- PD 169316
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- $5.00 / 5KG
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2019-09-04
- CAS:152121-53-4
- Min. Order: 1KG
- Purity: 99%
- Supply Ability: 1ton
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| | PD 169316 Basic information |
| | 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 |
| 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. |
| | PD 169316 Preparation Products And Raw materials |
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