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PD 169316

CAT: 0804-HY-10578-01Size: 5 mgDry Ice: NoHazardous: No
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CAT#:0804-HY-10578-01Size:5 mg
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24/48H Stock Items & 2 to 6 Weeks non Stock Items.
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Description
PD 169316 is a potent, cell-permeable and selective p38 MAP kinase inhibitor, with IC50 of 89 nM. PD169316 selectively inhibits the kinase activity of the phosphorylated p38 without hindering upstream kinases to phosphorylate p38. PD169316 shows antiviral activity against Enterovirus71. PD169316 shows antiviral activity against Enterovirus71.
CAS Number
152121-53-4
UNSPSC
12352005
Hazard Statement
H301, H315, H318, H335
Target
Autophagy; Enterovirus; p38 MAPK
Type
Reference compound
Related Pathways
Anti-infection; Autophagy; MAPK/ERK Pathway
Applications
Cancer-Kinase/protease
Field of Research
Cancer
Assay Protocol
https://www.medchemexpress.com/pd-169316.html
Purity
98.60
Solubility
DMSO : 12.5 mg/mL (ultrasonic)
Smiles
FC(C=C1)=CC=C1C2=C(C3=CC=NC=C3)NC(C4=CC=C([N+]([O-])=O)C=C4)=N2
Molecular Formula
C20H13FN4O2
Molecular Weight
360.34
Precautions
H301, H315, H318, H335
References & Citations
[1]Fu Y, et al. The p38 MAPK inhibitor, PD169316, inhibits transforming growth factor beta-induced Smad signaling in human ovarian cancer cells. Biochem Biophys Res Commun. 2003 Oct 17;310 (2) :391-7.|[2]Hu W, et al. Suppression of Nestin reveals a critical role for p38-EGFR pathway in neural progenitor cell proliferation. Oncotarget. 2016 Dec 27;7 (52) :87052-87063.|[3]Kummer JL, et al. Apoptosis induced by withdrawal of trophic factors is mediated by p38 mitogen-activated protein kinase. J Biol Chem. 1997 Aug 15;272 (33) :20490-4.|[4]Khan JA, et al. p38 and p42/44 MAPKs differentially regulate progesterone receptor A and B isoform stabilization. Mol Endocrinol. 2011 Oct;25 (10) :1710-24.|[5]Zhang Z, et al. PD169316, a specific p38 inhibitor, shows antiviral activity against Enterovirus71. Virology. 2017 Aug;508:150-158.
Shipping Conditions
Room Temperature
Storage Conditions
-20°C, 3 years; 4°C, 2 years (Powder)
Scientific Category
Reference compound1
Clinical Information
No Development Reported

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