Micafungin

1270.28

1269.438354

1806241-263-5

R10H71BSWG

C1850

J02AX05|J - Antiinfectives for systemic use

518.52000

-7.49

Solid

1.6±0.1 g/cm3

1.707

Freely soluble as sodium salt (> 200mg/mL)

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.

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.

Indicated for the treatment of candidemia, acute disseminated candidiasis, and certain other invasive Candida infections, as well as esophageal candidiasis, and prophylaxis of Candida 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. Indicated for the prophylaxis of Candida infections in patients undergoing hematopoietic stem cell transplantation.|FDA Label|Mycamine is indicated for:Adults, adolescents ≥ 16 years of age and elderlytreatment of invasive candidiasis;treatment of oesophageal candidiasis in patients for whom intravenous therapy is appropriate;prophylaxis of Candida infection in patients undergoing allogeneic haematopoietic stem-cell transplantation or patients who are expected to have neutropenia (absolute neutrophil count < 500 cells/µl) for 10 or more days.Children (including neonates) and adolescents < 16 years of agetreatment of invasive candidiasis.prophylaxis of Candida infection in patients undergoing allogeneic haematopoietic stem-cell transplantation or patients who are expected to have neutropenia (absolute neutrophil count < 500 cells/µl) for 10 or more days.The decision to use Mycamine should take into account a potential risk for the development of liver tumours. Mycamine should therefore only be used if other antifungals are not appropriate.

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 essential for fungal cell-wall synthesis. Depending on its concentration, micafungin may be fungicidal against some Candida, but is usually fungistatic against Apergillus. Micafungin can be used concomitantly with a variety of other drugs, including the HIV protease inhibitor ritonavir and the transplant medications cyclosporine and tacrolimus.

Substances that destroy fungi by suppressing their ability to grow or reproduce. They differ from FUNGICIDES, INDUSTRIAL because they defend against fungi present in human or animal tissues. (See all compounds classified as Antifungal Agents.)

Not absorbed orally|Fecal excretion is the major route of elimination (total radioactivity at 28 days was 71% of the administered dose).|0.39 ± 0.11 L/kg [adult patients with esophageal candidiasis]|0.359 +/- 0.179 mL/min/kg [Adult Patients with IC with 100 mg]

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.

14-17 hours

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.

FK 463

Human drugs -> Mycamine -> EMA Drug Category|Antimycotics for systemic use -> Human pharmacotherapeutic group|Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients