PD 169316 Chemical Properties

Boiling point:

583.1±50.0 °C(Predicted)

Density 

1.354±0.06 g/cm3(Predicted)

storage temp. 

2-8°C

solubility 

DMSO: >10mg/mL

pka

9.09±0.10(Predicted)

form 

solid

color 

light orange

Safety Information

Hazard Codes 

Xn

Risk Statements 

22-37/38-41

Safety Statements 

26-39

RIDADR 

UN 2811 6.1/PG 3

WGK Germany 

3

HS Code 

2933399990

PD 169316 Usage And Synthesis

Description

p38 is a member of the mitogen-activated protein kinase (MAPK) superfamily of enzymes that play an important role in signal transduction. PD 169316 is a selective inhibitor of p38 MAPK. It inhibits p38 MAPK with an IC₅₀ of 89 nM, whereas the IC₅₀s are >100-fold higher for extracellular signal-regulated kinase (ERK) and >1,000-fold higher for protein kinase A (PKA) and PKCα. PD 169316 inhibits apoptosis of neuronal and non-neuronal cells deprived of specific trophic factors such as potassium or nerve growth factor.

Uses

PD 169316 is a highly selective, potent inhibitor of p38 MAP kinase. PD 169316 inhibits transforming growth factor β-induced Smad signaling in human ovarian cancer cells. PD 169316 acts as an an endogenous suppressor of apoptosis by mimicking CD9, a membrane tetraspanin. Studies show that PD 169316 reduces myocardial ischemia/reperfusion induced voltage-dependent anion channel(VDAC) phosphorylation

Uses

PD 169316 has been used for the inhibition of p38 enzyme in human hepatocytes. It has been used in culture media to promote embryoid bodies differentiation.

Definition

ChEBI: 4-[4-(4-fluorophenyl)-2-(4-nitrophenyl)-1H-imidazol-5-yl]pyridine is a member of imidazoles.

General Description

PD 169316 is a pyridinyl imidazole compound. It is a potential inhibitor of p38 mitogen-activated protein kinases. It also inhibits signalling transforming growth factor β (TGFβ), particularly in human ovarian cancer cells.

Biochem/physiol Actions

Potent, cell-permeable and selective p38 MAP kinase inhibitor (IC50 = 89 nM).

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]

IC 50

a potent, selective and cell-permeable suppressor of p38 map kinase, with the ic50 value of 89 nm.

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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