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The term Multiple fungal proteins and membranes refers to a broad set of molecular structures and biosynthetic pathways essential for the survival and structural integrity of fungal pathogens. Key components include the fungal cell membrane, where the sterol ergosterol provides stability and is a primary target for polyene antibiotics like Amphotericin B [1]. Another critical component is the fungal cell wall, composed of chitin and beta-glucans, which is targeted by echinocandins to cause cell lysis [2]. This collective target also includes vital enzymes such as lanosterol 14-alpha demethylase (CYP51), which is inhibited by azole antifungals to prevent ergosterol synthesis [3]. Furthermore, it encompasses intracellular targets like those involved in nucleic acid synthesis, which are disrupted by agents such as flucytosine [5]. These targets are essential for maintaining the osmotic balance and protective barrier of the fungus against the host environment [4]. Drugs acting on these multiple sites are used to treat a variety of infections, including invasive candidiasis and aspergillosis [1, 3]. However, the complexity of these targets and their occasional similarity to human cellular components can lead to significant side effects, such as nephrotoxicity, hepatotoxicity, and drug-drug interactions [1, 3, 5].
Inhibition of ergosterol synthesis, direct membrane pore formation, inhibition of cell wall beta-glucan synthesis, and interference with nucleic acid synthesis.
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