Enoxacin (Sesquihydrate) is a new quinolone carboxylic acid compound. It inhibited 90% Escherichia coli, Klebsiella sp., Aeromonas sp., Enterobacter spp., Serratia spp., Proteus mirabilis, and Morganella morganii at less than or equal to 0.8 micrograms/ml. Enoxacin inhibited organisms resistant to cefotaxime, moxalactam, gentamicin, and piperacillin[3]. It has a broad spectrum of in vitro antibacterial activity, and is particularly potent against Gram-negative organisms and staphylococci. Significantly (p less than 0.01) more clinical and/or bacteriological cures were effected by enoxacin than pipemidic acid in acute cystitis and complicated urinary tract infection[4]. Enoxacin and bis-enoxacin trigger the release of EVs (Extracellular vesicles) from 4T1 cancer cells that inhibit osteoclastogenesis[5]. UVA (ultraviolet A) irradiation activates enoxacin, after which activated enoxacin induces apoptosis of AsPC1 cells through generation of reactive oxygen species[6].
Enoxacin Sesquihydrate/依诺沙星 倍半水合物 细胞实验
Cell Line
Concentration
Treated Time
Description
References
C2C12 myotubes
100 μM
During differentiation
Upregulated Ppargc1a and oxidative metabolism-related genes, increased maximum mitochondrial respiration and proton leak
Sci Adv. 2020 Dec 2;6(49):eabc6250
Human adipose-derived stem cells (hASC)
50 μM
10 days after differentiation
Increased UCP1 and PPARGC1A mRNA levels
Sci Adv. 2020 Dec 2;6(49):eabc6250
Mouse brown preadipocytes (9B)
50 μM
During differentiation
Increased Elovl3 expression but did not affect Ucp1 and Ppargc1a
Sci Adv. 2020 Dec 2;6(49):eabc6250
Mouse subcutaneous preadipocytes (9W)
50 μM
During differentiation (days 2 to 8)
Promoted expression of brown/beige adipocyte markers (Ucp1, Dio2, Prdm16, Ppargc1a)
Sci Adv. 2020 Dec 2;6(49):eabc6250
human neural progenitor cells (hNPCs)
100 µM
48 hours
To evaluate the inhibitory effect of Enoxacin on ZIKV infection, results showed that Enoxacin significantly inhibited ZIKV replication in hNPCs
Cell Res. 2019 Apr;29(4):265-273
HCT-116 cells
40 μg/mL (124 μM)
Enoxacin showed dose-dependent growth inhibition in HCT-116 cells
Redox Biol. 2018 Sep;18:84-92
NSC-34 cells
100 μM
72 hours
To test whether enoxacin could reverse the negative effect of ALS-causing mutant proteins on miRNA processing. Results showed that enoxacin partially ameliorated the impairments in pre-miRNA processing induced by ALS-causing mutants FUS R495X, TDP-43 A315T, or SOD1 G93A.
EMBO J. 2015 Nov 3;34(21):2633-51
SW1736 cells
40 µg/mL
5 days
Enoxacin significantly inhibited proliferation, migration, and invasion in SW1736 cells, and decreased the expression of EMT markers.
Oncogene. 2019 Jul;38(27):5486-5499
TPC1 cells
40 µg/mL
5 days
Enoxacin significantly inhibited proliferation, migration, and invasion in TPC1 cells, and decreased the expression of EMT markers.
Oncogene. 2019 Jul;38(27):5486-5499
Cal62 cells
40 µg/mL
5 days
Enoxacin significantly inhibited proliferation, migration, and invasion in Cal62 cells, and decreased the expression of EMT markers.
Oncogene. 2019 Jul;38(27):5486-5499
Human primary lung epithelial cells
200 μM
48 hours
Enoxacin reduced the expression of squamous differentiation markers induced by Doxorubicin
Cell Death Discov. 2023 Jan 21;9(1):21
Human primary lung epithelial cells
200 μM
24 hours
Enoxacin attenuated DNA damage and squamous differentiation response induced by Doxorubicin by enhancing DNA repair
Cell Death Discov. 2023 Jan 21;9(1):21
Enoxacin Sesquihydrate/依诺沙星 倍半水合物 动物实验
Species
Animal Model
Administration
Dosage
Frequency
Description
References
Mice (C57BL/6)
High-fat diet-induced obesity model
Intraperitoneal injection
10 mg/kg body weight/day
5 times/week for 10 weeks
Mitigated obesity, increased energy expenditure, improved glucose tolerance and insulin sensitivity, promoted BAT activation and beige adipogenesis
Sci Adv. 2020 Dec 2;6(49):eabc6250
Caenorhabditis elegans (C. elegans)
Wild-type N2 Bristol and other mutants
Added to NGM medium
100 μg/mL
Continuous administration starting from day 0 of adulthood
Enoxacin extended the lifespan of C. elegans and promoted survival under normal and oxidative stress conditions, achieved by inhibiting miR-34-5p and promoting mitohormesis.
Redox Biol. 2018 Sep;18:84-92
Mice
SOD1 G93A ALS mouse model
Oral
800 mg/kg bodyweight/day
Once daily, starting from day 42
To test whether enoxacin has a beneficial effect on neuromuscular function in the SOD1 G93A mouse model of ALS. Results showed that the enoxacin-treated group had a ~7-day delay in the onset of neurological symptoms, weight peak, and onset of weight decline compared to the control group. The neurological score was superior in the enoxacin-treated cohort, and performance was better in rotarod tests and gait analysis.
EMBO J. 2015 Nov 3;34(21):2633-51
Mice
Orthotopic mouse model of human thyroid cancer
Intraperitoneal injection
15 mg/kg
Daily over 28 days
Enoxacin significantly diminished tumor growth, upregulated the expression of critical miRNAs in tumors, and downregulated the EMT markers fibronectin and N-cadherin and the proliferation marker PCNA.
Oncogene. 2019 Jul;38(27):5486-5499
Female C57BL/6 mice
DHEA-induced PCOS mouse model
Intraperitoneal injection
100 mg/kg/day
Once daily for 3 weeks
Enoxacin ameliorated reproductive endocrine disorder, glucose intolerance, and ovarian dysfunction in DHEA-induced PCOS mice. By promoting white fat browning and improving metabolic disorders, it ameliorated DHEA-induced reproductive dysfunction. These beneficial effects might be associated with the restoration of gut dysbiosis.
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