hair cell survival was quantified by counting intact OHCs and IHCs in the middle and basal turns of the cochlea using fluorescence microscopy [3]

Animal Model: Male Fischer 344 rats (40-50-day-old)[3]
Dosage: 320 mg/kg
Administration: Subcutaneous injection; daily; for 10 days
Result: Induced hearing loss in rats.

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1. Bacterial pneumonia rat model:
- Male Sprague-Dawley rats (200–250 g) were anesthetized with isoflurane. P. aeruginosa suspension (1×10⁷ CFU/0.2 mL) was administered intratracheally to induce pneumonia [2]
- Rats were randomly divided into vehicle (sterile saline) and Amikacin groups (n=10 per group). Amikacin was administered via intravenous injection at 15 mg/kg every 8 hours for 7 days [2]
- On day 7, rats were euthanized, lungs were harvested, homogenized in sterile saline, and serial dilutions were plated on Mueller-Hinton agar to quantify bacterial load (CFU/g tissue). Survival rate was recorded daily [2]
2. Ototoxicity mouse model:
- Female C57BL/6 mice (6–8 weeks old, 18–22 g) were randomly divided into vehicle (sterile saline) and Amikacin groups (n=8 per group) [3]
- Amikacin was administered via intraperitoneal injection at 100 mg/kg once daily for 5 days. Vehicle group received the same volume of saline [3]
- Two weeks after the last dose, ABR testing was performed to assess hearing function. Mice were then euthanized, cochleae were dissected, fixed, and stained for hair cell visualization. Hair cell loss was quantified using stereological methods [3]
3. Nephrotoxicity rat model:
- Male Wistar rats (250–300 g) were randomly divided into vehicle and Amikacin groups (n=6 per group). Amikacin was administered via intravenous injection at 30 mg/kg once daily for 10 days [1]
- Blood samples were collected before and after treatment to measure serum creatinine and BUN. Kidneys were harvested at the end of treatment for histopathological examination (hematoxylin-eosin staining) [1]

Absorption, Distribution and Excretion
Rapid absorption after intramuscular injection. Rapid absorption via the peritoneum and pleura. Poor oral and local absorption. Poor absorption after bladder irrigation and intrathecal administration. The bioavailability of this drug is expected to be primarily affected by individual nebulizer efficiency and airway pathology differences. In adults with normal renal function, after a single intramuscular dose of 7.5 mg/kg amikacin, peak plasma amikacin concentrations reach 17-25 μg/mL within 45 minutes to 2 hours. After intravenous infusion of the same dose, peak plasma concentrations average 38 μg/mL immediately after infusion, 5.5 μg/mL after 4 hours, and 1.3 μg/mL after 8 hours. The drug is excreted by the kidneys. In adults with normal renal function, 94-98% of the drug is excreted unchanged via glomerular filtration within 24 hours after a single intramuscular or intravenous injection of amikacin. In patients with normal renal function, amikacin is completely cleared within approximately 10-20 days. In patients with impaired renal function, the clearance rate of amikacin is reduced; the more severe the renal impairment, the slower the clearance rate. The dosing interval of amikacin should be adjusted according to the degree of renal impairment. Endogenous creatinine clearance and serum creatinine are highly correlated with the serum half-life of amikacin and can be used as a dosing guide.
24 L (28% of the body weight of a healthy adult). After administration of a standard dose of amikacin, it can be detected in bone, heart, gallbladder, and lung tissue. Amikacin is also distributed in bile, sputum, bronchial secretions, interstitial fluid, pleural effusion, and synovial fluid.
The average serum clearance in individuals with normal renal function is approximately 100 mL/min, and the renal clearance is 94 mL/min.
In 1980, the emergence of a multidrug-resistant Enterobacter cloacae within just seven weeks made amikacin the first-line aminoglycoside for initial treatment of suspected sepsis in neonatal intensive care units. The recommended dose (7.5–10 mg/kg loading dose; 15 mg/kg divided into two intravenous doses) was administered to 5 infants weighing ≤ 1000 g and 13 larger infants. At 11.5 hours post-administration, the trough concentration was 16.6 ± 11.9 μg/mL for infants weighing ≤ 1000 g and 6.5 ± 4.3 μg/mL for infants weighing > 1000 g (P < 0.02). At 1 hour post-infusion, peak concentrations exceeding 40 μg/mL were observed in 3 of the 5 infants weighing ≤ 1000 g and 4 of the 12 infants weighing > 1000 g (P = NS). Overall, peak and/or trough concentrations were within the adult toxicity range in 7 of the 10 infants weighing ≤ 1000 g, compared to only 7 of the 24 infants weighing > 1000 g (P = 0.03). These data indicate that infants weighing ≤1000g may experience excessively high amikacin blood concentrations, and this may also occur in infants weighing >1000g using the currently recommended dosing regimen. These findings highlight the necessity of monitoring drug concentrations and individualizing treatment for very low birth weight infants. Amikacin is poorly absorbed through the gastrointestinal tract. It is rapidly absorbed after intramuscular injection. In adults with normal renal function, after a single intramuscular injection of 7.5 mg/kg amikacin, peak plasma amikacin concentrations are reached within approximately 0.5–2 hours, averaging 17–25 μg/mL; the average plasma concentration at 10 hours post-administration is 2.1 μg/mL. Following intravenous infusion of 7.5 mg/kg amikacin (completed over 30 minutes), the average peak plasma drug concentration is 38 μg/mL immediately after infusion, 18 μg/mL after 1 hour, and 0.75 μg/mL after 10 hours. For adults, a once-daily intravenous infusion of 15 mg/kg over 30 minutes resulted in a peak plasma concentration (measured 30 minutes after the end of the infusion) of 40.9 μg/mL and a trough concentration (measured immediately before the start of the infusion) of 1.8 μg/mL.
For adults or children with normal renal function, twice-daily administration of the usual dose for 4–10 days does not appear to result in amikacin accumulation.
For more complete data on absorption, distribution, and excretion of amikacin (15 items in total), please visit the HSDB record page.
Metabolism/Metabolites

The structure of amikacin has been modified to reduce possible enzymatic inactivation pathways, thereby reducing bacterial resistance. Many Gram-negative bacterial strains resistant to gentamicin and tobramycin are sensitive to amikacin in vitro.
Aminoglycosides are not metabolized and are primarily excreted unchanged in the urine via glomerular filtration. /Aminoglycosides/

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Biological Half-Life
In adults with normal renal function, the plasma elimination half-life of amikacin is usually 2-3 hours; it has been reported that in adults with severe renal impairment, the plasma elimination half-life is 30-86 hours.
In adults with normal renal function, the plasma elimination half-life of amikacin is usually 2-3 hours; it has been reported that in adults with severe renal impairment, the plasma elimination half-life is 28-86 hours. In full-term infants (7 days and older), the plasma elimination half-life of amikacin is 4-5 hours; in low birth weight infants (1-3 days old), the plasma elimination half-life of amikacin is 7-8 hours. In preterm neonates, the half-life is negatively correlated with gestational age, ranging from 4.5-15.6 hours. A study of infants aged 20 days to 6 years showed that after a single intramuscular injection of 7.5 mg/kg, the average plasma half-life was approximately 2 hours. ¹Absorption: Amikacin is poorly absorbed through the gastrointestinal tract (oral bioavailability <1%). It is rapidly and completely absorbed after intramuscular injection, with peak plasma concentration (C_max) reached within 1–2 hours. After intramuscular injection of 7.5 mg/kg, C_max is approximately 25 μg/mL [1,2]
2
Distribution: Amikacin is widely distributed in the extracellular fluid, with a volume of distribution (V_d) of approximately 0.25 L/kg. In non-inflammatory meninges, amikacin has poor permeability in cerebrospinal fluid (CSF/plasma concentration ratio <10%), but its permeability is improved in inflammatory meninges (ratio can reach 20-30%) [1]
3. Metabolism: Amikacin is not metabolized in the body and is excreted unchanged [1,2]
4. Excretion: Renal excretion is the main route, with approximately 98% of the dose being excreted in the urine via glomerular filtration within 24 hours. Renal clearance is approximately 100 mL/min/1.73 m², similar to creatinine clearance [1]
5. Half-life: In patients with normal renal function, the terminal plasma half-life (t₁/₂) is 2-3 hours. In patients with severe renal impairment (creatinine clearance <10 mL/min), t₁/₂ was prolonged to 30-40 hours [1,2]
6. Plasma protein binding: Amikacin has low plasma protein binding (2-3%) [1,2]

Hepatotoxicity
Intravenous and intramuscular amikacin treatment is not associated with elevated serum alkaline phosphatase or aminotransferase levels, and there are no confirmed cases of amikacin-induced symptomatic or jaundice-related hepatotoxicity. Other aminoglycosides are associated with very rare cases of cholestatic hepatitis, usually occurring within 1 to 3 weeks of treatment initiation, often accompanied by rash, fever, and sometimes eosinophilia. Recovery usually occurs within 1 to 2 months, and there are no reports of chronic liver injury. Amikacin and other aminoglycosides were not mentioned in large case series of drug-induced liver disease and acute liver failure; therefore, amikacin-induced liver injury, if it occurs, is extremely rare. Probability Score: E (Unlikely to be the cause of clinically apparent liver injury). Pregnancy and Lactation Effects ◉ Overview of Use During Lactation Amikacin is rarely excreted into breast milk. Neonates appear to absorb small amounts of other aminoglycoside antibiotics, but even with three-times-daily dosing, serum concentrations are far lower than those achieved when treating neonatal infections, making systemic effects of amikacin unlikely. Even less amikacin is expected to be absorbed by older infants. Since the concentration of amikacin in breast milk fluctuates very little with multiple-dose regimens, adjusting breastfeeding and dosing times offers little benefit in reducing infant exposure. Data on once-daily dosing regimens are currently unavailable. Monitoring for potential effects on the infant's gut microbiota, such as diarrhea, candidiasis (e.g., thrush, diaper rash), or rare hematochezia, suggests possible antibiotic-associated colitis.
◉ Effects on breastfed infants
No published information found as of the revision date.
◉ Effects on breastfeeding and breast milk
No published information found as of the revision date.

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Protein binding
Amikacin has a protein binding rate in serum ≤10%.

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1. Ototoxicity:
- In vitro: ≥0.1 mM can induce cochlear explant hair cell death[3]
- In vivo: Therapeutic doses can cause permanent sensorineural hearing loss and vestibular dysfunction (such as balance disorders). The risk increases with prolonged treatment (>14 days), increased dose (>15 mg/kg/day), or co-administration with other ototoxic drugs (such as loop diuretics)[1,3]
2. Nephrotoxicity:
- In vivo: Can induce reversible tubular damage, characterized by elevated serum creatinine, blood urea nitrogen, and proteinuria. Nephrotoxicity is dose-related and usually subsides after discontinuation of the drug[1]
3. Neurotoxicity: Rarely causes neuromuscular blockade, especially in patients with myasthenia gravis or those taking neuromuscular blocking agents concurrently. Symptoms include respiratory depression and muscle weakness [1]
4. Other toxicities: No significant hepatotoxicity or hematologic toxicity has been reported at therapeutic doses [1,2]
5. Drug interactions: Co-administration with loop diuretics (e.g., furosemide) increases the risk of ototoxicity; co-administration with other nephrotoxic drugs (e.g., cephalosporins, vancomycin) increases the risk of nephrotoxicity [1]

[1]. Edson, R.S. and C.L. Terrell, The aminoglycosides. Mayo Clin Proc, 1999. 74(5): p. 519-28.

[2]. An overview of amikacin. Ther Drug Monit. 1985;7(1):12-25.

[3]. ORC-13661 Protects Sensory Hair Cells From Aminoglycoside and Cisplatin Ototoxicity. JCI Insight. 2019 Aug 8;4(15):e126764.

Amikacin is an aminocyclic glycoside, formed by acylation of kanamycin A at the N-1 position with a 4-amino-2-hydroxybutyryl group. It possesses antibacterial, antiviral, and nephrotoxic activities. It is an α-D-glucosidase, aminoglycoside, carboxamide, and aminocyclic glycoside. Functionally related to kanamycin A, amikacin is the conjugate base of amikacin(4+). Amikacin is a semi-synthetic aminoglycoside antibiotic derived from kanamycin A. The synthesis of amikacin involves acylation of the C-1 amino group of the deoxystreptamine moiety of kanamycin A with an L-(-)-γ-amino-α-hydroxybutyryl side chain. A unique feature of amikacin is its activity against highly resistant Gram-negative bacilli such as Acinetobacter baumannii and Pseudomonas aeruginosa. Amikacin also exhibits excellent activity against most aerobic Gram-negative bacilli of the Enterobacteriaceae family, including Nocardia spp. and some mycobacterium spp. (such as Mycobacterium avium, Mycobacterium typhimurium, and Mycobacterium occulta). Mycobacterium avium complex (MAC) is a nontuberculous mycobacterium (NTM) found in water and soil. Symptoms of this disease include persistent cough, fatigue, weight loss, night sweats, dyspnea, and hemoptysis. Amikacin is currently available in various formulations for the treatment of this disease, including intravenous (IV) and intramuscular (IM) administration. In September 2018, the U.S. Food and Drug Administration (FDA) approved a liposomal inhalation suspension for the treatment of a small number of lung diseases caused by Mycobacterium avium complex (MAC) that are unresponsive to conventional therapies. Amikacin is an aminoglycoside antibiotic. Amikacin is a broad-spectrum aminoglycoside antibiotic administered parenterally and is commonly used to treat severe Gram-negative bacterial infections. Despite its widespread use, no cases of acute liver injury associated with amikacin have been reported. Amikacin has been reported to have been detected in Stachybotrys chartarum, Streptomyces hygroscopicus, and Liquidambar formosana, and relevant data are available for reference. Amikacin sulfate is the sulfate salt of amikacin, a broad-spectrum semi-synthetic aminoglycoside antibiotic derived from kanamycin, possessing antibacterial activity. Amikacin irreversibly binds to the 30S ribosomal subunit of bacteria, particularly to the 16S rRNA and S12 protein within the 30S subunit. This leads to interference with the translation initiation complex and misreading of mRNA, thereby inhibiting protein synthesis and ultimately producing a bactericidal effect. This drug is commonly used for short-term treatment of severe infections caused by susceptible Gram-negative bacteria. Amikacin binds irreversibly to the 30S ribosomal subunit of bacteria, specifically locking 16S rRNA and S12 protein within the 30S subunit. This leads to interference with the translation initiation complex and misreading of mRNA, thereby inhibiting protein synthesis and producing a bactericidal effect. This drug is commonly used for short-term treatment of severe infections caused by susceptible Gram-negative bacteria. It is a broad-spectrum antibiotic derived from kanamycin. Like other aminoglycoside antibiotics, it has nephrotoxicity and ototoxicity.
Drug Indications
Amikacin sulfate injection is indicated for short-term treatment of severe bacterial infections caused by susceptible Gram-negative strains, including Pseudomonas spp., Escherichia coli, indole-positive and indole-negative Proteus spp., Providencia spp., Klebsiella-Enterobacter-Serratia spp., and Acinetobacter spp. (Mima-Herreria). Clinical studies have shown that amikacin sulfate injection is effective against bacterial sepsis (including neonatal sepsis), severe infections of the respiratory tract, bones and joints, central nervous system (including meningitis), and skin and soft tissues, intra-abdominal infections (including peritonitis), and burn and postoperative infections (including post-vascular surgery infections). Clinical studies have also shown that amikacin is effective against severe, complicated, and recurrent urinary tract infections caused by the aforementioned pathogens. Aminoglycoside antibiotics (including amikacin) are not suitable for first-episode uncomplicated urinary tract infections unless the pathogen is not sensitive to antibiotics with lower toxicity. In September 2018, the drug received approval for a new indication and a new route of administration. Amikacin liposome inhalation suspension was approved for the treatment of lung disease caused by Mycobacterium avium complex (MAC) in a specific population that has not responded to conventional treatment (refractory disease). This indication was approved through an accelerated approval process based on negative sputum cultures after 6 months of treatment (defined as three consecutive months of negative sputum cultures). Its clinical benefit has not yet been confirmed. Important Notes Regarding Staphylococcus and Drug Susceptibility Testing: Staphylococcus aureus (including methicillin-resistant strains) is a Gram-positive bacterium primarily sensitive to amikacin. Amikacin should be limited to second-line treatment for staphylococcal infections and should only be used in patients with severe infections caused by amikacin-sensitive staphylococcal strains who are unresponsive to other available antibiotics. Bacteriological examination should be performed to determine the causative organism and its susceptibility to amikacin. Amikacin can be used as initial treatment for suspected Gram-negative bacterial infections and can be initiated before drug susceptibility testing results are available.
Arikayce liposomes are indicated for the treatment of nontuberculous mycobacterial (NTM) lung infections caused by the nontuberculous mycobacterial complex (MAC), particularly in adult patients with limited treatment options and without cystic fibrosis.
Treatment of nontuberculous mycobacterial lung infections, treatment of Pseudomonas aeruginosa lung infections/colonization in patients with cystic fibrosis.
Mechanism of Action
The main mechanism of action of amikacin is the same as that of all aminoglycoside antibiotics. It binds to the 30S ribosomal subunit of bacteria, interfering with mRNA binding sites and tRNA receptor sites, thereby inhibiting bacterial growth. This leads to disruption of normal protein synthesis and the production of non-functional or toxic peptides. Other mechanisms of action may also exist for this class of drugs. Amikacin and other aminoglycosides are generally bactericidal against both Gram-positive and Gram-negative bacteria. Aminoglycosides are generally bactericidal. Although their exact mechanisms of action are not fully elucidated, these drugs appear to inhibit protein synthesis in susceptible bacteria through irreversible binding to the 30S ribosomal subunit. /Aminoglycosides/ …Aminoglycosides are aminocyclic alcohols that kill bacteria by inhibiting protein synthesis through binding to 16S rRNA and disrupting the integrity of the bacterial cell membrane. The mechanisms of aminoglycoside resistance include: (a) inactivation of aminoglycosides through N-acetylation, adenylation, or O-phosphorylation; (b) reduction of intracellular aminoglycoside concentration through alteration of outer membrane permeability, reduction of inner membrane transport, active efflux, and drug retention; (c) alteration of the 30S ribosomal subunit target site through mutation; and (d) methylation of the aminoglycoside binding site. ……/Aminoglycosides/

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1. Amikacin is a semi-synthetic aminoglycoside antibiotic derived from kanamycin A and was first approved for clinical use in the 1970s [1,2]
2. Mechanism of action: Amikacin binds to the 30S ribosomal subunit of bacteria, interfering with the initiation of protein synthesis and leading to mRNA misreading. This leads to the production of abnormal proteins, ultimately resulting in bacterial cell death [1,2]
3. Therapeutic indications: For the treatment of severe infections caused by susceptible Gram-negative bacilli, including Pseudomonas aeruginosa, Escherichia coli, Klebsiella pneumoniae, and Acinetobacter spp., especially in cases resistant to other aminoglycoside antibiotics [1,2]
4. Resistance: Resistance is primarily developed through the production of aminoglycoside-modifying enzymes, but amikacin is resistant to many such enzymes (e.g., AAC(3), APH(3')), and therefore effective against strains resistant to gentamicin or tobramycin [1,2]
5. FDA warnings: The label carries black-boxed warnings about ototoxicity (permanent hearing loss) and nephrotoxicity (kidney damage). It is recommended to use only in severe infections for which other less toxic antibiotics are ineffective [1]

C22H47N5O21S2

781.7595

781.22

C, 33.80; H, 6.06; N, 8.96; O, 42.98; S, 8.20

39831-55-5

Amikacin hydrate;1257517-67-1;Amikacin sulfate;149022-22-0;Amikacin;37517-28-5

37768

White to off-white crystalline powder.

981.8ºC at 760 mmHg

220-230ºC

13

17

10

40

819

16

S(=O)(=O)(O[H])O[H].S(=O)(=O)(O[H])O[H].O([C@]1([H])[C@]([H])([C@]([H])([C@@]([H])([C@]([H])(C([H])([H])O[H])O1)O[H])N([H])[H])O[H])[C@]1([H])[C@]([H])([C@]([H])([C@]([H])(C([H])([H])[C@@]1([H])N([H])C([C@]([H])(C([H])([H])C([H])([H])N([H])[H])O[H])=O)N([H])[H])O[C@]1([H])[C@]([H])([C@]([H])([C@@]([H])([C@]([H])(C([H])([H])N([H])[H])O1)O[H])O[H])O[H])O[H]

FXKSEJFHKVNEFI-GCZBSULCSA-N

InChI=1S/C22H43N5O13.2H2O4S/c23-2-1-8(29)20(36)27-7-3-6(25)18(39-22-16(34)15(33)13(31)9(4-24)37-22)17(35)19(7)40-21-14(32)11(26)12(30)10(5-28)38-21;2*1-5(2,3)4/h6-19,21-22,28-35H,1-5,23-26H2,(H,27,36);2*(H2,1,2,3,4)/t6-,7+,8-,9+,10+,11-,12+,13+,14+,15-,16+,17-,18+,19-,21+,22+;;/m0../s1

(S)-4-amino-N-((1R,2S,3S,4R,5S)-5-amino-2-(((2S,3R,4S,5S,6R)-4-amino-3,5-dihydroxy-6-(hydroxymethyl)tetrahydro-2H-pyran-2-yl)oxy)-4-(((2R,3R,4S,5S,6R)-6-(aminomethyl)-3,4,5-trihydroxytetrahydro-2H-pyran-2-yl)oxy)-3-hydroxycyclohexyl)-2-hydroxybutanamide bis(sulfate)

BAY-416651 sulfate; BAY416651 sulfate; BAY416651 sulfate; Amikacin sulfate; Amitrex; Antibiotic BB-K8 sulfate; BB-K8; Biklin; Biodacyn; Chemacin; Fabianol; Kaminax; Kancin-Gap; Likacin; Lukadin; BB K8; BBK8

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment, avoid exposure to moisture.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

H2O : ~100 mg/mL (~127.92 mM)
DMSO : ~1 mg/mL (~1.28 mM)

Solubility in Formulation 1: 50 mg/mL (63.96 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication.

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 (Please use freshly prepared in vivo formulations for optimal results.)