Gentamicin

Freely soluble in water

Soluble in pyridine, dimethylformamide, in acidic media with salt formation; moderately soluble in methanol, ethanol, acetone; practically insoluble in benzene, halogenated hydrocarbons

1.26e+01 g/L

Breast Feeding; Lactation; Milk, Human; Anti-Infective Agents; Antibacterial Agents; Aminoglycosides

Access group antibiotics

Active Ingredients (Gentamicin) -> FDA Greenbook

Pharmaceuticals -> Animal Drugs -> Approved in Taiwan

When heated to decomposition it emits acrid smoke and irritating fumes.

Melts with decomposition between 220 °C and 240 °C. /Gentamycin sulfate/

102-108 °C

105 °C (decomposition)

Danger

H317 (47.6%): May cause an allergic skin reaction [Warning Sensitization, Skin]

P203, P233, P260, P261, P264, P270, P271, P272, P273, P280, P284, P302+P352, P304+P340, P318, P319, P321, P333+P317, P342+P316, P362+P364, P391, P403, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 103 reports by companies from 5 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including gentamicin sulfate, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Gentamicin sulfate/

The Generic Animal Drug and Patent Restoration act requires that each sponsor of an approved animal drug must submit to the FDA certain information regarding patents held for the animal drug or its method of use. The Act requires that this information, as well as a list of all animal drug products approved for safety and effectiveness, be made available to the public. Gentamicin sulfate is included on this list. /Gentamicin sulfate/

Oral dosage form new animal drugs. Gentamicin sulfate oral solution. ... Indications for use. In weanling swine for control and treatment of colibacillosis caused by strains of Escherichia coli sensitive to gentamicin, and in swine for control and treatment of swine dysentery associated with Treponema hyodysenteriae. ... Limitations. Do not slaughter treated swine for food for at least 3 days following treatment. Federal law restricts this drug to use by or on the order of a licensed veterinarian. /Gentamicin sulfate/

Oral dosage form new animal drugs. Gentamicin sulfate pig pump oral solution. ... Indications for use. In neonatal swine 1 to 3 days of age for control and treatment of colibacillosis caused by strains of Escherichia coli sensitive to gentamicin. ... Limitations. For use in neonatal swine only. Do not slaughter treated swine for food for at least 14 days following treatment. /Gentamicin sulfate/

For more FDA Requirements (Complete) data for Gentamicin (11 total), please visit the HSDB record page.

Protect from light and store away from heat. Store at controlled room temperature 15 deg - 30 °C (59 deg - 86 °F). /Gentamicin, ophthalmic preparations/

Store at 20 deg to 25 °C (68 deg to 77 °F) /Gentamicin, injectable preparations; Gentamicin, topical preparations/

SRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.

One in vitro study indicates that cytarabine may antagonize the activity of gentamicin against Klebsiella pneumoniae.

Gentamicin appears to be more readily inactivated by antipseudomonal penicillins (eg, ticarcillin) than amikacin both in vitro and in vivo in patients with renal failure.

Concomitant and/or sequential use of an aminoglycoside and other systemic, oral, or topical drugs that have neurotoxic, ototoxic, or nephrotoxic effects (e.g., other aminoglycosides, acyclovir, amphotericin B, bacitracin, capreomycin, certain cephalosporins, colistin, cisplatin, methoxyflurane, polymyxin B, vancomycin) may result in additive toxicity and should be avoided, if possible. /Aminoglycosides/

Because of the possibility of an increased risk of ototoxicity due to additive effects or altered serum and tissue aminoglycoside concentrations, aminoglycosides should not be given concomitantly with potent diuretics such as ethacrynic acid, furosemide, urea, or mannitol. It has been suggested that concomitant use of certain anti-emetics that suppress nausea and vomiting of vestibular origin and vertigo (e.g., dimenhydrinate, meclizine) may mask symptoms of aminoglycoside-associated vestibular ototoxicity. /Aminoglycosides/

For more Interactions (Complete) data for Gentamicin (12 total), please visit the HSDB record page.

Intravenous and intramuscular therapy with gentamicin has been linked to mild and asymptomatic elevations in serum alkaline phosphatase levels, but rarely affects aminotransferase levels or bilirubin, and changes resolve rapidly once gentamicin is stopped. Only isolated case reports of acute liver injury with jaundice have been associated with aminoglycoside therapy including gentamicin, most of which are not very convincing. The hepatic injury described in these reports is typically mixed but can evolve into a cholestatic hepatitis. The latency to onset is rapid, occurring within 1 to 3 weeks and is typically associated with skin rash, fever and sometimes eosinophilia. Recovery typically occurs within 1 to 2 months and chronic injury has not been described. Aminoglycosides are not listed or mentioned in large case series of drug induced liver disease and acute liver failure; thus, hepatic injury due to gentamicin is rare if it occurs at all.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 10(SRC), determined from a structure estimation method(2), indicates that gentamicin is expected to have very high mobility in soil(SRC). The estimated pKb of gentamicin is 9.0(3), indicating that this compound will exist partially in the cation form in the environment and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4). Volatilization of gentamicin from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 9.8X10-31 atm-cu m/mole(SRC), using a fragment constant estimation method(5). Gentamicin is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 1.8X10-13 mm Hg at 25 °C(SRC), determined from a fragment constant method(2). Biodegradation data in soil were not available(SRC, 2017).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 10(SRC), determined from a structure estimation method(2), indicates that gentamicin is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 9.8X10-31 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 3(SRC), from an estimated log Kow of -1.88(2) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Biodegradation data in water were not available(SRC, 2017).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), gentamicin, which has an estimated vapor pressure of 1,8X10-13 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase gentamicin may be removed from the air by wet and dry deposition(SRC). Gentamicin does not contain chromophores that absorb at wavelengths >290 nm(4) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC).

Skin Sensitizer - An agent that can induce an allergic reaction in the skin.

Characteristically, gentamicin reaches high concentrations in the renal cortex and the inner ear. The latter may be injured, leading to auditory and, especially, vestibular dysfunction. The first manifestation of cochlear damage is often high-pitched tinnitus, which may last a few weeks after the gentamicin is interrupted. A high-frequency hearing loss may be present in almost two-thirds of patients receiving aminoglycosides, including gentamicin, but only a small number report hearing impairment. The vestibular toxicity manifests as nausea, vomiting, balance disorder, and vertigo within the first 2 weeks. A chronic phase, which may persist for about 2 months, is marked by ataxia and, not infrequently, leaves residual dysfunction. Gentamicin tends to accumulate in renal proximal tubular cells and can cause damage. Hence, mild proteinuria and a reduction in glomerular filtration rate are potential consequences of gentamicin use, with 14% of users experiencing these effects in a review. Once proximal tubular cells retain regenerative capacity, renal injury and its consequences are often reversible. Compared with the high-dose and extended-interval dosing approach, the divided-dose scheme implies a longer duration of gentamicin serum concentrations above the toxicity threshold, resulting in a higher risk of ototoxicity and nephrotoxicity.

IDENTIFICATION AND USE: Gentamicin sulfate is an aminoglycoside antibiotic. Gentamicin is widely used in the treatment of severe infections. It is active against many strains of Gram-negative bacteria and Streptococus aureus. It is inactive against anaerobes and poorly active against Streptococus hemolyticus and Pneumococcus. HUMAN EXPOSURE AND TOXICITY: Main risks and target organs: The main toxic effects are vestibular damage, deafness and renal dysfunction. The damage on the vestibular portion of the eighth cranial nerve appears to be greater than that on the cochlear portion. The main target organs are the eighth cranial nerves and the kidneys. Damage to eighth cranial nerve (both divisions) resulting in tinnitus, deafness, nausea, vomiting, vertigo, dizziness and nystagmus, and nephrotoxicity causing acute tubular necrosis resulting in renal failure. Loss of hearing, dizziness, vertigo, ataxia, nausea, vomiting and renal impairment developing in a patient on gentamicin therapy suggests a diagnosis of gentamicin toxicity. Other toxic features are muscular paralysis and respiratory depression. As gentamicin accumulates in the renal cortex, a critical concentration is reached when the concentrating ability of the kidney becomes impaired. Nephrotoxicity appears to be related to the duration for which the trough serum concentration exceeds 2 ug/ml. The exact mechanism of toxicity is unknown. Ototoxicity and vestibular toxicity seem most highly correlated with elevated peak concentrations (greater than 10 ug/mL) of gentamicin. Gentamicin accumulates in endolymph and perilymph and progressive destruction of ventricular and cochlear cells occurs. Repeated courses of gentamicin may produce progressive destruction of cells leading to deafness. Gentamicin appears to damage the vestibular portion more than the cochlear portion. Neuromuscular blockade with acute muscular paralysis and apnea may occur rarely. Most episodes have occurred in association with anesthesia or administration of other neuromuscular blockers but may also occur after intrapleural or intraperitoneal instillation of large doses of gentamicin or other aminoglycosides. This phenomenon may occur after intravenous or intramuscular administration. ANIMAL STUDIES: Clinical signs of intoxication in rodents included convulsions, prostration, hypoactivity, polydipsia, dyspnoea and ataxia. Dogs exhibited muscle tremors, salivation, and anorexia. Histopathological examination of kidneys from dogs that died up to 13 days after dosing revealed necrosis of the proximal convoluted tubule. Groups of 3 female Rhesus monkeys were injected i.m. with doses of 0, 6 or 30 mg/kg bw/day gentamicin in an aqueous vehicle for 3 weeks. Adverse clinical signs were limited to the 30 mg/kg bw/day group, which included pronounced facial paling and ptosis, markedly disturbed equilibrium from day 20, and depressed food intake and body- weight gain from week 2 onwards. Electron microscopy of renal tubules from the 30 mg/kg bw/day monkeys revealed myeloid bodies present in both tubular cells and lumen, increased phagosomes, disappearance of brush borders and sloughing of epithelial cells from the basement membrane. Groups of beagle dogs (4/sex/group) were administered oral doses of 0, 2, 10, or 60 mg/kg bw/day gentamicin in capsules for 14 weeks. Emesis and diarrhoea were observed occasionally in treated dogs. The only postmortem change was interstitial nephritis observed in 2 animals in the high-dose group. Gentamicin had negative effects on sperm parameters and testis apoptosis in rats. No treatment-related changes in pregnancy rate, litter size and weight, prenatal mortality or fetal abnormalities were reported in 2 generation study in rats. Gentamicin was tested in vitro for its ability to induce forward gene mutation in Chinese hamster ovary cells at concentrations of 128-5000 ug/mL and chromosomal aberrations in these cells at concentrations of 800-5000 ug/mL, both with and without metabolic activation. It was also tested in vivo for its ability to induce nuclear anomalies in mouse bone-marrow cells at intravenous doses of 20-80 mg/kg bw, the highest dose being the maximum tolerated dose. There was no indication of mutagenic activity.

The main toxicity that occurs from gentamicin systemic use is nephrotoxicity. Although a rare event, hypersensitivity reactions secondary to gentamicin administration can be severe, to the extent that cases requiring intensive care unit admissions exist in the literature. There is no antidote for gentamicin toxicity, and the approach for gentamicin-induced hypersensitivity reaction is drug suspension combined with supportive treatment. The possible hypersensitivity manifestations are urticaria, eosinophilia, delayed-type hypersensitivity reaction (Stevens-Johnson syndrome and toxic epidermal necrolysis), angioedema, and anaphylactic shock. The clinical manifestations should guide the treatment strategy. In case of hypotension or even anaphylactic shock, intravenous fluids and vasoactive agents are the primary therapeutic options. Oxygen supplementation or mechanical ventilation may be necessary if respiratory distress occurs. When Stevens-Johnson syndrome or toxic epidermal necrolysis develops, the mainstay of treatment includes wound care, pain control, fluid and electrolyte management, and monitoring of superinfections. Nephrotoxicity, one of the most common adverse effects of gentamicin use, is associated with the therapy duration and not with serum concentrations. Generally, the glomerular filtration rate decrement is small and transient, and rarely progresses to oliguric-anuric renal failure. Likewise, ototoxicity is more common in long-term gentamicin therapy. Furthermore, cochlear and vestibular damage sometimes is irreversible and can be accumulated after repetitive gentamicin exposure; aspirin use may attenuate this ototoxicity risk.

Using a structure estimation method based on molecular connectivity indices(1), the Koc of gentamicin can be estimated to be 10(SRC). According to a classification scheme(2), this estimated Koc value suggests that gentamicin is expected to have very high mobility in soil. The estimated pKb of gentamicin is 9.0(3), indicating that this compound will exist partially in the cation form in the environment and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4). Aromatic amines are expected to bind strongly to humus or organic matter in soils due to the high reactivity of the aromatic amino group(5,6), suggesting that mobility may be much lower in some soils(SRC).

/SIGNS AND SYMPTOMS/ Serious adverse effects on both vestibular and auditory branches of the eighth nerve have been reported, primarily in patients with renal impairment (especially if dialysis is required), and in patients on high doses and/or prolonged therapy. Symptoms include dizziness, vertigo, tinnitus, roaring in the ears and hearing loss, which, as with other aminoglycosides, may be irreversible. Hearing loss is usually manifested initially by diminution of high-tone acuity. Other factors which may increase the risk of toxicity include excessive dosage, dehydration and previous exposure to other ototoxic drugs. Peripheral neuropathy or encephalopathy, including numbness, skin tingling, muscle twitching, convulsions and a myasthenia gravis-like syndrome, have been reported.

/SIGNS AND SYMPTOMS/ Serious sensitivity reactions, such as anaphylaxis and dermatologic reactions including exfoliative dermatitis, toxic epidermal necrolysis, erythema multiforme, angioedema, and Stevens-Johnson syndrome, have been reported rarely in patients receiving aminoglycosides; fatalities have occurred rarely. Cross-sensitivity occurs among the aminoglycosides. /Aminoglycosides/

/CASE REPORTS/ A 65-year-old man with end-stage renal disease on continuous ambulatory peritoneal dialysis accidentally received an acute massive overdose of gentamicin as a treatment of peritonitis. The patient developed acute vestibular dysfunction and hearing loss following the overdose. His serum gentamicin had reached the extremely toxic level of 220 ug/mL. To remove the gentamicin, the patient received hemodialysis and hemoperfusion immediately. This was followed by two more courses of hemodialysis during the following 2 days. The gentamicin level was brought down to 10 ug/mL after the third hemodialysis. Moderate and persistent high-frequency hearing loss was documented with serial audiograms. The patient made a gradual but incomplete recovery from the vestibular dysfunction. ....

/CASE REPORTS/ A healthy 14-month-old girl received gentamicin 500 mg (56 mg/kg) intravenously as empiric therapy given fever. The overdosage was quickly recognized and the child transferred to a pediatric referral center. Two hours after administration, serum creatinine was 0.3 mg/dL, though serum gentamicin level was 89 mg/L. Hemodialysis was initiated approximately 4 hr after gentamicin was given and stopped 4 hr later, with a serum gentamicin level of 3.4 mg/L. Gentamicin level 4 hr after completion of hemodialysis was 2.3 mg/L. Three months later, the child's serum creatinine was 0.3 mg/dL, urinalysis showed no blood or protein, and audiometry showed normal hearing bilaterally at all frequencies. This child demonstrated the highest gentamicin level recorded in a patient with normal renal function. Her case demonstrates that prompt hemodialysis in this circumstance rapidly clears gentamicin without rebound. If left untreated, long-term adverse sequellae for hearing or renal function were possible; hemodialysis may have altered these outcomes.

For more Human Toxicity Excerpts (Complete) data for Gentamicin (17 total), please visit the HSDB record page.

Drug-Induced Liver Injury Severity and Toxicity (DILIst)

Gentamicin

DILI Negative

Intramuscular; Intravenous

DOI:10.1016/j.drudis.2019.09.022

The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including gentamicin sulfate, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Gentamicin sulfate/

The Generic Animal Drug and Patent Restoration act requires that each sponsor of an approved animal drug must submit to the FDA certain information regarding patents held for the animal drug or its method of use. The Act requires that this information, as well as a list of all animal drug products approved for safety and effectiveness, be made available to the public. Gentamicin sulfate is included on this list. /Gentamicin sulfate/

Oral dosage form new animal drugs. Gentamicin sulfate oral solution. ... Indications for use. In weanling swine for control and treatment of colibacillosis caused by strains of Escherichia coli sensitive to gentamicin, and in swine for control and treatment of swine dysentery associated with Treponema hyodysenteriae. ... Limitations. Do not slaughter treated swine for food for at least 3 days following treatment. Federal law restricts this drug to use by or on the order of a licensed veterinarian. /Gentamicin sulfate/

Oral dosage form new animal drugs. Gentamicin sulfate pig pump oral solution. ... Indications for use. In neonatal swine 1 to 3 days of age for control and treatment of colibacillosis caused by strains of Escherichia coli sensitive to gentamicin. ... Limitations. For use in neonatal swine only. Do not slaughter treated swine for food for at least 14 days following treatment. /Gentamicin sulfate/

For more FDA Requirements (Complete) data for Gentamicin (11 total), please visit the HSDB record page.

J - Antiinfectives for systemic use

D - Dermatologicals

S - Sensory organs

S - Sensory organs

S - Sensory organs

QD - Dermatologicals

There are 3 key phases of aminoglycoside entry into cells. The first “ionic binding phase” occurs when polycationic aminoglycosides bind electrostatically to negatively charged components of bacterial cell membranes including with lipopolysaccharides and phospholipids within the outer membrane of Gram-negative bacteria and to teichoic acids and phospholipids within the cell membrane of Gram-positive bacteria. This binding results in displacement of divalent cations and increased membrane permeability, allowing for aminoglycoside entry. The second “energy-dependent phase I” of aminoglycoside entry into the cytoplasm relies on the proton-motive force and allows a limited amount of aminoglycoside access to its primary intracellular target - the bacterial 30S ribosome. This ultimately results in the mistranslation of proteins and disruption of the cytoplasmic membrane. Finally, in the “energy-dependent phase II” stage, concentration-dependent bacterial killing is observed. Aminoglycoside rapidly accumulates in the cell due to the damaged cytoplasmic membrane, and protein mistranslation and synthesis inhibition is amplified. The necessity of oxygen-dependent active transport explains why aminoglycosides are ineffective against anaerobic bacteria. Hence, aminoglycosides have both immediate bactericidal effects through membrane disruption and delayed bactericidal effects through impaired protein synthesis; observed experimental data and mathematical modeling support this two-mechanism model. Inhibition of protein synthesis is a key component of aminoglycoside efficacy. Structural and cell biological studies suggest that aminoglycosides bind to the 16S rRNA in helix 44 (h44), near the A site of the 30S ribosomal subunit, altering interactions between h44 and h45. This binding also displaces two important residues, A1492 and A1493, from h44, mimicking normal conformational changes that occur with successful codon-anticodon pairing in the A site. Overall, aminoglycoside binding has several negative effects including inhibition of translation, initiation, elongation, and ribosome recycling. Recent evidence suggests that the latter effect is due to a cryptic second binding site situated in h69 of the 23S rRNA of the 50S ribosomal subunit. Also, by stabilizing a conformation that mimics correct codon-anticodon pairing, aminoglycosides promote error-prone translation. Mistranslated proteins can incorporate into the cell membrane, inducing the damage discussed above.

Aminoglycosides are usually bactericidal in action. Although the exact mechanism of action has not been fully elucidated, the drugs appear to inhibit protein synthesis in susceptible bacteria by irreversibly binding to 30S ribosomal subunits. /Aminoglycosides/

... Aminoglycosides are aminocyclitols that kill bacteria by inhibiting protein synthesis as they bind to the 16S rRNA and by disrupting the integrity of bacterial cell membrane. Aminoglycoside resistance mechanisms include: (a) the deactivation of aminoglycosides by N-acetylation, adenylylation or O-phosphorylation, (b) the reduction of the intracellular concentration of aminoglycosides by changes in outer membrane permeability, decreased inner membrane transport, active efflux, and drug trapping, (c) the alteration of the 30S ribosomal subunit target by mutation, and (d) methylation of the aminoglycoside binding site. ... /Aminoglycosides/

One study assessing the pharmacokinetics of gentamicin in children and adults reported a mean half-life of 75 minutes after intravenous administration. The mean half-life associated with intramuscular administration was about 29 minutes longer. Fever and anemia may result in a shorter half-life although dose adjustments are not usually necessary. Severe burns are also associated with a shorter half-life and may result in lower gentamicin serum concentrations.

The plasma elimination half-life of gentamicin is usually 2-4 hours in adults with normal renal function and is reported to range from 24-60 hours in adults with severe renal impairment. The serum half-life of gentamicin averages 3-3.5 hours in infants 1 week to 6 months of age and 5.5 hours in full-term infants and large premature infants less than 1 week of age. In small premature infants, the plasma half-life is approximately 5 hours in those weighing over 2 kg, 8 hours in those weighing 1.5-2 kg, and 11.5 hours in those weighing less than 1.5 kg.

... terminal elimination half-lives of greater than 100 hours have been reported in adults with normal renal function following repeated IM or IV administration of the drug.

Gentamicin undergoes little to no metabolism.

Gentamicin is not metabolized. It is excreted by glomerular filtration in an active, unchanged form.

T6Z9V48IKG

GENTAMICIN

Established Pharmacologic Class [EPC] - Aminoglycoside Antibacterial

Chemical Structure [CS] - Aminoglycosides

Gentamicin is an Aminoglycoside Antibacterial.

GENTAMICIN

Compounds which inhibit the synthesis of proteins. They are usually ANTI-BACTERIAL AGENTS or toxins. Mechanism of the action of inhibition includes the interruption of peptide-chain elongation, the blocking the A site of ribosomes, the misreading of the genetic code or the prevention of the attachment of oligosaccharide side chains to glycoproteins.

Substances that inhibit the growth or reproduction of BACTERIA.

Gentamicin is excreted primarily by the kidneys. In patients with normal renal function, 70% or more of an initial gentamicin dose can be recovered in the urine within 24 hours. Excretion of gentamicin is significantly reduced in patients with renal impairment.

The renal clearance of gentamicin is comparable to individual creatinine clearance.

/MILK/ Gentamicin is distributed into milk following IM administration.

Gentamicin is distributed into cerebrospinal fluid (CSF) in low concentrations following IM or IV administration. CSF concentrations of gentamicin following intrathecal administration depend on the dose administered, the site of injection, the volume in which the dose is diluted, and the presence or absence of obstruction to CSF flow. There may be considerable interpatient variation in concentrations achieved. In one study, intrathecal administration of 4 mg of gentamicin resulted in CSF concentrations of the drug of 19-46 ug/mL for 8 hours and less than 3 ug/mL at 20 hours. Gentamicin crosses the placenta.

Following parenteral administration of usual dosages of gentamicin, the drug can be detected in lymph, subcutaneous tissue, lung, sputum, and bronchial, pleural, pericardial, synovial, ascitic, and peritoneal fluids. Concentrations in bile may be low, suggesting minimal biliary excretion. In patients with ventilator-associated pneumonia receiving IV gentamicin (240 mg once daily), drug concentrations in alveolar lining fluid were 32% of serum concentrations and averaged 4.24 ug/mL 2 hours after a dose. Only minimal concentrations of gentamicin are attained in ocular tissue following IM or IV administration.

Accumulation of gentamicin does not appear to occur in patients with normal renal function receiving 1-mg/kg doses every 8 hours for 7-10 days. However, accumulation may occur with higher doses and/or when the drug is given for prolonged periods, especially in patients with renal impairment.

For gentamycin (USEPA/OPP Pesticide Code: 006324) there are 0 labels match. /SRP: Not registered for current use in the U.S., but approved pesticide uses may change periodically and so federal, state and local authorities must be consulted for currently approved uses./

MEDICATION (VET)

MEDICATION

Anti-Bacterial Agents; Protein Synthesis Inhibitors

Use (kg; approx.) in Germany (2009): >250

Antibiotic complex produced by fermentation of Micromonospora purpurea or M. echinospora and variants thereof.

Recovered from a fermentation broth produced when submerged cultures of two subspecies of Micromonospora purpurea are grown in a yeast extract-cerelose medium.

Table: Gentamicin Sulfate Preparations [Table#4414]

Table: Gentamicin Sulfate in Sodium Chloride Preparations [Table#4415]

Animal Drugs -> FDA Approved Animal Drug Products (Green Book) -> Active Ingredients

Veterinary Drug -> ANTIMICROBIAL_AGENT -> JECFA Functional Classes

Veterinary Drug -> ANTIMICROBIAL_AGENT -> JECFA Functional Classes

Veterinary Drug -> ANTIMICROBIAL_AGENT -> JECFA Functional Classes

Veterinary Drug -> ANTIMICROBIAL_AGENT -> JECFA Functional Classes

Pharmaceuticals -> Animal Drugs -> Approved in Taiwan

Gentamicin or gentamicin sulfate, is a mixture of gentamicin C1 (25876-10-2), gentamicin C2 (25876-11-3), and gentamicin C1a (26098-04-4) isolated from Micromonospora purpurea and related species. Note that compounds obtained from Micromonospora species are given names ending in -micin; those isolated from Streptomyces end in -mycin.

Consists of 3 closely related components, gentamicins C1, C2, C1a, and also gentamicin a which differs from other members of complex but is similar to kanamycin C.