B I09, an IRE-1 RNase inhibitor with an IC50 of 1230 nM, inhibits splicing of XBP1 mRNA in human WaC3 cells and expression of xbp-1 in LPS-stimulated B cells. B I09 can be used to simulate the defects of XBP-1 in CLL cells., an IRE-1 RNase inhibitor with an IC50 of 1230 nM, inhibits splicing of XBP1 mRNA in human WaC3 cells and expression of xbp-1 in LPS-stimulated B cells. B I09 can be used to simulate the defects of XBP-1 in CLL cells., an IRE-1 RNase inhibitor with an IC50 of 1230 nM, inhibits splicing of XBP1 mRNA in human WaC3 cells and expression of xbp-1 in LPS-stimulated B cells. B I09 can be used to simulate the defects of XBP-1 in CLL cells.

IRE1 Rnase:1230 nM

B I09 is an IRE-1 RNase inhibitor, with an IC50 of 1230 nM[1] and it also is highly effective in inhibiting splicing of XBP1 mRNA in human WaC3 cells and the expression of XBP-1s in LPS stimulated B cells[2]. Treatment of CLL cells with this inhibitor (B I09) mimick XBP-1 deficiency, including upregulation of IRE-1 expression and compromised BCR signaling.

B I09 has a halflife of approximately 1.5 hours and reaches its peak concentration of approximately 39 μM in mouse plasma serum 15 minutes after administration. Administration of B I09 to CLL tumor-bearing mice suppress leukemic progression by inducing apoptosis. And it do not cause systemic toxicity[2].