Marizomib (Salinosporamide A) (0.15 mg/kg; i.v; twice a week for three weeks) significantly decreases tumor growth, and is not associated with any toxicity[3]. Animal Model: CB-17 SCID-male mice (4-6 weeks old)[3] Dosage: 0.15 mg/kg Administration: i.v; twice a week for three weeks Result: Significantly decreased tumor growth, and was not associated with any toxicity.
In Vitro
Marizomib (Salinosporamide A) (0.1-10000 nM; 72 hours) effectively reduces survival of D-54 and U-251 cells in a dose-dependent manner. The IC50s are ∼52 nM for U-251 and ∼20 nM for D-54[1]. Marizomib (24 hours; 60 nM) induces apoptosis and caspase-3 activation in glioma cells[1]. Cell Proliferation Assay[1] Cell Line: U-251 and D-54 cells Concentration: 0.1, 1, 10, 100, 1000, 10000 nM Incubation Time: 72 hours Result: Effectively reduced survival of D-54 and U-251 cells in a dose-dependent manner. Apoptosis Analysis[1] Cell Line: D-54 cells Concentration: 60 nM Incubation Time: 24 hours Result: Induces D-54 cells apoptosis. Western Blot Analysis[1] Cell Line: D-54 cells Concentration: 60 nM Incubation Time: 24 hours Result: Led to increased activity of caspase-3 in a dose-dependent manner.
Kinase Assay
Cell Assay
Animal Administration
References
[1]. Di K, et al. Marizomib activity as a single agent in malignant gliomas: ability to cross the blood-brainbarrier. Neuro Oncol. 2016 Jun;18(6):840-8.
[2]. Kale AJ, et al. Molecular mechanisms of acquired proteasome inhibitor resistance. J Med Chem. 2012 Dec 13;55(23):10317-27.
[3]. Singh AV, et al. Pharmacodynamic and efficacy studies of the novel proteasome inhibitor NPI-0052 (marizomib) in a human plasmacytoma xenograft murine model. Br J Haematol. 2010 May;149(4):550-9.
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