Active Ingredients: Ciprofloxacin
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Both trifluoperazine and methdilazine tend to cause accumulation and retention of antimycobacterial drugs in macrophages. Thus there should be approaches for developing more effective and less harmful derivatives of such drugs that can be used as an alternative to trigger the function of the compound.
Although chlorpromazine was found to kill M. Chlorpromazine was largely replaced by the neuroleptic drug thioridazine, which is less toxic and is much more effective in in vitro systems against all forms of antibiotic resistant strains of M.
Thus the interest in thioridazine began; this compound promotes the killing of multidrug-resistant M. In the murine model, thioridazine has been found to be effective against both antibiotic susceptible and multidrugresistant tuberculosis infection.
Chlorpromazine has been found to affect the bacterial efflux pump; therefore, it reduces the resistance to antibiotics in bacterial strains.
The result was found to be similar in the case of phenothiazines.
They could inhibit Nor A efflux pump of Staphylococcus aureus and the QAC efflux pump of plasmid-carrying multidrug-resistant Staphylococcus aureus.
The Acr AB efflux pump of E. These phenothiazines could also inhibit the main efflux pump of M.
Since it affects the survival genes of M. Phenothiazines act by inhibiting the activity of calcium-dependent ATPase, which leads to the acidification of phagolysosome and its subsequent activation of the hydrolases, resulting in the inhibition of replication of the bacterium.
Thioridazine inhibits the EmrE-encoded efflux pump in M.
Further, thioridazine treated cell cause the expression of Rv 3065 gene, which encodes the multidrug transport integral membrane protein EmrE, and that of another putative efflux pump gene Rv 1634.
When Rv 3065 homologue is deleted in M. During the macrophage infection by M.