<unk>  is a first-generation triazole antifungal medication. It differs from earlier azole antifungals (such as ketoconazole) in that its structure contains a triazole ring instead of an imidazole ring. While the imidazole antifungals are mainly used topically,<unk>  and certain other triazole antifungals are preferred when systemic treatment is required because of their improved safety and predictable absorption when administered orally.<unk> 's spectrum of activity includes most Candida species (but not Candida krusei or Candida glabrata), Cryptococcus neoformans, some dimorphic fungi, and dermatophytes, among others. Common uses include: * The treatment of non-systemic Candida infections of the vagina ("yeast infections"), throat, and mouth. * Certain systemic Candida infections in people with healthy immune systems, including infections of the bloodstream, kidney, or joints. Other antifungals are usually preferred when the infection is in the heart or central nervous system, and for the treatment of active infections in people with weak immune systems. * The prevention of Candida infections in people with weak immune systems, such as those neutropenic due to cancer chemotherapy, those with advanced HIV infections, transplant patients, and premature infants. * As a second-line agent for the treatment of cryptococcal meningoencephalitis, a fungal infection of the central nervous system. Resistance Fungal resistance to drugs in the azole class tends to occur gradually over the course of prolonged drug therapy, resulting in clinical failure in immunocompromised patients (e.g., patients with advanced HIV receiving treatment for thrush or esophageal Candida infection). In C. albicans, resistance occurs by way of mutations in the ERG11 gene, which codes for 14α-demethylase. These mutations prevent the azole drug from binding, while still allowing binding of the enzyme's natural substrate, lanosterol. Development of resistance to one azole in this way will confer resistance to all drugs in the class. Another resistance mechanism employed by both C. albicans and C. glabrata is increasing the rate of efflux of the azole drug from the cell, by both ATP-binding cassette and major facilitator superfamily transporters. Other gene mutations are also known to contribute to development of resistance. C. glabrata develops resistance by up regulating CDR genes, and resistance in C. krusei is mediated by reduced sensitivity of the target enzyme to inhibition by the agent. The full spectrum of fungal susceptibility and resistance to<unk>  can be found in the product data sheet. According to the United States Centers for Disease Control,<unk>  resistance among Candida strains in the U.S. is about 7%.
Fluconazole
Itraconazole
Miconazole
Terbinafine
Posaconazole
Micafungin
Sertaconazole
Fosravuconazole