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| Pronunciation | /eɪˌnɪdjʊləˈfʌndʒɪn/ ay-NID-yuu-lə-FUN-jin |
| Trade names | Eraxis, Ecalta |
| Other names | (4R,5S)-4,5-Dihydroxy-N2-[[4''-(pentyloxy)-p-terphenyl-4-yl]carbonyl]-L-ornithyl-L-threonyl-trans-4-hydroxy-L-prolyl-(S)-4-hydroxy-4-(p-hydroxyphenyl)-L-threonyl-L-threonyl-(3S,4S)-3-hydroxy-4-methyl-L-proline cyclic (6→1)-peptide[1] 1-[(4R,5R)-4,5-Dihydroxy-N2-[[4''-(pentyloxy)[1',1':4',1''-terphenyl]-4-yl]carbonyl]-L-ornithine]echinocandin B[2] |
| AHFS/Drugs.com | Monograph |
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| Routes of administration | Intravenous |
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| Bioavailability | 100% (intravenous use only) |
| Protein binding | Extensive (>99%) |
| Metabolism | Hepatic metabolism not observed, CYP system not involved |
| Elimination half-life | 27 hours; 40–50 hours (terminal) |
| Excretion | Feces (~30%), urine (<1%) |
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| ECHA InfoCard | 100.184.856  |
| Chemical and physical data | |
| Formula | C58H73N7O17 |
| Molar mass | 1140.254 g·mol−1 |
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Anidulafungin (INN)[1]: 42 (trade names Eraxis, Ecalta) is a semisynthetic echinocandin used as an antifungal drug. It was previously known as LY303366.[3][4][5] It may also have application in treating invasive Aspergillus infection when used in combination with voriconazole.[6] It is a member of the class of antifungal drugs known as the echinocandins; its mechanism of action is by inhibition of (1→3)-β-D-glucan synthase, an enzyme important to the synthesis of the fungal cell wall.[7]
It is on the World Health Organization's List of Essential Medicines.[8]
Anidulafungin has not been studied in endocarditis, osteomyelitis, and meningitis due to Candida, and has not been studied in sufficient numbers of neutropenic patients to determine efficacy in this group.[2]
Anidulafungin significantly differs from other antifungals in that it undergoes chemical degradation to inactive forms at body pH and temperature. Because it does not rely on enzymatic degradation or hepatic or renal excretion, the drug is safe to use in patients with any degree of hepatic or renal impairment.[9]
| Parameter | Value |
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| Volume of distribution (L) | 30–50 L.[10] |
| Plasma protein binding (%) | 99%[10] |
| Elimination half-life [h] | 24 hours[10] |
Anidulafungin is not evidently metabolized by the liver. This specific drug undergoes slow chemical hydrolysis to an open-ring peptide which lacks antifungal activity. The half-life of the drug is 27 hours. About 30% is excreted in the feces (10% as unchanged drug). Less than 1% is excreted in the urine.[11][12][13]
Anidulafungin inhibits glucan synthase, an enzyme important in the formation of (1→3)-β-D-glucan, a major fungal cell wall component. Glucan synthase is not present in mammalian cells, so it is an attractive target for antifungal activity.[14]
Anidulafungin is manufactured via semi-synthesis. The starting material is echinocandin B (alipopeptide fermentation product of Aspergillus nidulans or the closely related species, A. rugulosus), which undergoes deacylation (cleavage of the linoleoyl side chain) by the action of a deacylase enzyme from the bacterium Actinoplanes utahensis;[15] in three subsequent synthetic steps, including a chemical reacylation, the antifungal drug anidulafungin[14][16] is synthesized.
Anidulafungin was originally discovered at Lilly laboratories by Turner and Debono and licensed to Vicuron Pharmaceuticals who submitted it to the FDA.[17] Pfizer acquired the drug upon its acquisition of Vicuron in the fall of 2005.[18] Pfizer gained approval by the Food and Drug Administration (FDA) on February 21, 2006.[19]
