Antimicrobial resistance among microorganisms is an alarming and increasing problem throughout the world [1-3]. The widespread use of antibiotics led to the development of multi-drug resistant (MDR) organisms, nullifying the action of drugs formerly considered highly active. Infections involving MDR bacteria are a significant concern for most hospitals and healthcare facilities since they contribute not only to an increase in morbidity and mortality compared to the underlying diseases alone but also have an impact on the length of stay and associated healthcare costs. There are various drugs such as aminoglycosides, cephalosporin, and tetracycline for the treatment, but due to increased resistance against them, there is a need to develop either new drugs or restore the sensitivity of the currently available cornerstone drugs. MDR among bacteria may develop due to either of these two mechanisms: first, these bacteria may accumulate multiple genes, each coding for resistance to a single drug, within a single cell. This accumulation occurs on-resistance (R) plasmids, typically, and secondly, multi-drug resistance may also occur by the increased expression of genes coding for multi-drug efflux pumps, extruding a wide range of drugs [4]. These efflux pumps efflux out the drugs to decrease their concentration inside the cytoplasm [5]. The majority of gram-negative Bacterial efflux pump families, such as K. pneumonia, reduce antibiotic intracellular concentrations, resulting in intrinsic or acquired resistance to a variety of antibiotic classes [6-10]. Drug resistance to chloramphenicol, fluoroquinolones, tetracyclines, glycylcyclines, and florfenicol is caused by efflux pumps belonging to the MFS (Cml and Flo) and RND families (AcrAB-TolC, Acr AB, Mex XY, OprM, MexABOpM, MexCD-OprJ, Oqxb). Efflux pump-mediated drug resistance is an increasing problem, and to overcome this problem, the development and discovery of efflux pump inhibitors is an urgent necessity.