Entation of the traditional antifungal agents, their targets, and actions. AntimetaboFigure
Entation with the standard antifungal agents, their targets, and actions. AntimetaboFigure 1.1. Schematic representation in the traditional antifungal agents, their targets, and actions. Antimetabolite, 5-Fluorocytosine (5-FC), is usually a S1PR3 Agonist Compound fluorinated pyrimidine analog with fungicidal activity by means of interfering the pyrimidine melite, 5-Fluorocytosine (5-FC), is actually a fluorinated pyrimidine analog with fungicidal activity by way of interfering the pyrimidine tabolism, RNA/DNA and protein synthesis. Initial, 5-FC is taken up by fungal cells by way of a cytosine permease (encoded by metabolism, RNA/DNA and protein synthesis. Initial, 5-FC isistaken up by fungal by UMP a cytosine permease (engene FCY2) and is converted to 5-fluorouracil (5-FU), and then transformed cells via pyrophosphorylase into coded by gene FCY2) and is converted to 5-fluorouracil (5-FU),incorporated into RNAs by inhibitpyrophosphorylase into and is then transformed to UMP the protein synthesis. mTOR Modulator web 5-fluorourdine monophosphate (5-FUMP). Then, 5-FUMP is 5-fluorourdine monophosphatereductase enables 5-FUMP is incorporated into into 5-fluorodeoxyuridine monophosphate Furthermore, ribonucleotide (5-FUMP). Then, the conversion of 5-FUMP RNAs to inhibit the protein synthesis. Addi(5-FdUMP), a potent reductase enables the conversion that inhibits fungal DNA synthesis and nuclear division. Azoles tionally, ribonucleotideinhibitor of thymidylate synthase of 5-FUMP into 5-fluorodeoxyuridine monophosphate (5-FdUMP), a are inhibitors for of thymidylate synthase that enzyme lanosterol 14-demethylase nuclear division. Azoles ERG11 gene, potent inhibitor cytochrome P450-dependent inhibits fungal DNA synthesis and (CYP51) encoded by the are inhibitors and hence blockP450-dependent of lanosterol to ergosterol. Allylamines block ergosterol biosynthesis via inhibiting squafor cytochrome the conversion enzyme lanosterol 14-demethylase (CYP51) encoded by the ERG11 gene, and thus block lene epoxidase (ERG1) that result in squalene accumulation and elevated permeability could cause the disruption of celthe conversion of lanosterol to ergosterol. Allylamines block ergosterol biosynthesis through inhibiting squalene epoxidase lular organization. Echinocandins act as noncompetitive inhibitors of -(1, 3)-D-glucan synthase enzyme complicated and (ERG1) that cause squalene accumulation and elevated permeability might lead to the disruption of cellular organization. leads to disruption from the cell wall structure, resulting in osmotic instability and fungal cell death. Polyenes particularly Echinocandins actbilayer and kind a complex with-(1,ergosterol creating pores that leads to and disruption of the cell bind towards the lipid as noncompetitive inhibitors with the 3)-D-glucan synthase enzyme complicated the results in disruption on the cell wall structure, resulting in osmotic instability and fungal cell death. Polyenes specifically bindB (AmB) binds ermembrane, leakage in the cytoplasmic, contents and oxidative harm in fungal cells. Amphotericin towards the lipid bilayer and type and forms an extra-membranous fungicidal pores that results in the disruption on the cell membrane, leakage of gosterol a complicated with all the ergosterol making sterol sponge destabilizing membrane function. the cytoplasmic, contents and oxidative harm in fungal cells. Amphotericin B (AmB) binds ergosterol and types an Common clinical antifungal drugs have extra-membranous fungicidal sterol sponge destabilizing membrane function. distinct molecular targets and can be di-vided.
