PD 169316 |
Katalog-Nr.GC17737 |
PD 169316 ist ein potenter, zellgÄngiger und selektiver p38-MAP-Kinase-Inhibitor mit einem IC50-Wert von 89 nM. PD169316 hemmt selektiv die KinaseaktivitÄt des phosphorylierten p38, ohne stromaufwÄrts gelegene Kinasen daran zu hindern, p38 zu phosphorylieren. PD169316 zeigt antivirale AktivitÄt gegen Enterovirus71. PD169316 zeigt antivirale AktivitÄt gegen Enterovirus71.
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 152121-53-4
Sample solution is provided at 25 µL, 10mM.
IC50: A potent, selective and cell-permeable suppressor of p38 MAP kinase, with the IC50 value of 89 nM.
PD169316, a specific p38 MAPK inhibitor, blocks signal transduction mediated by both TGF-β and Activin A, but not bone morphogenetic protein (BMP) 4. Suppression on TGF-β signaling in a dose-dependent manner may then reduce Smad2 and Smad3 phosphorylation, block nuclear translocation and increase the expression of TGF-β target gene. [1]
In vitro: It was reported that pretreatment of CaOV3 cells with 10 M PD169316 caused a significant decrease in Smad2 and Smad3 phosphorylation which was mediated by TGF-β. The inhibitory effect of PD 169316 was proved to act in a dose-dependent manner. Study also demonstrated that PD169316 at 5 M or higher dose directly suppressed TGF-β signaling activity. [1]
In vivo: Based on an amyloid β (Aβ) rat model of Alzheimer's disease, the effect of PD 169316 on apoptosis induced by amyloid beta was examined. It was demonstrated that caspase-3 and Bax/Bcl-2 ratio, two marks of apoptosis, were significantly decreased in the rats pre-treated with PD169316 intracerebroventricularly. This study suggested the potential neuroprotective role of PD 169316 against the neuronal toxicity induced by Aβ. [2]
Clinical trial: So far, no clinical trial has been conducted.
References:
[1]Fu YX, O’Connor LM, Shepherd TG and Nachtigal MW. The p38 MAPK inhibitor, PD169316, inhibits transforming growth factor β-induced Smad signaling in human ovarian cancer cells. Biochem Bioph Res Co. 2003. 310: 3917.
[2]Ashabi G, Alamdary SZ, Ramin M and Khodagholi F. Reduction of hippocampal apoptosis by intracerebroventricular administration of extracellular signal-regulated protein kinase and/or P38 inhibitors in amyloid beta rat model of Alzheimer’s disease: involvement of nuclear-related factor-2 and nuclear factor-κb. Basic Clin. Pharmacol. Toxicol. 2013 Aug. 112: 145–55.
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