Last update 21 Nov 2024

Lomefloxacin Hydrochloride

Last update 21 Nov 2024

Overview

R&D Status

Clinical Result

Translational Medicine

Overview

Basic Info

Drug Type

Small molecule drug

Synonyms

(±)-1-ethyl-6,8-difluoro-1,4-dihydro-7-(3-methyl-1-piperazinyl)-4-oxo-3-quinolinecarboxylic acid, 1,4-Dihydro-6,8-difluoro-1-ethyl-7-(3-methyl-1-piperazinyl)-4-oxo-3-quinolinecarboxylic acid, LFLX

+ [64]

Target

Bacterial DNA gyrase x Top II

Mechanism

Bacterial DNA gyrase inhibitors, Top II inhibitors(Topoisomerase II inhibitors)

Therapeutic Areas

Infectious DiseasesEye DiseasesRespiratory Diseases+ [1]

Active Indication

BlepharitisCorneal UlcerDacryocystitis+ [6]

Inactive Indication-

Originator Organization

Pfizer Inc.

Active Organization

Novartis Ophthalmics, Inc.Senju Pharmaceutical Co., Ltd.

Pfizer Inc.

+ [1]

Inactive Organization

Pharmacia Corp.

Drug Highest PhaseApproved

First Approval Date

(01 Jan 1989),

Bacterial InfectionsBronchitisSurgical Wound Infection+ [1]

Regulation-

Structure

Molecular FormulaC17H20ClF2N3O3

InChIKeyKXEBLAPZMOQCKO-UHFFFAOYSA-N

CAS Registry98079-52-8

View All Structures (2)

100 Clinical Results associated with Lomefloxacin Hydrochloride

100 Translational Medicine associated with Lomefloxacin Hydrochloride

100 Patents (Medical) associated with Lomefloxacin Hydrochloride

1,019

Literatures (Medical) associated with Lomefloxacin Hydrochloride

01 Dec 2024·Environmental Pollution

Toxicological mechanisms and molecular impacts of tire particles and antibiotics on zebrafish

Article

Author: Fenech, Adam ; Ding, Xiaowen ; Wen, Jingya ; Gao, Jiaxuan ; Li, Tong ; Li, Yu ; Pu, Qikun ; Liu, Yajing

Tire microplastics (TMPs) and antibiotics are emerging pollutants that widely exist in water environments. The coexistence of these pollutants poses severe threats to aquatic organisms. However, the toxicity characteristics and key molecular factors of the combined exposure to TMPs in aquatic organisms remain unknown. Therefore, the joint toxicity of styrene-butadiene rubber TMPs (SBR-TMPs) and 32 antibiotics (macrolides, fluoroquinolones, β-lactams, sulfonamides, tetracyclines, nitroimidazoles, highly toxic antibiotics, high-content antibiotics, and common antibiotics) in zebrafish was investigated using a full factorial design, molecular docking, and molecular dynamics simulation. Sixty-four combinations of antibiotics were designed to investigate the hepatotoxicity of the coexistence of SBR-TMPs additives and antibiotics in zebrafish. Results indicated that low-order effects of antibiotics (e.g., enoxacin-lomefloxacin and ofloxacin-enoxacin-lomefloxacin) had relatively notable toxicity. The van der Waals interaction between additives and zebrafish cytochrome P450 enzymes primarily affected zebrafish hepatotoxicity. Zebrafish hepatotoxicity was also affected by the ability of SBR-TMPs to adsorb antibiotics, the relation between antibiotics, the affinity of antibiotics docking to zebrafish cytochrome P450 enzymes, electronegativity, atomic mass, and the hydrophobicity of the antibiotic molecules. This study aimed to eliminate the joint toxicity of TMPs and antibiotics and provide more environmentally friendly instructions for using different chemicals.

01 Dec 2024·Bioresource Technology

Quinolone antibiotics stimulate bacterial mercury methylation by Geobacter metallireducens GS-15

Article

Author: Ding, Lingyun ; Zhang, Lijuan ; Huang, Zhishan ; He, Ningning ; Hung Wong, Ming ; Pi, Bin ; Xu, Nan ; Zhang, Lele ; Tao, Huchun ; Zhang, Yaoyu ; Fang, Fang

Bacterial mercury (Hg) methylation is critical for bioremediating Hg pollution, but the impact of emerging antibiotics on this process has rarely been reported. This study innovatively investigated the interactions between Hg-methylating bacteria of Geobacter metallireducens GS-15 and two quinolone antibiotics: lomefloxacin (LOM) and ciprofloxacin (CIP) at 5 μg/L. Short-term LOM exposure increased methylmercury (MeHg) yield by 36 % compared to antibiotic-free conditions, caused by hormesis to alter bioactivities of single GS-15 cells. Long-term CIP exposure led to more antibiotic resistance and mercury tolerance in GS-15 cells, doubling MeHg productivity and significantly increasing expression of Hg methylation (hgcA by 95 folds) and antibiotic resistance (gyrA by 54 folds) genes, while mercury resistance gene merA only increased by 2.5 folds than without selective pressure. These results suggest quinolone antibiotics at environmentally contaminated concentrations stimulate bacterial Hg methylation to form highly toxic MeHg, raising considerable concern for the Hg-antibiotic complex in contaminated environments.

01 Nov 2024·Archives of Biochemistry and Biophysics

Aldose reductase with quinolone antibiotics interaction: In vitro and in silico approach of its relationship with diabetic complications

Article

Author: Türkeş, Cüneyt

Aldose reductase (AR, EC1.1.1.21), a member of the aldo-keto reductase family, is critically implicated in the pathogenesis of chronic complications associated with diabetes mellitus, including neuropathy, nephropathy, and retinopathy. Hyperglycemia-induced AR overactivity results in intracellular sorbitol accumulation, NADPH depletion, and oxidative stress. Consequently, AR is recognized as a key mediator of oxidative and inflammatory signaling pathways involved in diverse human pathologies such as cardiovascular diseases, inflammatory disorders, and cancer. This has sparked renewed interest in developing novel AR inhibitors (ARIs) with enhanced therapeutic profiles. In this study, we evaluated the inhibitory potential of five quinolone antibiotics-gatifloxacin, lomefloxacin, nalidixic acid, norfloxacin, and sparfloxacin-as ARIs relevant to various physiological and pathological conditions. Through comprehensive in vitro and in silico analyses, we explored these antibiotics' binding interactions and affinities within the AR active site. Our findings reveal that these quinolones moderately inhibit AR at micromolar concentrations, with inhibition constants (K_Is) ranging from 1.03 ± 0.13 μM to 4.12 ± 0.51 μM, compared to the reference drug epalrestat (K_I of 0.85 ± 0.06 μM). The combined in vitro and in silico results underscore significant interactions between these drugs and AR, suggesting their potential as therapeutic agents against the aforementioned pathological conditions. Furthermore, these insights will aid in optimizing clinical dosing regimens and mitigating unexpected drug-drug interactions when these antibiotics are co-administered with other treatments.

100 Deals associated with Lomefloxacin Hydrochloride

External Link

KEGG	Wiki	ATC	Drug Bank
D00873	Lomefloxacin Hydrochloride	J01MA07 S01AE04	DB00978

R&D Status

10 top approved records.

to view more data

Indication	Country/Location	Organization	Date
Blepharitis	JP	Senju Pharmaceutical Co., Ltd.	10 Sep 2007
Corneal Ulcer	JP	Senju Pharmaceutical Co., Ltd.	10 Sep 2007
Dacryocystitis	JP	Senju Pharmaceutical Co., Ltd.	10 Sep 2007
Hordeolum	JP	Senju Pharmaceutical Co., Ltd.	10 Sep 2007
Conjunctivitis	BR	Novartis Ophthalmics, Inc.	21 Nov 1999
Conjunctivitis	GB	Novartis Ophthalmics, Inc.	21 Nov 1999
Bacterial Infections	-	Pfizer Inc.	01 Jan 1989
Bronchitis	-	Pfizer Inc.	01 Jan 1989
Surgical Wound Infection	-	Pfizer Inc.	01 Jan 1989
Urinary Tract Infections	-	Pfizer Inc.	01 Jan 1989

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


ARVO2002	Not Applicable	-	-	Levofloxacin 0.5%	(isnhtnqiza) = idmpirzvep oubvkucvir (ssdaivrzqv, 3.53)	-	01 Dec 2002
				Norfloxacin 0.3%	(isnhtnqiza) = sgzzdpbmpa oubvkucvir (ssdaivrzqv, 1.18)

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Lomefloxacin Hydrochloride

Overview

Basic Info

Structure

Related

External Link

R&D Status

Clinical Result

Translational Medicine

Deal

Core Patent

Clinical Trial

Approval

Regulation