GSK-J5 hydrochloride is a cell-permeable ester derivative of GSK J2 (HY-15648A), inactive. GSK-J5 hydrochloride is also an isomer of GSK-J4 (HY-15648B) and often used as a negative group^[1].

GSK-J5 (25 μM) has no effects at inhibiting the LPS-induced response of human primary macrophages derived from healthy volunteers. While GSK-J4 significantly reduced the expression of 16 of 34 LPS-driven cytokines as assessed by PCR array, such as TNF-α^[1].
GSK-J5 (30 μM; 6 hours) is the inactive isomer of GSK-J4, has no effect on TNF-α protein production. But neither GSK-J4 nor GSK-J5 directly affects the levels of LPS-induced JMJD3 or of LPS-independent UTX and EZH2^[1].
GSK-J5 (30 μM; 1 hour) can not prevent the LPS-induced loss of H3K27me3 associated with the TNFA TSS or block the recruitment of RNA polymerase II to this locus but GSK-J5 can. Finally, GSK-J4, but not GSK-J5, blocks the production of TNF-α by macrophages derived from patients with rheumatoid arthritis^[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

453.96

C₂₄H₂₈ClN₅O₂

1797983-32-4

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Laurens Kruidenier, et al. A selective jumonji H3K27 demethylase inhibitor modulates the proinflammatory macrophage response. Nature. 2012 Aug 16;488(7411):404-8.