Brands, Medical Use, Clinical Data
- Antineoplastic Agents
Brands / Synonyms
DHAD; DHAQ; DHAQ HCl; Dihydroxyanthraquinone; Immunex; Mitox; Mitoxanthrone; Mitoxantron; Mitoxantrona [Inn-Spanish]; Mitoxantrone 2HCl; Mitoxantrone dihydrochloride; Mitoxantrone HCl; Mitoxantrone hydrochloride; Mitoxantronum [Inn-Latin]; Mitozantrone; Mitozantrone hydrochloride; Novantron; Novantrone; Novantrone
For the treatment of secondary (chronic) progressive, progressive relapsing, or worsening relapsing-remitting multiple sclerosis
Mitoxantrone has been shown in vitro to inhibit B cell, T cell, and macrophage proliferation and impair antigen presentation, as well as the secretion of interferon gamma, TNFa, and IL-2.
Mechanism of Action
Mitoxantrone, a DNA-reactive agent that intercalates into deoxyribonucleic acid (DNA) through hydrogen bonding, causes crosslinks and strand breaks. Mitoxantrone also interferes with ribonucleic acid (RNA) and is a potent inhibitor of topoisomerase II, an enzyme responsible for uncoiling and repairing damaged DNA. It has a cytocidal effect on both proliferating and nonproliferating cultured human cells, suggesting lack of cell cycle phase specificity.
Poorly absorbed following oral administration
Severe leukopenia with infection.
Biotrnasformation / Drug Metabolism
NOVANTRONEâ is contraindicated in patients who have demonstrated prior
hypersensitivity to it.
Mitoxantrone and its metabolites are excreted in bile and urine, but it is not known whether the metabolic or
excretory pathways are saturable, may be inhibited or induced, or if mitoxantrone and its metabolites undergo
enterohepatic circulation. To date, post-marketing experience has not revealed any significant drug interactions in
patients who have received NOVANTRONEâ for treatment of cancer. Information on drug
interactions in patients with multiple sclerosis is limited.
Following concurrent administration of NOVANTRONEâ with corticosteroids, no
evidence of drug interactions has been observed.