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Cat No.
Product Overview
DMAT also displays submicromolar IC50 values with almost all of the other kinases with special reference to PKD1, PIM3 and PIM1.Protein kinase CK2 is involved in cell proliferation and survival, and found overexpressed in virtually all types of human cancer, including breast cancer. We demonstrate that inhibition of CK2 with 2-dimethylamino-4,5,6,7-tetrabromo-benzimidazole (DMAT), a potent and specific CK2 inhibitor, results in caspase-mediated killing of human breast cancer cells with acquired resistance to antiestrogens. Clinical trial: Prostate cancer diagnosis among men with isolated high-grade intraepithelial neoplasia enrolled onto a 3-year prospective phase III clinical trial of oral toremifene.
Molecular Weight
Store at -20°C
Casein kinase II Inhibitor; CK2 Inhibitor
Molecular Formula
Chemical Name
Soluble in DMSO
Shipping Conditions
Evaluation sample solution: ship with blue ice. All other available size: ship with RT, or blue ice upon request
In vitro
Treatment with DMAT decreases the secretion of aldosterone, dehydroepiandrosterone sulfate, and androstendione in H295R human adrenocortical cancer cell line and results in an accumulation of 17-OH-progesterone. Cell growth as measured by the MTT and 5-bromo-2'-deoxyuridine incorporation assays is inhibited, and cell cycle analysis has revealed a slight induction of apoptosis. PIM1 is also inhibited by DMAT by a mechanism which is competitive with respect to ATP. However, IC50 determinations at increasing ATP concentration denote weak competition by ATP which, at almost physiological concentration (0.6 mM), causes only a 5.3-fold decrease in DMAT inhibition, as compared with 1 μM ATP concentration, whereas in the same range of ATP concentration the IC50 with CK2 increases 22.1-fold, doubling the value calculated with PIM1 (1.2 μM).
In vivo
Similar to Sorafenib, DMAT interfered with NFκ B activation and Wnt-signaling. Of the kinases inhibited by DMAT at almost equimolar IC50, CK2 and PIM-3 were found to be over-expressed or more active in hepatoma cells and human HCC tissue. Knockdown of PIM-3 or CK2 by shRNA revealed that both kinases are important for hepatoma cell proliferation and survival. DMAT, might represent a promising therapeutic approach in future HCC therapy.
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