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    Mitoxantrone HCl (mitozantrone)
    Mitoxantrone HCl (mitozantrone)

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V1404
    CAS #: 70476-82-3 Purity ≥98%

    Description: Mitoxantrone HCl (formerly NSC-301739; NSC301739; DHAQ; CL-232325; Mitroxone; Neotalem; Onkotrone; Pralifan; Novantrone), the hydrochloride salt of Mitoxantrone which is an anthracenedione anticancer agent, is a potent type II topoisomerase inhibitor with potential antitumor activity. It inhibits TOPO II with IC50s of 2.0 μM, 0.42 mM in HepG2 and MCF-7/wt cells, respectively. It is used as an anti-neoplastic drug for leukemia and other types of cancer, and a proven drug for multiple sclerosis. Mitoxantrone suppressed the leukemia via inhibiting DNA synthesis and cell cycle progression. It had effect on different immune cells (e.g. T cell, B cell and macrophage etc.). It interfered with TOPO-II-mediated DNA cleavage and led to multiple DSB (DNA strand breaks), chromatin structure changes etc.

    References: Curr Opin Rheumatol. 1999 May;11(3):226-32; Neurology. 2004 Dec 28;63(12 Suppl 6):S15-8.

    Related CAS#:65271-80-9 (free base); 70476-82-3 (HCl salt)

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    Molecular Weight (MW)517.4 
    CAS No.70476-82-3 (HCl salt); 
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 89 mg/mL (172.0 mM)
    Water: 89 mg/mL (172.0 mM)
    Ethanol: <1 mg/mL
    Solubility (In vivo)Saline: 30 mg/mL 

    NSC-301739; CL-232325; NSC301739; CL 232325; NSC 301739; DHAQ; CL232325; Mitozantrone; Mitoxantrone HCl; Mitoxantrone dihydrchloride; US brand name: Novantrone. NSC 301739; DHAQ; CL232325; Foreign brand names: Mitroxone; Neotalem; Onkotrone; Pralifan;

    Chemical Name: 1,4-dihydroxy-5,8-bis((2-((2-hydroxyethyl)amino)ethyl)amino)anthracene-9,10-dione dihydrochloride


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    In Vitro

    In vitro activity: Mitoxantrone induces DNA fragmentation and the proteolytic cleavage of poly(ADP-ribose) polymerase (PARP), a marker of the activation of caspases, in all the patients studied, demonstrating that the cytotoxic effect of mitoxantrone is due to induction of apoptosis. Mitoxantrone activates NFkappaB and stimulates IkappaBalpha degradation in the promyelocytic leukemia cell line HL60 but not in the variant cells, HL60/MX2 cells, which lack the beta isoform of topoisomerase II and express a truncated alpha isoform that results in an altered subcellular distribution. Mitoxantrone inhibits proliferation of activated PBMCs, B lymphocytes, or antigen-specific T-cell lines (TCLs) stimulated on antigen-presenting cells (APCs) in a dose-dependent manner. Mitoxantrone induces apoptosis of PBMCs, monocytes and DCs at low concentrations, whereas higher doses causes cell lysis.

    Kinase Assay: Mitoxantrone inhibits PKC in a competitive manner with respect to histone H1, and its Ki value is 6.3 μM and in a non-competitive manner with respect to phosphatidylserine and ATP. Treatment of B-CLL cells for 48 h with mitoxantrone (0.5 μg/mL) induces a decrease in cell viability. Mitoxantrone induces DNA fragmentation and the proteolytic cleavage of poly(ADP-ribose) polymerase (PARP), demonstrating that the cytotoxic effect of mitoxantrone is due to induction of apoptosis. Mitoxantrone shows cytotoxicity to human breast carcinoma cell lines MDA-MB-231 and MCF-7 with IC50 values of 18 and 196 nM, respectively.

    Cell Assay: The human breast carcinoma cell lines MDA-MB-231 and MCF-7 are seeded in standard 96-well plates. One day after seeding, the culture medium is changed and replaced by medium containing different concentration of Mitoxantrone (10-5 to 5 μM) with or without DHA (30 μM) during 7 days. Viability of cells are measured as a whole by the tetrazolium salt assay.

    In Vivo Mitoxantrone given IP at the optimal dose (1.6 mg/kg/day; as a free base) produces a statistically significant number of 60-day survivors (curative effect) in mice with IP implanted L1210 leukemia. In SC implanted Lewis lung carcinoma, mitoxantrone and ADM administered IV also shows effective antitumor activities and produces a 60% and a 45% ILS, respectively.
    Animal model Mice
    Formulation & Dosage 1.6 mg/kg/day; i.p. or i.v.
    ReferencesCurr Opin Rheumatol. 1999 May;11(3):226-32; Arthritis Rheum. 1989 Sep;32(9):1065-73; Cancer Chemother Pharmacol. 1982;8(2):157-62.

    These protocols are for reference only. InvivoChem does not independently validate these methods.


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