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A narrow-spectrum antibiotic against enteric bacteria called nalidixic acid is used to treat simple urinary tract infections (UTIs). The groundbreaking development of fluoroquinolones during the 1970s and 1980s greatly increased the coverage of the quinolone class.
It is recommended to use NegGram (nalidixic acid, USP) to treat urinary tract infections brought on by gram-negative germs, such as the majority of E. Coli, Enterobacter species, Klebsiella species, and Proteus species.
Bacterial infections are treated with nalidixic acid. Additionally, it treats infections of the lungs, skin, soft tissues, female genital organ, tonsils, sinuses, nose, and throat (pneumonia). An antibiotic is nalidixic acid. It functions by inhibiting the activity of the DNA-gyrase enzyme found in bacteria.
NALIDIXIC ACID is a member of the antibiotic medication class used to treat bacterial urinary tract infections (UTIs). The most typical microbe-caused infection in people is a urinary tract infection, which can affect any component of the urinary tract, including the bladder, urethra, kidneys, or ureters.
The first synthetic quinolone, nalidixic acid, was largely used to treat urinary tract infections brought on by Gram-negative bacteria. However, due to bacterial resistance and the introduction of more potent antibiotics, it is no longer used in clinical settings.
The Global NALIDIXIC ACID market accounted for $XX Billion in 2023 and is anticipated to reach $XX Billion by 2030, registering a CAGR of XX% from 2024 to 2030.
Nalidixic acid was found to be the most bactericidal against several kinds of gram-negative bacteria. Increases in nalidixic acid concentration above this range had the opposite impact on all species tested: they decreased, rather than increased, the bactericidal action of the drug, making it rather bacteriostatic at concentrations about 400 g/ml.
In order to better understand how nalidixic acid works, several concentrations were studied. Deoxyribonucleic acid synthesis, but not ribonucleic acid (RNA) or protein synthesis, was shown to be inhibited at the highest bactericidal concentration.
However, it was shown that both RNA and protein production were suppressed at higher dosages, where the medication is least bactericidal.
Results are presented that imply that the drug’s ability to inhibit RNA synthesis is a secondary manifestation of its ability to inhibit protein synthesis, and that when bacteria are exposed to the drug in high concentrations, RNA synthesis is most likely the second target site for the drug’s action.