⭐ The "Holy Grail" of antifungal design is finding targets like the cell wall or ergosterol that exist in fungi but not in humans to minimize side effects.
Target the cell wall by inhibiting glucan synthesis; generally well-tolerated. antifungal agent
for specific infections (like Aspergillosis or Candidiasis ) Molecular mechanisms of drug resistance New drug developments currently in clinical trials ⭐ The "Holy Grail" of antifungal design is
Inhibit ergosterol synthesis; primarily fungistatic. The clinical importance of these agents has grown
The clinical importance of these agents has grown alongside the rising prevalence of invasive fungal infections, particularly in immunocompromised populations such as transplant recipients and chemotherapy patients. However, the "antifungal armamentarium" is relatively small compared to the vast array of available antibiotics. This limited selection is further threatened by the emergence of drug-resistant strains, such as Candida auris . Resistance can occur through various mechanisms, including mutations in the target enzymes, the upregulation of efflux pumps that expel the drug from the cell, or the formation of protective biofilms.