Interactions
Like other fluoroquinolones, delafloxacin chelates metals including aluminum, magnesium, sucralfate, iron, zinc, and divalent and trivalent cations like didanosine; using this drugs with antacids, some dietary supplements, or drugs buffered with any of these ions will interfere with available amounts of delafloxacin. Pharmacology
The half-life varies in around 8 hours at normal doses. Excretion is 65% through urine, mostly in unmetabolized form, and 28% via feces. Clearance is reduced in people with severe kidney disease.Delafloxacin is more active (lower MIC90) than other quinolones against Gram-positive bacteria such as methicillin-resistant Staphylococcus aureus (MRSA). In contrast to most approved fluoroquinolones, which are zwitterionic, delafloxacin has an anionic character, which results in a 10-fold increase in delafloxacin accumulation in both bacteria and cells at acidic pH. This property is believed to confer to delafloxacin an advantage for the eradication of Staphylococcus aureus in acidic environments, including intracellular infections and biofilms. Chemistry
The chemical name is 1-deoxy-1 (methylamino)-D-glucitol, 1-(6-amino-3,5-difluoropyridin-2-yl)-8-chloro-6-fluoro-7-(3-hydroxyazetidin-1-yl)-4-oxo-1,4-dihydroquinoline-3-carboxylate (salt).The injectable form of delafloxacin is sold as the meglumine salt of the active ingredient and its United States Adopted Name, delafloxacin meglumine, reflects that; the injection formulation also includes EDTA and sulfobutylether-β-cyclodextrin. The tablet is made of delafloxacin, citric acid anhydrous, crospovidone, magnesium stearate, microcrystalline cellulose, povidone, sodium bicarbonate, and sodium phosphate monobasic monohydrate. History
Delafloxacin was known as ABT-492, RX-3341, and WQ-3034 while it was under development.Rib-X Pharmaceuticals acquired delafloxacin from Wakunaga Pharmaceutical in 2006. Rib-X was renamed to Melinta Therapeutics in 2013.
Sialuria is a group of disorders resulting in an accumulation of free sialic acid. One type, known as the Finnish type or Salla disease has been described in northeastern Finland and is due to a mutation in gene SLC17A5 on chromosome 6q4-15. The "French type sialuria" (Online Mendelian Inheritance in Man (OMIM): 269921), is a very rare condition presenting in infancy with failure to thrive, yellowish skin, large liver, low blood count, recurrent chest infections, bowel upsets, dehydration and characteristic facial features. References


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