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XMD8-92BMK1/ERK5 inhibitor,highly selective

XMD8-92

Catalog No. A3943
Size Price Stock Qty
10mM (in 1mL DMSO) $110.00 In stock
10mg $75.00 In stock
50mg $300.00 In stock
100mg $460.00 In stock

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Sample solution is provided at 25 µL, 10mM.

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Chemical structure

XMD8-92

Biological Activity

Description XMD8-92 is a potent and selective inhibitor of BMK1/ERK5 with Kd of 80 nM.
Targets BMK1/ERK5          
IC50 Kd=80 nM          

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Chemical Properties

Cas No. 1234480-50-2 SDF Download SDF
Chemical Name 2-[2-ethoxy-4-(4-hydroxypiperidin-1-yl)anilino]-5,11-dimethylpyrimido[4,5-b][1,4]benzodiazepin-6-one
Canonical SMILES CCOC1=C(C=CC(=C1)N2CCC(CC2)O)NC3=NC=C4C(=N3)N(C5=CC=CC=C5C(=O)N4C)C
Formula C26H30N6O3 M.Wt 474.57
Solubility >23.8mg/mL in DMSO Storage Store at -20°C
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
Shipping Condition Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request

Background

IC50: 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 [1].
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.
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 [2].
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 [3].
Clinical trial: XMD8-92 is still at preclinical development stage up to this point.
Reference:
[1] Yang Q, Lee JD. Targeting the BMK1 MAP kinase pathway in cancer therapy. Clin Cancer Res. 2011;17(11):3527-32.
[2] Sureban SM, May R, Weygant N, Qu D, Chandrakesan P, Bannerman-Menson E, Ali N, Pantazis P, Westphalen CB, Wang TC, Houchen CW. XMD8-92 inhibits pancreatic tumor xenograft growth via a DCLK1-dependent mechanism. Cancer Lett. 2014;351(1):151-61.
[3] Yang Q, Deng X, Lu B, Cameron M, Fearns C, Patricelli MP, et al. Pharmacological inhibition of
BMK1 suppresses tumor growth through promyelocytic leukemia protein. Cancer Cell. 2010;18:258–67.