(2R,3R,4S,5S,6R)-4-Amino-2-[(1S,2S,3R,4S,6R)-4,6-diamino-3-[(2R,3R,6S)-3-amino-6-(aminomethyl)oxan-2-yl]oxy-2-hydroxy-cyclohexyl]oxy-6-(hydroxymethyl)oxane-3,5-diol

Dibekacin was synthesized in 1967 by Umezawa et al. by the removal of the 3 - and 4 -hydroxyl groups of kanamycin B. Studies by the same workers on the mechanisms of bacterial resistance to kanamycin-group antibiotics preceded the discovery. Dibekacin shows excellent activity, as expected, against a variety of bacteria, including kanamycin-resistant strains. It shows higher activity than kanamycin against Pseudomonas aeruginosa, Proteus, and other pathogens.

Dideoxykanamycin B is an antibacterial compound.

ChEBI: A kanamycin that is kanamycin B lacking the 3- and 4-hydroxy groups on the 2,6-diaminosugar ring.

3′,4′-Dideoxy kanamycin B. A semisynthetic aminoglycoside closely related to the natural compound tobramycin (3′-deoxy kanamycin B). Supplied as the sulfate.
It is active against staphylococci including methicillinresistant strains, a wide range of enterobacteria, Acinetobacter and Pseudomonas spp. It is also active against M. tuberculosis and the M. avium complex (MICs 4–16 mg/L). It exhibits the usual aminoglycoside properties of bactericidal activity at concentrations close to the MIC and bactericidal synergy with selected β-lactam antibiotics.
Absence of hydroxyl groups present in the parent kanamycin B renders dibekacin resistant to phosphorylation by APH(3′). It is also resistant to some forms of ANT(4′). However, the type of this enzyme, ANT(4′), found in some Gram-positive organisms modifies dibekacin at the 2″-hydroxyl group; nevertheless dibekacin has much greater activity than tobramycin against organisms that produce the enzyme.
A 1 mg/kg intravenous bolus dose achieves a peak plasma concentration of around 5 mg/L. The plasma half-life is 2.3 h. Protein binding is 3–12%. It is eliminated principally by the renal route, 75–80% of the dose appearing in the urine in the first 24 h. Elimination is inversely related to renal function. In patients maintained on chronic hemodialysis, the half-life rises to 54 h between dialyses and falls to 6–7 h on dialysis.
Toxic effects are those typical of aminoglycosides with a frequency similar to or less than those of gentamicin.
It is used for severe infections caused by susceptible microorganisms, especially those resistant to established aminoglycosides, but availability is limited.

Poison by intraperitoneal, subcutaneous, intramuscular, and intravenous routes. Moderately toxic by ingestion. Experimental teratogenic and reproductive effects. An antibacterial agent. When heated to decomposition it emits toxic fumes of NOx.