Disease relevance of rokitamycin

• Flow cytometric assessment of susceptibilities of Streptococcus pyogenes to erythromycin and rokitamycin [1].
• In vitro activity of rokitamycin, a new macrolide, against Borrelia burgdorferi [2].
• Effects of rokitamycin and other macrolide antibiotics on Mycoplasma pneumoniae in L cells [3].
• In vitro susceptibility of Campylobacter jejuni to rokitamycin [4].
• Inactivation of the macrolide antibiotics erythromycin, midecamycin, and rokitamycin by pathogenic Nocardia species [5].

High impact information on rokitamycin

• The present study demonstrates the in vitro effectiveness of the macrolide rokitamycin and the phenothiazine compound chlorpromazine against Acanthamoeba castellanii [6].
• In general, 14-membered macrolides such as erythromycin, clarithromycin, and flurithromycin were more active against streptococci and Bordetella pertussis than was the 15-membered macrolide azithromycin, which was more active than 16-membered macrolides such as miocamycin and rokitamycin [7].
• Bactericidal activity of levofloxacin, gatifloxacin, penicillin, meropenem and rokitamycin against Bacillus anthracis clinical isolates [8].
• Isolates with non-inducible resistance (those with only the mefE gene) had an intermediate level of resistance to 14-membered macrolides, and were susceptible to rokitamycin, a 16-membered macrolide [9].
• However, whether rokitamycin would inhibit the CYP3A-mediated drug metabolism in vivo requires further investigations in patients [10].

Chemical compound and disease context of rokitamycin

• The effects of rokitamycin, a macrolide antibiotic, on the binding of bilirubin to albumin were examined in vitro using blood plasma from young rats with hyperbilirubinemia, bilirubin-supplemented serum separated from human cord blood, and the human serum from a newborn infant with icterus gravis neonatorum [11].

Biological context of rokitamycin

• An in vitro study on the metabolism and possible drug interactions of rokitamycin, a macrolide antibiotic, using human liver microsomes [10].
• However, rokitamycin, LMA7, erythromycin, and clarithromycin inhibited the CYP3A4-catalyzed triazolam alpha-hydroxylation with IC50 (Ki) values of 5.8 (2.0), 40, 33 (20), and 56 (43) microM, respectively [10].
• They also indicated that, as the PAEs of rokitamycin on the M phenotype and inducible resistant strains were comparable with those on susceptible strains, no re-evaluation of therapeutic dosing regimens was required [12].
• Effects of rokitamycin on phagocytosis and release of oxidant radicals of human polymorphonuclear leukocytes [13].
• The drug bound reversibly, not cohesively, to the ribosomes from both strains S704 and 8325MMT7, confirming our earlier hypothesis that rokitamycin can cause bacteriostasis or cell death depending upon whether it binds reversibly or cohesively to the ribosomes of a given strain [14].

Anatomical context of rokitamycin

• Phagocytosis and intracellular killing of rokitamycin-exposed staphylococci by human polymorphonuclear leukocytes [15].
• Implication of cohesive binding of a macrolide antibiotic, rokitamycin, to ribosomes from Staphylococcus aureus [14].
• Rokitamycin uptake by alveolar macrophages [16].

Associations of rokitamycin with other chemical compounds

• In vitro evaluation of the effectiveness of the macrolide rokitamycin and chlorpromazine against Acanthamoeba castellanii [6].
• Sensitive determination of josamycin and rokitamycin in plasma by high-performance liquid chromatography with fluorescence detection [17].
• X-ray crystallographies of leucomycin A5 and rokitamycin monomethylacetal [18].
• EM and AZM, both of which have been shown to be clinically effective in the treatment of Diffuse panbronchiolitis (DPB), significantly suppressed active oxygen generation and chemotaxis of neutrophils at low concentrations equivalent to therapeutic doses (0.5 approximately 1.0 microgram/ml, p < 0.05), whereas the clinically ineffective RKM did not [19].

Gene context of rokitamycin

• Although in this in-vitro animal study CYP3A activity was barely inhibited by rokitamycin, the possibility cannot be totally discounted in man when rokitamycin is co-administered with drugs metabolized by CYP3A [20].

Analytical, diagnostic and therapeutic context of rokitamycin

• Although she was treated with 35 mg/kg/day rokitamycin, TWAR was repeatedly isolated after treatment [21].
• Morphological changes in H. pylori induced by rokitamycin incubation at these MICs and times were also investigated by scanning electron microscopy [22].
• Detection of rokitamycin-induced morphostructural alterations in Helicobacter pylori by atomic force microscopy [23].
• The pharmacokinetics of rokitamycin tablets were studied in 12 healthy volunteers in a randomized cross-over design [24].

References