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CLASSES OF MEDICATION

POLYENE ANTIFUNGALS
AMPHOTERICIN B CANDICIDIN FILIPIN HAMYCIN NATAMYCIN NYSTATIN RIMOCIDIN

IMIDAZOLES
BIFONAZOLE BUTOCONAZOL E CLOTRIMAZOL E ECONAZOLE E LULICONAZOLE MICONAZOLE OMOCONAZOL E OXICONAZOLE SERTACONAZO LE SULCONAZOLE TIOCONAZOLE

TRIAZOLES
ALBACONAZO LE FLUCONAZOL E ISAVUCONAZ OLE ITRACONAZOL E POSACONAZO LE RAVUCONAZO LE TERCONAZOL E VORICONAZO LE

FENTICONAZO LE ISOCONAZOLE KETOCONAZOL

CLASSES OF MEDICATION
ALLYLAMINES
AMOROLFIN

ECHINOCANDINS

OTHERS
BENZOIC ACID CICLOPIROX FLUCYTOSINE OR 5 FLUOROCYTO SINE GRISEOFULVI N HALOPROGIN POLYGODIAL TOLNAFTATE

BUTENAFINE
NAFTIFINE TERBINAFINE

ANIDULAFUNGI N CASPOFUNGIN MICAFUNGIN

UNDECYLENI C ACID
CRYSTAL VIOLET

MECHANISM OF ACTION

FUNGAL CELL STRUCTURE AND TARGETS Knowledge of fungal cell structure and function is essential for understanding the pharmacology of antifungal agents. Like mammalian cells, fungi are eukaryotes with DNA organized into chromosomes within the cell nucleus and have distinct cytoplasmic organelles including endoplasmic reticulum, golgi apparatus, mitochondria, and storage vacuoles. This homology to mammalian cells also extends to biosynthetic pathways, where fungi share similar mechanisms for DNA replication and protein synthesis.

FUNGAL CELL MEMBRANE


Fungi and mammalian cells both contain a cell membrane that serves and important role in cell structure, division, and metabolism. Complex lipid particles, called sterols, account for approximately 25% of the weight of the cell membrane. However, the sterol content between mammalian cells and fungal cells is different. Whereas mammalian cell membranes contain primarily cholesterol, ergosterol is the predominant sterol in many pathogenic fungi. This difference in sterol content has been exploited as the target of antifungal drug action by several classes of antifungal agents currently used to treat superficial and invasive fungal infections including the polyenes, azoles, and allylamines.

POLYENE ANTIFUNGALS
Polyene antifungals such as amphotericin B act by binding to ergosterol in the fungal cell membrane. This binding results in depolarization of the membrane and formation of pores that increase permeability to proteins and monovalent and divalent cations, eventually leading to cell death. Amphotericin B may also induce oxidative damage in fungal cells and has been reported to stimulate of host immune cells. Toxicities of polyene antifungals are an extension of their mechanism of action. Stimulation of the host immune cells by amphotericin B causes release of inflammatory cytokines by circulating monocytes resulting in fever, chills, rigor, nausea, vomiting, myalgias, arthralgias, and headache during intravenous infusions. At higher concentrations, amphotericin B binds to cholesterol in mammalian cell membranes leading to various organ toxicities, most importantly nephrotoxicity.

AZOLE ANTIFUNGALS
Azole antifungals inhibit the fungal cytochrome P-450 3-A dependent enzyme 14-alpha demethylase, thereby interrupting the synthesis of ergosterol. Inhibition of this critical enzyme in the ergosterol synthesis pathway leads to the depletion of ergosterol in the cell membrane and accumulation of toxic intermediate sterols, causing increased membrane permeability and inhibition of fungal growth. Azole antifungals can also inhibit many mammalian cytochrome p450-dependent enzymes involved in hormone synthesis or drug metabolism. Therefore, azole antifungals are particularly susceptible to clinically-significant drug interactions with other medications metabolized through the P450 pathway.

FUNGAL CELL WALL


GLUCAN SYNTHESIS INHIBITORS

DNA/RNA SYNTHESIS
ANTIMETABOLITES This class has only one example, flucytosine or 5-fluorocytosine (5-FC). Flucytosine was originally developed in the 1950's as a potential antineoplastic agent. Although ineffective against tumors it was later found to have antifungal activity. This small molecule is transported into susceptible fungal cells by a specific enzyme cytosine permease and converted in the cytoplasm by cytosine deaminase to 5-fluorouracil (5-FU)- a pyrimidine anti-metabolite used as chemotherapy for many types

The glucan synthesis inhibitors are, collectively, agents that are presumed to block fungal cell wall synthesis by inhibiting the enzyme 1,3-beta glucan synthase. Inhibition of this enzyme results in depletion of glucan polymers in the fungal cell, resulting in an abnormally

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