Trovafloxacin An official website of the United States government Here's how you know Log inAccess keysNCBI HomepageMyNCBI HomepageMain ContentMain NavigationBookshelfSearch databaseBooksAll DatabasesAssemblyBiocollectionsBioProjectBioSampleBooksClinVarConserved DomainsdbGaPdbVarGeneGenomeGEO DataSetsGEO ProfilesGTRHomoloGeneIdentical Protein GroupsMedGenMeSHNLM Levels and EffectsSummary of Use during LactationNo information is available on the clinical use of trovafloxacin during breastfeeding; however, amounts in breastmilk appear to be low. Fluoroquinolones have traditionally not been used in infants because of concern about adverse effects on the infants' developing joints. However, recent studies indicate little risk.[1,2] The calcium in milk might
Trovafloxacin attenuates neuroinflammation and improves outcome after traumatic brain injury in mice Trovafloxacin is a broad-spectrum antibiotic, recently identified as an inhibitor of pannexin-1 (Panx1) channels. Panx1 channels are important conduits for the adenosine triphosphate (ATP) release from live and dying cells that enhances the inflammatory response of immune cells. Elevated extracellular levels ATP released upon injury activate purinergic pathways in inflammatory cells that promote migration, proliferation, phagocytosis, and apoptotic signals. Here, we tested whether trovafloxacin administration attenuates the neuroinflammatory response and improves outcomes after brain trauma. The murine controlled cortical impact (CCI) model was used to determine whether in vivo delivery
Trovafloxacin acyl-glucuronide induces chemokine (C-X-C motif) ligand 2 in HepG2 cells Trovafloxacin is an antibiotic that was withdrawn from the market relatively soon after its release due to the risk of hepatotoxicity. Trovafloxacin is mainly metabolized to its acyl-glucuronide by uridine 5'-diphosphate (UDP)-glucuronosyltransferase (UGT) 1A1. In this study, we examined whether the acyl -glucuronide is involved in the development of hepatotoxicity. A UGT1A1-induced cell model was developed and the toxicity of trovafloxacin acyl-glucuronide was evaluated. The UGT1A1-induced cell model was developed by treating HepG2 cells with chrysin for 48 h. Chemokine (C-X-C motif) ligand 2, a cytokine involved in drug-induced liver injury, was uniquely induced by trovafloxacin in the UGT1A1-induced HepG2
Trovafloxacin Enhances Lipopolysaccharide-Stimulated Production of Tumor Necrosis Factor-α by Macrophages: Role of the DNA Damage Response Trovafloxacin (TVX) is a drug that has caused idiosyncratic, drug-induced liver injury (IDILI) in humans. In a murine model of IDILI, otherwise nontoxic doses of TVX and the inflammagen lipopolysaccharide (LPS) interacted to produce pronounced hepatocellular
Trovafloxacin Potentiation of Lipopolysaccharide-Induced Tumor Necrosis Factor Release from RAW 264.7 Cells Requires Extracellular Signal-Regulated Kinase and c-Jun N-Terminal Kinase Trovafloxacin (TVX) is a fluoroquinolone antibiotic known to cause idiosyncratic, drug-induced liver injury (IDILI) in humans. The mechanism underlying this toxicity remains unknown. Previously, an animal model
Molecular Mechanisms of Hepatocellular Apoptosis Induced by Trovafloxacin-Tumor Necrosis Factor-alpha Interaction Idiosyncratic drug-induced liver injury (IDILI) continues to be a significant human health problem. IDILI is characterized as occurring in a minority of individuals exposed to a drug, yet it accounts for as much as 17% of all cases of acute liver failure. Despite these concerns , the mechanisms underlying IDILI remain unknown. Trovafloxacin (TVX), which causes IDILI in humans, also causes hepatocellular death in vitro when combined with tumor necrosis factor-alpha (TNF) treatment. However, the molecular mechanisms involved in this toxicity are not fully characterized. The purpose of this study was to identify mechanisms by which TVX and TNF interact to cause hepatocellular death
Clinical evaluation of the tolerability and efficacy of trovafloxacin compared with sparfloxacin in the treatment of lower respiratory tract infections. To evaluate the clinical tolerability and efficacy of trovafloxacin compared with sparfloxacin in the treatment of lower respiratory tract infections. This was a randomised, double-blind, controlled, parallel study. 92 patients with lower respiratory tract infection were enrolled in three centres. 45 patients received trovafloxacin 200mg once daily orally for 10 days and 43 patients received sparfloxacin 400mg on the first day and 200mg once daily orally for 9 days. Clinical evaluation was performed for fever, dyspnoea, pulmonary symptoms, cough and sputum on days 1, 3, 6 and 12 of the study along with bacteriological evaluation on days 1
al.Clinical Nutrition 41 (2022) 468e488478CommentaryThe site of an enteral tube tip and therefore the site of drugdelivery is an important factor when establishing likely drug effi-cacy. For example, a study of trovafloxacin administered into thestomach yielded similar efficacy with or without simultaneousenteral formula, but administration through a tube directly into theduodenum rather than through a tube
and metastasis in lung and bladder cancer cells. Silencing this kinase, through either RNA interference or CRISPR, sensitized tumor cells to chemotherapy and hindered metastasis in vitro and in vivo in a tail vein injection model. Drug screening revealed several floxacin antibiotics as potent RSK4 activation inhibitors, and trovafloxacin reproduced all effects of RSK4 silencing in vitro and in/ex vivo using
that trovafloxacin was found in the breast milk of three lactating subjects. The average measurable breast milk concentration was 0.8 mcg/mL (range 0.3 to 2.1 mcg/mL) after a single intravenous alatrofloxacin dose equivalent to 300 mg of trovafloxacin. Further details on the study are not available.Infant Levels. Relevant published information was not found as of the revision date.Effects in Breastfed informationPubMedSimilar articles in PubMedReview Trovafloxacin.[Drugs and Lactation Database (...]Review Lomefloxacin.[Drugs and Lactation Database (...]Review Enoxacin.[Drugs and Lactation Database (...]Review Sparfloxacin.[Drugs and Lactation Database (...]Review Moxifloxacin.[Drugs and Lactation Database (...]See reviews...See all...Recent ActivityClearTurn OffAlatrofloxacin - Drugs and Lactation Database (LactMed®
, Olafsson JHM, Thorarinsson HM, Ryan RWP, Johnson RBM, Tilton RCP. Single Dose Azithromycin Treatment of Gonorrhea and Infections Caused by C. trachomatis and U. urealyticum in Men. Sexually Transmitted Diseases. 1994;21(1):43-6. 71. Bebear CM, Renaudin H, Charron A, Gruson D, Lefrancois M, Bebear C. In vitro activity of trovafloxacin compared to those of five antimicrobials against mycoplasmas including
that there was no statistical difference between fluoroquinolone and non-fluoroquinolone groups in terms of musculoskeletal adverse events in children (risk ratio = 1.145, 95% confidence interval = 0.974 - 1.345, P = .101). Subgroup analysis was performed using a random-effects model. Here, the effects on the trovafloxacin and levofloxacin groups were significantly different from that of the control group. However
activation is responsible for the secretion of ATP and UTP from apoptotic cells, which function as “find me” signals to recruit phagocytes to perform efferocytosis. In order to determine the role of PANX1 activation in the apoptotic secretome, prior to UV irradiation, PANX1 was inhibited in Jurkat cells using two methods: pharmacological inhibition with the drugs trovafloxacin (Trovan) or spironolactone