Echinocandins: A ray of hope in antifungal drug therapy
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Invasive fungal infections are on the rise. Amphotericin B and azole antifungals have been the mainstay of antifungal therapy so far. The high incidence of infusion related toxicity and nephrotoxicity with amphotericin B and the emergence of fluconazole resistant strains of Candida glabrata egged on the search for alternatives. Echinocandins are a new class of antifungal drugs that act by inhibition of beta (1, 3)-D- glucan synthase, a key enzyme necessary for integrity of the fungal cell wall.Caspofungin was the first drug in this class to be approved. It is indicated for esophageal candidiasis, candidemia, invasive candidiasis, empirical therapy in febrile neutropenia and invasive aspergillosis. Response rates are comparable to those of amphotericin B and fluconazole. Micafungin is presently approved for esophageal candidiasis, for prophylaxis of candida infections in patients undergoing hematopoietic stem cell transplant (HSCT) and in disseminated candidiasis and candidemia. The currently approved indications for anidulafungin are esophageal candidiasis, candidemia and invasive candidiasis.The incidence of infusion related adverse effects and nephrotoxicity is much lower than with amphotericin B. The main adverse effect is hepatotoxicity and derangement of serum transaminases. Liver function may need to be monitored. They are, however, safer in renal impairment. Even though a better pharmacoeconomical choice than amphotericin B, the higher cost of these drugs in comparison to azole antifungals is likely to limit their use to azole resistant cases of candidial infections and as salvage therapy in invasive aspergillosis rather than as first line drugs.
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Echinocandins inhibit fungal wall synthesis by noncompetitive blockage of (1,3)-β-D-glucan synthase, leading to impaired structural integrity and osmotic lysis.
“Echinocandins (caspofungin, micafungin, and anidulafungin) are lipopeptidic antifungal agents that inhibit the synthesis of fungal wall by noncompetitive blockage of the (1,3)-β-D-glucan synthase (Figure 1). This enzyme inhibition leads to the formation of fungal cell walls with impaired structural integrity, which finally results in cell vulnerability to osmotic lysis [24].”
From <i>Candida</i>Infections, Causes, Targets, and Resistance Mechanisms: Traditional and Alternative Antifungal Agents (2013) · cites this paper as [24]
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Bioengineering Towards Fighting Against Superbugs
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A REVIEW ON DIAGNOSIS & THEIR TREATMENT: FUNGAL INFECTIONS
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- Authors
- Grover, N.
- Affiliations
- Bharati Vidyapeeth (Deemed to be University) (IN)
- Corresponding author
- Grover, NeetaD
- Venue
- Indian Journal of Pharmacology
- Published
- 2010
- Volume
- 42
- Issue
- 1
- Pages
- 9
- ISSN
- 0253-7613 (ISSN-L)
- PMC
- PMC2885632
- OpenAlex
- W2004949243
- Cited by
- 75
- References
- 34
- Citations by year
- 2026: 3 · 2025: 10 · 2024: 13 · 2023: 12 · 2022: 5 · 2021: 3 · 2020: 5 · 2019: 7 · 2018: 2 · 2016: 4 · 2015: 1 · 2014: 1 · 2013: 2 · 2012: 1
- FWCI
- 1.87
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- cc-by
- Locations
- Indian Journal of Pharmacology (publishedVersion)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Bioline International (Bioline International) (submittedVersion)
- TSpace (University of Toronto) (submittedVersion)
- Topics
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Health Sciences › Medicine › Epidemiology › Fungal Infections and Studies
- Life Sciences › Agricultural and Biological Sciences › Ecology, Evolution, Behavior and Systematics › Fungal Plant Pathogen Control
- Keywords
- echinocandins, antifungal therapy, invasive fungal infections, caspofungin, micafungin, anidulafungin, candidiasis, invasive aspergillosis, candidemia, esophageal candidiasis, fluconazole resistance, Candida glabrata, amphotericin B nephrotoxicity, hepatotoxicity, febrile neutropenia
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