Disease relevance of CI 919

• Oral treatment of systemic Pseudomonas aeruginosa infection with enoxacin [1].
• Use of enoxacin in a patient with cystic fibrosis [2].
• The cleavage mechanisms of these structurally diverse compounds were analyzed by purifying and characterizing stable ternary complexes of enoxacin and CcdB protein with gyrase bound to a strong gyrase binding site from bacteriophage Mu [3].
• While the clinical efficacy of each agent must be considered in the light of risk of adverse events and potential drug interactions, ciprofloxacin, enoxacin, ofloxacin, and temafloxacin appear to be most useful for cutaneous bacterial infections [4].
• Signs of central nervous system toxicity caused by temafloxacin were absent in two rodent studies, during which clonic convulsions were induced by concomitant use of fenbufen plus enoxacin or ciprofloxacin, and in human subjects evaluated by positron emission tomography [5].

Psychiatry related information on CI 919

• At doses of 30, 100, and 300 mg/kg p.o., temafloxacin HCl and enoxacin had no effect on locomotor activity of rats, but oxolinic acid markedly stimulated locomotor activity [6].

High impact information on CI 919

• Incubation of Mu DNA with gyrase and enoxacin revealed a cleavage site 18.1 kilobases from the left end of the 37.2-kilobase genome [7].
• 1) Enoxacin binds to the DNA active site and alters the breakage/reunion activity of the enzyme [3].
• In comparative studies, lomefloxacin, a new difluorinated quinolone, exhibits broad antibacterial activity in vitro, similar or superior to that of other quinolones (enoxacin, ofloxacin, pipemidic acid, nalidixic acid, and norfloxacin) but less than that of ciprofloxacin [8].
• A positive correlation exists between the doses of enoxacin or ciprofloxacin and the prolongation (increases) in the caffeine elimination half-life [9].
• METHODS: A randomized 3-period change-over study was conducted in 12 healthy young volunteers on the steady-state interactions between pefloxacin or enoxacin (400 mg twice a day) with caffeine (183 mg once daily), a validated marker of CYP1A2 [10].

Chemical compound and disease context of CI 919

• Comparative evaluation of ciprofloxacin, enoxacin, and ofloxacin in experimental Pseudomonas aeruginosa pneumonia [11].
• The MICs of QA-241 for 90% of staphylococci, Enterococcus faecalis isolates, and streptococcal species ranged from 1.56 to 6.25 micrograms/ml, and the activity of QA-241 was similar to those of norfloxacin and enoxacin but two to four times less potent than those of ofloxacin and ciprofloxacin [12].
• Pefloxacin, in contrast, caused azoospermia and testicular damage in dogs, and enoxacin caused testicular atrophy in rats and reduced spermatogenesis in dogs [13].
• Proposed criteria for interpretation of susceptibilities of strains of Neisseria gonorrhoeae to ciprofloxacin, ofloxacin, enoxacin, lomefloxacin, and norfloxacin [14].
• Thus, eae-positive, necrotoxigenic, and verotoxigenic (except for nalidixic acid) E. coli strains were significantly more sensitive to nalidixic acid, enoxacin, and enrofloxacin than nonfimbriated, nontoxigenic, eae-negative strains [15].

Biological context of CI 919

• Ranitidine pretreatment reduced enoxacin oral bioavailability by an average of 26% [16].
• Pharmacokinetics of enoxacin and its oxometabolite following intravenous administration to patients with different degrees of renal impairment [17].
• In conclusion, our study revealed considerable differences in the distribution kinetics of enoxacin among various excretory sites [18].
• Pyridonecarboxylic acids as antibacterial agents. 2. Synthesis and structure-activity relationships of 1,6,7-trisubstituted 1,4-dihydro-4-oxo-1,8-naphthyridine-3-carboxylic acids, including enoxacin, a new antibacterial agent [19].
• The substituent at position 8 was found to determine the molecular conformations of the fluoroquinolones, and the planarity in molecular shape decreased in the same order as the inhibitory activity (enoxacin > 8-Hy > 8-F1) [20].

Anatomical context of CI 919

• Tissue penetration and clinical efficacy of enoxacin in urinary tract infections [21].
• The mean ratios of enoxacin concentrations in sputum to those in serum at various time intervals for all groups were as follows: at 2 h, 0.55 +/- 0.34; at 5 h, 1.04 +/- 0.72; at 9 h, 0.97 +/- 0.62 [22].
• Structure-related inhibitory effect of antimicrobial enoxacin and derivatives on theophylline metabolism by rat liver microsomes [20].
• The uptake of [3H]thymidine into DNA (trichloroacetic acid precipitable) was significantly increased in phytohemagglutinin-stimulated human lymphocytes when they were exposed to eight new 4-quinolone derivatives, ciprofloxacin, norfloxacin, ofloxacin, A-56619, A-56620, amifloxacin, enoxacin, and pefloxacin, at 1.6 to 6.25 micrograms/ml for 5 days [23].
• The evaluation of the clinical activity of enoxacin is still relatively new, but published studies reveal a good deal of potential in the treatment of infections caused by susceptible bacteria in the urinary tract, upper and lower respiratory tracts, bones and joints, and the gastrointestinal tract [24].

Associations of CI 919 with other chemical compounds

• Ciprofloxacin and enoxacin showed the strongest inhibitory effects in vitro, whereas ofloxacin had the lowest inhibitory effect [9].
• The pharmacokinetic profile of enoxacin is similar to that of ofloxacin, achieving higher plasma and tissue concentrations and possessing a longer half-life than norfloxacin or ciprofloxacin [25].
• Difloxacin significantly reduced bacterial counts of vegetations compared with enoxacin [26].
• Strains with enzymatic resistance to amikacin were more resistant to beta-lactams (except enoxacin and imipenem) than were strains with decreased permeability [27].
• Difloxacin significantly reduced bacterial counts of vegetations, as compared with enoxacin and cefoperazone [28].

Gene context of CI 919

• Enoxacin, even at subminimal inhibitory concentrations, induces the bacterial SOS system, even in partially resistant gyrA strains [29].
• Following the use of norfloxacin, enoxacin, and ofloxacin, the MIC90s of norfloxacin, ofloxacin, and ciprofloxacin against 46 isolates of MRSA collected during 1989-1990 increased to 64, 16, and 32 micrograms/ml, respectively, and the rates of resistant strains to these three agents were 37.0%, 30.4%, and 34.8%, respectively [30].
• The inducing compounds of the SOS genes, such as bleomycin, captan, ciprofloxacin, enoxacin, hydroxyurea, N-methyl-N'-nitro-N-nitrosoguanidine, mitomycin C, nalidixic acid, ofloxacin and hexavalent chromium compounds also trigger the expression of the nrdA gene [31].
• Using these strains, we have found that, like nalidixic acid, ofloxacin, enoxacin and ciprofloxacin are strong inducers of the SOS genes tested, umuC gene expression being the highest [32].
• Moreover, eae-positive strains were significantly more sensitive to enoxacin and enrofloxacin than F5-positive strains [15].

Analytical, diagnostic and therapeutic context of CI 919

• Blood specimens collected over 24 hours after the final dose of enoxacin and urine collected during the 12-hour dose interval after the final dose were assayed for enoxacin by HPLC [33].
• In a four-subject, four-way crossover study enoxacin was administered every 12 hours at four levels (0, 25, 100, and 400 mg) for 14 doses [34].
• In a multicentre, open, non-comparative trial, clinical cure or improvement in skin or skin structure infections was achieved after oral administration of enoxacin 200 to 600 mg twice daily in 88% of 196 evaluable patients [35].
• Enoxacin concentrations were measured in serum and bone (cortical and cancellous) by high-pressure liquid chromatography [36].
• Enoxacin treatment for 3 or 5 days and vancomycin treatment for 5 days significantly reduced bacterial counts of vegetations compared with those in untreated control rabbits after 1 day of infection [37].

References