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QuickView for micafungin (compound)


PubChem
Name: micafungin
PubChem Compound ID: 11804463
Molecular formula: C56H71N9O23S
Molecular weight: 1270.28 g/mol
DrugBank
Identification
Name: micafungin
Name (isomeric): DB01141
Drug Type: small molecule
Synonyms:
FK-463
Brand: Mycamine
Category: Antifungal Agents, Antifungals
CAS number: 235114-32-6
Pharmacology
Indication: For use in the treatment of candidemia, acute disseminated candidiasis, and certain other invasive <i>Candida</i> infections, as well as esophageal candidiasis, and prophylaxis of <i>Candida</i> infections in patients undergoing hematopoietic stem cell transplantation. Micafungin is also used as an alternative for the treatment of oropharyngeal candidiases and has been used with some success as primary or salvage therapy, alone or in combination with other antifungals, for the treatment of invasive aspergillosis.
Pharmacology:
Formerly known as FK463, micafungin is a semisynthetic lipopeptide synthesized from a fermentation product of Coleophoma empetri that works as an antifungal agent. It is a glucan synthesis inhibitor of the echinocandin structural class. The U.S. Food and Drug Administration approved micafungin in March 2005. Micafungin inhibits an enzyme ess...
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Mechanism of Action: Micafungin inhibits the synthesis of beta-1,3-D-glucan, an essential component of fungal cell walls which is not present in mammalian cells. It does this by inhibiting beta-1,3-D-glucan synthase.
Absorption: Not absorbed orally
Protein binding: Highly (>99%) protein bound in vitro, independent of plasma concentrations over the range of 10 to 100 µg/mL. The primary binding protein is albumin; however, micafungin, at therapeutically relevant concentrations, does not competitively displace bilirubin binding to albumin. Micafungin also binds to a lesser extent to a1-acid-glycoprotein.
Biotransformation: Micafungin is metabolized to M-1 (catechol form) by arylsulfatase, with further metabolism to M-2 (methoxy form) by catechol-O-methyltransferase. M-5 is formed by hydroxylation at the side chain (w-1 position) of micafungin catalyzed by cytochrome P450 (CYP) isozymes. Even though micafungin is a substrate for and a weak inhibitor of CYP3A in vitro, hydroxylation by CYP3A is not a major pathway for micafungin metabolism in vivo.
Route of elimination: Fecal excretion is the major route of elimination (total radioactivity at 28 days was 71% of the administered dose).
Half Life: 14-17 hours
Clearance: 0.359 +/- 0.179 mL/min/kg [Adult Patients with IC with 100 mg] 0.321 +/- 0.098 mL/min/kg [HIV- Positive Patients with EC with 50 mg] 0.327 +/- 0.093 mL/min/kg [HIV- Positive Patients with EC with 100 mg] 0.340 +/- 0.092 mL/min/kg [HIV- Positive Patients with EC with 150 mg] 0.214 +/- 0.031 mL/min/kg [hematopoietic stem cell transplant recipients 3 mg/kg] 0.204 +/- 0.036 mL/min/kg [hematopoietic stem cell transplant recipients 4 mg/kg] 0.224 +/- 0.064 mL/min/kg [hematopoietic stem cell transplant recipients 6 mg/kg] 0.223 +/- 0.081 mL/min/kg [hematopoietic stem cell transplant recipients 8 mg/kg]
Toxicity: Intravenous LD50 in rats is 125mg/kg. In dogs it is >200mg/kg. No cases of overdosage have been reported. Repeated daily doses up to 8 mg/kg (maximum total dose of 896 mg) in adult patients have been administered in clinical trials with no reported dose-limiting toxicity. The minimum lethal dose is 125 mg/kg in rats, equivalent to 8.1 times the recommended human clinical dose for esophageal candidiasis based on body surface area comparisons.
Affected organisms: Aspergillis, Candida and other fungi

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