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| Pronunciation | /eɪˌnɪdjʊləˈfʌndʒɪn/ay-NID-yuu-lə-FUN-jin |
| Trade names | Eraxis, others |
| Other names | LY303366, (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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| Pharmacokinetic data | |
| Bioavailability | 100% (intravenous use only) |
| Protein binding | Extensive (>99%) |
| Metabolism | Hepatic metabolism not observed,CYP system not involved |
| Eliminationhalf-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 (sold under the brand nameEraxis among others, is asemisyntheticechinocandin used as anantifungal medication.[4][5][6] It may also have application in treating invasiveAspergillus infection when used in combination withvoriconazole.[7] It is a member of the class of antifungal drugs known as theechinocandins; 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.[8]
It is on theWorld Health Organization's List of Essential Medicines.[9]
Anidulafungin has not been studied inendocarditis,osteomyelitis, andmeningitis due toCandida, and has not been studied in sufficient numbers ofneutropenic patients to determine efficacy in this group.[2]
Anidulafungin significantly differs from other antifungals in that it undergoes chemical degradation to inactive forms at bodypH 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.[10]
| Parameter | Value |
|---|---|
| Volume of distribution (L) | 30–50 L.[11] |
| Plasma protein binding (%) | 99%[11] |
| Elimination half-life [h] | 24 hours[11] |
Anidulafungin is not evidently metabolized by theliver. This specific drug undergoes slow chemicalhydrolysis 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.[12][13][14]
Anidulafungin inhibitsglucan 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.[15]
Anidulafungin is manufactured via semi-synthesis. The starting material isechinocandin B (alipopeptide fermentation product ofAspergillus nidulans or the closely related species,A. rugulosus), which undergoes deacylation (cleavage of thelinoleoyl side chain) by the action of a deacylase enzyme from the bacteriumActinoplanes utahensis;[16] in three subsequent synthetic steps, including a chemical reacylation, the antifungal drug anidulafungin[15][17] is synthesized.
Anidulafungin was originally discovered at Lilly laboratories by Turner and Debono and licensed to Vicuron Pharmaceuticals who submitted it to the FDA.[18]Pfizer acquired the drug upon its acquisition of Vicuron in the fall of 2005.[19] Pfizer gained approval by theFood and Drug Administration (FDA) on 21 February 2006.[20]