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Fungal cell wall chitin is a primary structural homopolymer composed of beta-(1,4)-linked N-acetyl-D-glucosamine units, serving as a critical component of the fungal cell wall architecture. It provides the mechanical strength and rigidity necessary to maintain cellular integrity and protect the organism against osmotic stress, particularly during active growth phases such as budding and hyphal tip extension (Gow et al., 2017; [1, 10]). Because chitin is absent in mammalian cells, it represents an ideal target for selective antifungal therapy with minimal host toxicity. Current therapeutic approaches focus on inhibiting its biosynthesis via chitin synthase inhibitors like Nikkomycin Z, which competitively blocks the enzyme's active site by mimicking the natural substrate UDP-N-acetylglucosamine ([5, 7, 8]). Beyond its structural utility, chitin is recognized as a pathogen-associated molecular pattern (PAMP) by the host innate immune system, where it can modulate inflammatory responses or serve as a biomarker for diagnosing invasive fungal infections in clinical samples ([11, 13, 18]).
Competitive inhibition of chitin synthase (CHS) enzymes by substrate analogs to prevent polymerization, or direct enzymatic degradation of the polymer via chitinases.
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