Current research is underway to understand the biosynthesis of this antibiotic in an attempt to increase expression and force secretion of gentamicin for higher titer.

[13] Gentamicin is active against a wide range of bacterial infections, mostly Gram-negative bacteria including Pseudomonas, Proteus, Escherichia coli, Klebsiella pneumoniae, Enterobacter aerogenes, Serratia, and the Gram-positive Staphylococcus.

[16] Gentamicin is not used for Neisseria meningitidis or Legionella pneumophila bacterial infections (because of the risk of the person going into shock from lipid A endotoxin found in certain Gram-negative organisms).

[15] In the elderly, renal function should be assessed before beginning therapy as well as during treatment due to a decline in glomerular filtration rate.

[14] The risk of nephrotoxicity can be affected by the dose, frequency, duration of therapy, and concurrent use of certain medications, such as NSAIDs, diuretics, cisplatin, ciclosporin, cephalosporins, amphotericin, iodide contrast media, and vancomycin.

[22] The common symptoms of inner ear damage include tinnitus, hearing loss, vertigo, trouble with coordination, and dizziness.

[14] Factors that increase the risk of inner ear damage include:[14][15] Gentamicin is a bactericidal antibiotic that works by binding the 30S subunit of the bacterial ribosome, negatively impacting protein synthesis.

[25] However, when gentamicin binds at helix 44 of the 16S rRNA, it forces the adenosines to maintain the position they take when there is a correct, or cognate, match between aa-tRNA and mRNA.

[26] This leads to the acceptance of incorrect aa-tRNAs, causing the ribosome to synthesize proteins with wrong amino acids placed throughout (roughly every 1 in 500).

Moreover, it has been observed that gentamicin can cause a substantial slowdown in the overall elongation rate of peptide chains in live bacterial cells, independent of the misincorporation of amino acids.

[28] This finding indicates that gentamicin not only induces errors in protein synthesis but also broadly hampers the efficiency of the translation process itself.

Because of this lot-to-lot variability, it can be difficult to study various properties of gentamicin including pharmacokinetics and microorganism susceptibility if there is an unknown combination of chemically related but different compounds.

[34][33][35][40][41] Literature also agrees with the gentamicin biosynthesis pathway starting with D-Glucose-6-phosphate being dephopsphorylated, transaminated, dehydrogenated and finally glycosylated with D-glucosamine to generate paromamine inside Micromonospora echinospora.

[42][45][32][46] When X2 bypasses GenK and is directly dehydrogenated and aminated by the GenQ enzyme, the other pharmacologically relevant intermediate JI-20A is formed.

[32] The main components of the growth medium are carbon sources, mainly sugars, but several studies found increased gentamicin production by adding vegetable and fish oils and decreased gentamicin production with the addition of glucose, xylose and several carboxylic acids.

[32][35] Phosphate ions, metal ions (cobalt and a few others at low concentration), various vitamins (mostly B vitamins), purine and pyrimidine bases are also supplemented into the growth medium to increase gentamicin production, but the margin of increase is dependent on the species of Micromonospora and the other components in the growth medium.

[32][35] A range of pH from 6.8 to 7.5 is used for gentamicin biosynthesis and the aeration is determined by independent experimentation reliant on type of growth medium and species of Micromonospora.

It was discovered in 1963 by Weinstein, Wagman et al. at Schering Corporation in Bloomfield, N.J. while working with source material (soil samples) provided by Rico Woyciesjes.

[citation needed] It is synthesized by Micromonospora, a genus of Gram-positive bacteria widely present in the environment (water and soil).

According to the American Medical Association Committee on Generic Names, antibiotics not produced by Streptomyces should not use y in the ending of the name, and to highlight their specific biological origins, gentamicin and other related antibiotics produced by this genus (verdamicin, mutamicin, sisomicin, netilmicin, and retymicin) have their spellings ending in ~micin and not in ~mycin.

Gentamicin is one of the few heat-stable antibiotics that remain active even after autoclaving, which makes it particularly useful in the preparation of some microbiological growth media.