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PD 169316 CAS NO.152121-53-4
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- Min.Order: 100 Gram
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≥98.0%(100-500)Gram≥98.0%(1000-5000)Gram
- Product Details
Keywords
- PD 169316
- 4-[4-(4-Fluorophenyl)-2-(4-nitrophenyl)-1H-imidazol-5-yl]pyridine;4-[5-(4-fluorophenyl)-2-(4-nitrophenyl)-1H-iMidazol-4-yl]pyridine;Pyridine, 4-[4-(4-fluorophenyl)-2-(4-nitrophenyl)-1H-iMidazol-5-yl]-
- 152121-53-4
Quick Details
- ProName: PD 169316
- CasNo: 152121-53-4
- Molecular Formula: C20H13FN4O2
- Appearance: White crystal
- Application: CAS：152121-53-4； Aromatics;Heterocycl...
- DeliveryTime: 2 months
- PackAge: 100g,500g,1kg,25kg
- Port: shang hai
- ProductionCapacity: 1000 Gram/Month
- Purity: 98%
- Storage: Dry seal
- Transportation: shipping
- LimitNum: 100 Gram
Superiority
We are committed to provide excellence in researching, manufacturing and drug discovery process.
Our research team of scientists consists of western-trained Ph.D.s with experience and capabilities in drug R&D methodologies and medicinal chemistry.
Details
PD 169316 is a potent, cell-permeable and selective p38 MAP kinase inhibitor (IC50 = 89 nM).
IC50 Value: 89 nM
Target：p38 MAPK
in vitro: PD169316, a p38 MAPK inhibitor, abrogates signaling initiated by both TGFbeta and Activin A, but not bone morphogenetic protein (BMP) 4. Inhibition of TGFbeta signaling is dose dependent and results in reduced Smad2 and Smad3 phosphorylation, nuclear translocation, and up-regulation of the TGFbeta target gene Smad7. Reduced TGFbeta signaling is not due to abrogation of p38 MAPK activity, since blocking p38 MAPK activity with a dominant negative form of p38 MAPK has no effect on TGFbeta/Smad signaling. PD169316 at 5 μM or higher can block TGFβ signaling activity and thus caution must be used when attributing cellular activities exclusively to p38 MAPK signaling when these inhibitors are used experimentally [1]. PD169316 significantly attenuated apoptosis in potassium-deprived cells in a dose dependent manner [2]. PD169316 rescued the inhibitory effect of sphingosine on the formation of inositol phosphates by PGF(2alpha) or NaF in osteoblast-like MC3T3-E1 cells [3]. 6-keto-PGF(1alpha) release was increased in a concentration-dependent manner following LPS exposure (maximal at 10(-6)g/ml; EC(50) = 1 x 10(-9)g/ml), and was significantly inhibited by p38 MAPK blockade (reduced from 1.6+/-0.3 x 10(-9)g/ml to 4+/-1 x 10(-10)g/ml and 4+/-2 x 10(-10)g/ml with 10(-6) M SB203580 or 10(-6) M PD169316, respectively) [4].