Background:

Tetrabromocinnamic Acid (TBCA) is a new class of specific protein kinase CK2 inhibitors [1].

Protein kinases have been involved in catalyzing the phosphorylation of serine, threonine and tyrosine residues in protein substrates that play dominant roles in controlling nearly all cellular functions. The Ser/Thr-specific protein kinase CK2 has been implicated in signal transduction, gene expression, DNA repair, RNA and protein synthesis. CK2 is invariably elevated in a wide spectrum of tumours [1].

In vitro: TBCA was a selective, cell-permeable inhibitor of CK2 with an IC50 of 0.11 μM. The Ki value was 77 nM. TBCA showed minimal effect on a panel of 28 other kinases. TBCA induced cell death in Jurkat adult T cell leukemia cells with an DC50 of 7.7 μM [1]. TBCA dose-dependently inhibited platelet aggregation and secretion induced by various agonists including 2-MeSADP, AYPGKF, SFLLRN, and CRP [2]. TBCA also significantly inhibited agonist-induced thromboxane A2 (TxA2) generation and ERK phosphorylation. TBCA significantly inhibited platelet spreading on immobilized fibrinogen surface and clot retraction mediated by integrin αIIbβ3 signaling [2].

参考文献:
[1] Pagano M A, Poletto G, Di Maira G, et al.? Tetrabromocinnamic acid (TBCA) and related compounds represent a new class of specific protein kinase CK2 inhibitors[J]. Chembiochem, 2007, 8(1): 129-139.
[2] Ryu S Y, Kim S.? Evaluation of CK2 inhibitor (E)-3-(2, 3, 4, 5-tetrabromophenyl) acrylic acid (TBCA) in regulation of platelet function[J]. European journal of pharmacology, 2013, 720(1): 391-400.