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Anidulafungin and its role in candida infections.

Cappelletty DM, Jung R - Infect Drug Resist (2009)

Bottom Line: The decrease in 1,3-β-D-glucan results in the osmotic lysis of the cell, resulting in fungicidal activity against candida.The efflux pump associated with fluconazole resistance in Candida albicans can confer higher minimum inhibitory concentrations to caspofungin.Because it is available only parenterally its role in treating mucocutaneous candidiasis is primarily in patients unable to take oral therapy.

View Article: PubMed Central - PubMed

Affiliation: The University of Toledo, College of Pharmacy, Toledo, OH, USA.

ABSTRACT
Candida infections continue to play a significant role not only in critically ill and immunocompromised patients but also in non-compromised patients. The incidence of systemic fungal infections in the United States has been on the rise for the past 30 years. Anidulafungin and all echinocandins inhibit glucan synthase thus inhibiting the formation of 1,3-β-D-glucan which is an essential component of the fungal cell wall. The decrease in 1,3-β-D-glucan results in the osmotic lysis of the cell, resulting in fungicidal activity against candida. Anidulafungin is active against most species of candida and resistance to it is very rare. Two potential mechanisms conferring reduced susceptibility to the echinocandins are efflux and target alteration. The efflux pump associated with fluconazole resistance in Candida albicans can confer higher minimum inhibitory concentrations to caspofungin. The second mechanism of resistance is via mutations in the genes which code for 1,3 β-D-glucan synthase, specifically FKS1. Because of its spectrum of activity, fungicidal nature, and tolerability it is an attractive first-line therapeutic choice for treating candidemia in both non-neutropenic and neutropenic patients. Because it is available only parenterally its role in treating mucocutaneous candidiasis is primarily in patients unable to take oral therapy.

No MeSH data available.


Related in: MedlinePlus

Anidulafungin chemical structure.
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f1-idr-2-051: Anidulafungin chemical structure.

Mentions: The echinocandins are synthetically modified lipopeptides which were identified from the fermentation broths of various fungi. Anidulafungin (Figure 1) is derived from Aspergillus nidulans. It is a 1-[(4R,5R)-4,5-Dihydroxy-N2-[[4″ (pentyloxy)[1,1′:4′,1″-terphenyl]-4-yl]carbonyl]-L-ornithine]echinocandin B. Its molecular formula is C58H73N7O17, and its molecular weight is 1140.3.7 The echinocandins are only available parenterally and anidulafungin is available in both 50 and 100 mg vials.


Anidulafungin and its role in candida infections.

Cappelletty DM, Jung R - Infect Drug Resist (2009)

Anidulafungin chemical structure.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3108729&req=5

f1-idr-2-051: Anidulafungin chemical structure.
Mentions: The echinocandins are synthetically modified lipopeptides which were identified from the fermentation broths of various fungi. Anidulafungin (Figure 1) is derived from Aspergillus nidulans. It is a 1-[(4R,5R)-4,5-Dihydroxy-N2-[[4″ (pentyloxy)[1,1′:4′,1″-terphenyl]-4-yl]carbonyl]-L-ornithine]echinocandin B. Its molecular formula is C58H73N7O17, and its molecular weight is 1140.3.7 The echinocandins are only available parenterally and anidulafungin is available in both 50 and 100 mg vials.

Bottom Line: The decrease in 1,3-β-D-glucan results in the osmotic lysis of the cell, resulting in fungicidal activity against candida.The efflux pump associated with fluconazole resistance in Candida albicans can confer higher minimum inhibitory concentrations to caspofungin.Because it is available only parenterally its role in treating mucocutaneous candidiasis is primarily in patients unable to take oral therapy.

View Article: PubMed Central - PubMed

Affiliation: The University of Toledo, College of Pharmacy, Toledo, OH, USA.

ABSTRACT
Candida infections continue to play a significant role not only in critically ill and immunocompromised patients but also in non-compromised patients. The incidence of systemic fungal infections in the United States has been on the rise for the past 30 years. Anidulafungin and all echinocandins inhibit glucan synthase thus inhibiting the formation of 1,3-β-D-glucan which is an essential component of the fungal cell wall. The decrease in 1,3-β-D-glucan results in the osmotic lysis of the cell, resulting in fungicidal activity against candida. Anidulafungin is active against most species of candida and resistance to it is very rare. Two potential mechanisms conferring reduced susceptibility to the echinocandins are efflux and target alteration. The efflux pump associated with fluconazole resistance in Candida albicans can confer higher minimum inhibitory concentrations to caspofungin. The second mechanism of resistance is via mutations in the genes which code for 1,3 β-D-glucan synthase, specifically FKS1. Because of its spectrum of activity, fungicidal nature, and tolerability it is an attractive first-line therapeutic choice for treating candidemia in both non-neutropenic and neutropenic patients. Because it is available only parenterally its role in treating mucocutaneous candidiasis is primarily in patients unable to take oral therapy.

No MeSH data available.


Related in: MedlinePlus