Enzymes for Research, Diagnostic and Industrial Use


Cat No.
XMD8-92 is a potent and selective inhibitor of BMK1/ERK5 with Kd of 80 nM.
Product Overview
XMD8-92 has been synthesized as a potent inhibitor of Mitogen-activated protein kinase 7 (MAPK7/BMK1; Kd = 80 nM). XMD8-92 blocks EGF-induced activation of BMK1 with IC50 of 240 nM. The mitogen-activated protein kinases (MAPKs) are crucial components of signaling cascades that regulate numerous physiological processes. Four MAPK pathways have been identified thus far, including extracelluar-signal-regulated kinase 1/2 (ERK1/2), c-Jun-amino-terminal kinase (JNK), p38, and BMK1.XMD8-92 is a MAPKs kinase inhibitor with anti-cancer activity against lung and cervical cancers. Clinical trial: XMD8-92 is still at preclinical development stage up to this point.
Molecular Weight
Store at -20°C
Kd=80 nM
Molecular Formula
Chemical Name
Soluble in DMSO > 10 mM
Shipping Conditions
Evaluation sample solution: ship with blue ice. All other available size: ship with RT, or blue ice upon request
In vitro
In a previous study, XMD8-92 was shown to inhibit AsPC-1 cancer cell proliferation and tumor xenograft growth. In XMD8-92 treated tumors, significant downregulation of DCLK1was found and several of its downstream targets, including c-MYC, KRAS, NOTCH1, ZEB1, ZEB2, SNAIL, SLUG, OCT4, SOX2, NANOG, KLF4, LIN28, VEGFR1, and VEGFR2) via upregulation of tumor suppressor miRNAs, such as let-7a, miR-144, miR-200a-c, and miR-143/145.XMD8-92 was, however, not found to affect BMK1 downstream genes p21 and p53.These findings suggested that XMD8-92 treatment led to the inhibition of DCLK1 and downstream oncogenic pathways, which would be a promising chemotherapeutic agent against PDAC.
In vivo
In both immunocompetent and immunodeficient mice, XMD8-92 treatment was found to able to block the growth of lung and cervical xenograft tumors, respectively, by 95%. This remarkable anti-tumor effect of XMD8-92 in lung and cervical xenograft tumor models was due to its capacity to inhibit tumor cell proliferation through the PML suppressioninducted p21 checkpoint protein, as well as by blocking of the contribution of BMK1 in tumorassociated angiogenesis.
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