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Catalog No.S7525

12 publications

XMD8-92 Chemical Structure

CAS No. 1234480-50-2

XMD8-92 is a potent and selective BMK1/ERK5 inhibitor with Kd of 80 nM.

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Selleck's XMD8-92 has been cited by 12 publications

5 Customer Reviews

  • 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.

    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.

    (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.

  • Scutellarin activated extracellular-regulated kinase 5 (Erk5) pathway after subarachnoid hemorrhage (SAH). (A) Representative western blot bands of Kruppel-like factor 2 (KLF2), phosphorylated-Erk5 and Erk5 expression in the ipsilateral hemisphere. (B) Quantification analysis of KLF2 expression in the left/ipsilateral hemisphere at 48 h after SAH (n = 3). (C) Quantification analysis of p-Erk5 expression in the left/ipsilateral hemisphere at 48 h after SAH (n = 3). (D) Quantification analysis of Erk5 expression in the left/ipsilateral hemisphere at 48 h after SAH (n = 3). Sham (n = 15), not subjected to any treatment or intervention; SAH + vehicle (n = 24), intracerebroventricularly administered normal saline after SAH surgery; SAH + SCU (n = 22), intracerebroventricularly injected 100 mg/kg SCU (Sigma–Aldrich) at the concentration of 50 lM [16] immediately after SAH; and SAH + SCU + XMD8-92 (n = 23), intracerebroventricularly injected same amount of SCU plus 10 lM XMD8-92 (100 mg/kg; Selleck Chemicals) immediately after the SAH surgery. Erk5 = extracellular-regulated kinase 5, KLF2 = Kruppel-like factor 2, SCU = scutellarin; *p < 0.05 vs. sham; #p < 0.05 vs. SAH + vehicle; &p < 0.05 vs. SAH + SCU.

    J Clin Neurosci, 2016, 34:264-270. XMD8-92 purchased from Selleck.

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Choose Selective ERK Inhibitors

Biological Activity

Description XMD8-92 is a potent and selective BMK1/ERK5 inhibitor with Kd of 80 nM.
BMK1 [1]
(Cell-free assay)
80 nM(Kd)
In vitro

XMD8-92, via inhibition of BMK1 activation, significantly induces p21 expression in cells, and mediates suppression of cancer cell proliferation. [1] 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. [2]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
human HeLa cells NFrMU5RHfW6ldHnvckBie3OjeR?= NUHLR|hOUW6qaXLpeIlwdiCxZjDFS2YucW6mdXPl[EBDVUtzIHH1eI9xcG:|cHjvdplt[XSrb36gbY4hcHWvYX6gTIVN[SClZXzsd{BjgSCVRGOtVGFITSCjbnHsfZNqeyxiSVO1NF0xNjJ2IN88US=> MmO3NlE1OTJ2ME[=

... Click to View More Cell Line Experimental Data

Methods Test Index PMID
Western blot

PubMed: 22869143     

A549 cells were treated with XMD8-92 (4 μM) for 0, 8, 16, 24, 32 and 40 hours. Cell lysates were analyzed by western blot using anti-p53 or anti-GAPDH antibodies.

BMK1 / p-BMK1 ; 

PubMed: 22869143     

Tumor homogenates from Nod/Scid mice subcutaneously injected with HeLa or A549 cells and treated with control, doxorubicin, XMD8-92 or doxorubicin+XMD8-92 for 30 hr were used in western blot to detect BMK1, p53 and GAPDH expression. n = 3 mice per group. 


PubMed: 22869143     

Pml+/+ MEF and Pml−/− MEF cells were treated with XMD8-92 (4 μM) and/or doxorubicin (300 nM) for about 24 hr and stained using anti-PML, anti-MDM2, and anti-Nucleolin antibodies. Arrows indicate translocation of MDM2 to the nucleoli.

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. [1] XMD8-92 inhibits pancreatic tumor xenograft growth by significant downregulation of DCLK1 and several of its downstream targets. [3]


Animal Research:


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  • Animal Models: Nod/Scid mice bearing HeLa xenograft, C57Bl/6 mice bearing LL/2 xenograft
  • Dosages: ~50 mg/kg twice a day
  • Administration: i.p.
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 73 mg/mL warmed (153.82 mM)
Water Insoluble
Ethanol Insoluble

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 474.55


CAS No. 1234480-50-2
Storage powder
in solvent
Synonyms N/A
Smiles CCOC1=C(C=CC(=C1)N2CCC(CC2)O)NC3=NC=C4C(=N3)N(C5=CC=CC=C5C(=O)N4C)C

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ERK Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID