Molecular Weight(MW): 474.55
XMD8-92 is a potent and selective BMK1/ERK5 inhibitor with Kd of 80 nM.
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Representative images (20x magnification, scale bar 100 μm) of tumor histology (H&E and trichrome staining) and IHC staining for DNA double strand breaks (DSBs, γH2AX staining) from control and Hsp90i+Erk5i treated mice on day 13.
Oncotarget, 2014, 5(10): 3145-58. XMD8-92 purchased from Selleck.
HL60 or U937 cells were pretreated with either BIX02189 (10 uM), PD 98059 (20 uM) or XMD8-92 (5 uM)for 1 h, then 1,25D (1 nM) was added for an additional 96 h on the 1,25D-induced CD11b and CD14 levels. Data collected using the ERK5 auto-phosphorylation inhibitor XMD8-92 (5 μM) are also included. *, p< 0.05; and **, p< 0.01 versus control. ◆, p< 0.05; and ◆◆, p< 0.01 versus 1,25D alone.
J Cell Physiol, 2014, 229(7): 856-67. XMD8-92 purchased from Selleck.
The mRNA level of DCLK1 after MET or ERK5 inhibition in mesothelioma cells. The mRNA level of DCLK1 in (A) H290 and (B) H513 cells treated with MET inhibitor XL184 or ERK5 inhibitor XMD8-92 measured using quantitative real-time PCR (*P<0.0001, one-way ANOVA and Scheffe multiple comparisons).
Int J Oncol, 2017, 51(1):91-103. XMD8-92 purchased from Selleck.
(A) RAW264.7D clone cells were cultured with 50 ng/ml sRANKL in the presence or absence of BIX02189. The formation of TRAP-positive MNCs was inhibited when the concentration of BIX02189 reached 4 μM. (B) An experiment similar to A was conducted with XMD8-92. (C) The total proteins were extracted from the cells treated with BIX02189 for 6 hrs, and the phosphorylation of ERK5 and ERK1,2 was analyzed by Western blot analysis. (D) Cell viabilities during the experiments were analyzed. Cells were incubated with drugs for 1 day (dark gray bars) or 2 days (light gray ones).
PLoS One, 2015, 10(4):e0125054. XMD8-92 purchased from Selleck.
Purity & Quality Control
Choose Selective ERK Inhibitors
|Description||XMD8-92 is a potent and selective BMK1/ERK5 inhibitor with Kd of 80 nM.|
XMD8-92, via inhibition of BMK1 activation, significantly induces p21 expression in cells, and mediates suppression of cancer cell proliferation.  XMD8-92 markedly abrogates the inhibitive effects of hydroxysafflor yellow A (HSYA) on hepatic stellate cell (HSC) activation, and blockes the HSYA-mediated MEF2C down-regulation. 
|In vivo||XMD8-92 (50 mg/kg i.p.) significantly inhibit the growth of the xenografted human or syngeneic mouse tumors by blocking tumor cell proliferation and tumor-associated angiogenesis.  XMD8-92 inhibits pancreatic tumor xenograft growth by significant downregulation of DCLK1 and several of its downstream targets. |
|In vitro||DMSO||73 mg/mL warmed (153.82 mM)|
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