PD 153035 hydrochloride
Chemical Name: 4-[(3-Bromophenyl)amino]-6,7-dimethoxyquinazoline hydrochloride
Biological ActivityAn extremely potent inhibitor of epidermal growth factor (EGF) receptor tyrosine kinase, with an IC50 of 25 pM. Inhibits other purified tyrosine kinases only at micromolar or higher concentrations.
The technical data provided above is for guidance only.
For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Tyrosine kinase inhibitors. 8. An unusually steep structure-activity relationship for analogues of 4-(3-bromoanilino)-6,7-dimethoxyquinazoline (PD 153035), a potent inhibitor of the epidermal growth factor receptor.
Bridges et al.
PD153035, a tyrosine kinase inhibitor, prevents epidermal growth factor receptor activation and inhibits growth of cancer cells in a receptor number-dependent manner.
Bos et al.
Clin.Cancer Res., 1997;3:2099
A specific inhibitor of the epidermal growth factor receptor tyrosine kinase.
Fry et al.
Citations for PD 153035 hydrochloride
The citations listed below are publications that use Tocris products. Selected citations for PD 153035 hydrochloride include:
5 Citations: Showing 1 - 5
Analysis of the Intrinsic Self-Organising Properties of Mesenchymal Stromal Cells in Three-Dimensional Co-Culture Models with Endothelial Cells.
Authors: Marshall Et al.
Bioengineering (Basel) 2018;5
Signaling pathways induced by serine proteases to increase intestinal epithelial barrier function.
Authors: Lahey Et al.
PLoS One 2017;12:e0180259
Hepatic nonparenchymal cells drive metastatic breast cancer outgrowth and partial epithelial to mesenchymal transition.
Authors: Taylor Et al.
Breast Cancer Res Treat 2014;144:551
Inhibition of epidermal growth factor receptor tyrosine kinase ameliorates collagen-induced arthritis.
Authors: Swanson Et al.
J Immunol 2012;188:3513
EGFR activation results in enhanced cyclooxygenase-2 expression through p38 mitogen-activated protein kinase-dependent activation of the Sp1/Sp3 transcription factors in human gliomas.
Cancer Res 2007;67:6121
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