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PD 169316

P38 MAPK inhibitor CAS# 152121-53-4

PD 169316

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Chemical structure

PD 169316

3D structure

Chemical Properties of PD 169316

Cas No. 152121-53-4 SDF Download SDF
PubChem ID 4712 Appearance Powder
Formula C20H13FN4O2 M.Wt 360.34
Type of Compound N/A Storage Desiccate at -20°C
Solubility DMSO : 12.5 mg/mL (34.69 mM; Need ultrasonic)
H2O : < 0.1 mg/mL (insoluble)
Chemical Name 4-[4-(4-fluorophenyl)-2-(4-nitrophenyl)-1H-imidazol-5-yl]pyridine
SMILES C1=CC(=CC=C1C2=NC(=C(N2)C3=CC=NC=C3)C4=CC=C(C=C4)F)[N+](=O)[O-]
Standard InChIKey BGIYKDUASORTBB-UHFFFAOYSA-N
Standard InChI InChI=1S/C20H13FN4O2/c21-16-5-1-13(2-6-16)18-19(14-9-11-22-12-10-14)24-20(23-18)15-3-7-17(8-4-15)25(26)27/h1-12H,(H,23,24)
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of PD 169316

DescriptionPD 169316 is a potent, cell-permeable and selective p38 MAP kinase inhibitor, with IC50 of 89 nM.In Vitro:PD169316 (10 μM) inhibits TGFβ and Activin A, but not BMP4 signaling in CaOV3 cells. PD169316 (0.2-20 μM) inhibits TGFβ-induced Smad2 nuclear translocation, Smad7 mRNA induction, and reporter gene activity in CaOV3 cells[1]. PD169316 (10 μM) shows a significantly increased rate of proliferation in Nestin knockdown cells, and can rescue the effect of Nestin knockdown on cell viability in the absence of EGF[2]. PD169316 significantly inhibits p38 MAP kinase activity with no significant change in ERK activity in PC12 cells. PD169316 (10 μM) blocks apoptosis induced by trophic factor withdrawal in differentiated PC12 cells[3].In Vivo:PD169316 (30 ng/5 μL) or in combination with U0126 improves spatial learning in MWM in Aβ-injected rats, 20 days after Aβ-injection. Pretreatment with U0126 and PD169316 decreases the levels of phosphorylated form of ERK and p38 to about 77.7 and 64.2%, respectively, and causes a significant increase in c-fos, p-CREB, NRF-1 and TFAM protein levels, compared to the Aβ-injected group[4].

References:
[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]. PD 169316, et al. ERK and p38 inhibitors attenuate memory deficits and increase CREB phosphorylation and PGC-1α levels in Aβ-injected rats. Behav Brain Res. 2012 Jun 15;232(1):165-73. [5]. Ayumi Iwasaki, et al. Molecular Mechanism Responsible for Fibronectin-controlled Alterations in Matrix Stiffness in Advanced Chronic Liver Fibrogenesis. THE JOURNAL OF BIOLOGICAL CHEMISTRY VOL. 291, NO. 1, pp. 72-88, January 1, 2016 [6]. Zhang Z, et al. PD169316, a specific p38 inhibitor, shows antiviral activity against Enterovirus71. Virology. 2017 Aug;508:150-158.

Protocol

Kinase Assay [3]
Sixteen hours after the removal of serum from Rat-1 fibroblasts or NGF from differentiated PC12 cells, the cells are incubated in the absence or presence of insulin (50 ng/mL) for 15 min at 37°C. After washing with 2 mL of ice-cold PBS, the cells are solubilized in 400 μL of ice-cold immunoprecipitation buffer containing 10 mM Tris, pH 7.4, 1% Triton X-100, 0.5% Nonidet P-40, 150 mM NaCl, 1 mM EDTA, 1 mM EGTA, 0.2 mM sodium orthovanadate, and 0.2 mM phenylmethylsulfonyl fluoride. The cell lysates are centrifuged to remove insoluble material, and 200 μg of the supernatant protein (400 μL, total volume) are incubated with 1 μg of anti-p38 antibodies for 1 h at 4°C followed by incubation with 30 μL of Protein G Plus/Protein A-agarose for an additional hour. The immunocomplexes are pelleted and washed twice in immunoprecipitation buffer and then once in kinase ish buffer (50 mM β-glycerolphosphate, 1 mM EGTA, 20 mM MgCl2, 100 μM sodium orthovanadate). The protein kinase assay is initiated by the addition of 20 μL of 2× reaction buffer (50 mMβ-glycerolphosphate, 1 mM EGTA, 20 mM MgCl2, 100 μM sodium orthovanadate, 0.1 mg/mL ATF-2 (N-terminal half), 50 μg/mL IP20, a peptide inhibitor of c-AMP dependent protein kinase, 200 μM ATP, and 0.9 mCi/mL [32P]ATP) to 20 μL of immune complex. The reaction is allowed to proceed for 10 min at 30°C and then terminated by the addition of 2× LaemmLi sample buffer and analyzed by SDS-polyacrylamide gel electrophoresis using 12% acrylamide gels. After electrophoresis, the gels are dried and subjected to phosphoimaging.

Animal Administration [4]
Adult male albino Wistar rats weighing 210-280 g are used in these experiments. Animals are divided into six groups: (A) Aβ-injected group, which receives bilateral intra-CA1 injection of Aβ (30 ng/3 μL PBS per side), 4 h after unilateral i.c.v. administration of DMSO (5 μL/rat), without receiving any treatment; (B) vehicle group, which only receives carrier, DMSO in lateral ventricle and PBS (3 μL/side) in both CA1 regions; (C) ERK inhibitor group, which receives i.c.v. infusion of U0126 (30 μg/5 μL 1% DMSO in PBS) with PBS injection (3 μL/side in CA1); (D) p38 inhibitor group, which receives i.c.v. infusion of PD169316 (30 μg/5 μL 1% DMSO in PBS) with PBS injection (3 μL/side in CA1); and (E) treatment group which receives i.c.v. administration of U0126 (30 μg/5 μL 1% DMSO in PBS), 4 h prior to intra-hippocampal A (30 ng/3 μL PBS per side) injection; (F) treatment group which receives i.c.v. administration of PD169316 (30 μg/5 μL 1% DMSO in PBS), 4 h prior to intra-hippocampal A (30 ng/3 μL PBS per side) injection. The aforementioned groups enter two experimental protocols: behavioral experiments and molecular studies. All the groups of animals in molecular study are considered as 7 and 20-day experimental groups.

References:
[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]. PD 169316, et al. ERK and p38 inhibitors attenuate memory deficits and increase CREB phosphorylation and PGC-1α levels in Aβ-injected rats. Behav Brain Res. 2012 Jun 15;232(1):165-73. [5]. Ayumi Iwasaki, et al. Molecular Mechanism Responsible for Fibronectin-controlled Alterations in Matrix Stiffness in Advanced Chronic Liver Fibrogenesis. THE JOURNAL OF BIOLOGICAL CHEMISTRY VOL. 291, NO. 1, pp. 72-88, January 1, 2016 [6]. Zhang Z, et al. PD169316, a specific p38 inhibitor, shows antiviral activity against Enterovirus71. Virology. 2017 Aug;508:150-158.

PD 169316 Dilution Calculator

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PD 169316 Molarity Calculator

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Preparing Stock Solutions of PD 169316

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.7752 mL 13.8758 mL 27.7516 mL 55.5031 mL 69.3789 mL
5 mM 0.555 mL 2.7752 mL 5.5503 mL 11.1006 mL 13.8758 mL
10 mM 0.2775 mL 1.3876 mL 2.7752 mL 5.5503 mL 6.9379 mL
50 mM 0.0555 mL 0.2775 mL 0.555 mL 1.1101 mL 1.3876 mL
100 mM 0.0278 mL 0.1388 mL 0.2775 mL 0.555 mL 0.6938 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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Background on PD 169316

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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References on PD 169316

Pd-Catalyzed Acyl C-O Bond Activation for Selective Ring-Opening of alpha-Methylene-beta-lactones with Amines.[Pubmed:28375015]

Org Lett. 2017 Apr 21;19(8):1966-1969.

A Pd-catalyzed ring-opening of beta-lactones with various types of amines (primary, secondary, and aryl) to provide beta-hydroxy amides with excellent selectivity toward acyl C-O bond cleavage is reported. The utility of this protocol is demonstrated in an asymmetric kinetic resolution providing enantioenriched alpha-methylene-beta-lactones.

CD8 T-cell regulation by T regulatory cells and the programmed cell death protein 1 pathway.[Pubmed:28375543]

Immunology. 2017 Jun;151(2):146-153.

The primary function of the immune system is to protect the host from infectious microorganisms and cancers. However, a major component of the immune response involves the direct elimination of cells in the body and the induction of systemic inflammation, which may result in life-threatening immunopathology. Therefore, the immune system has developed complex mechanisms to regulate itself with a specialized subset of CD4 T lymphocytes (referred to as regulatory T cells) and immune checkpoint pathways, such as the programmed cell death protein 1 pathway. These immune regulatory mechanisms can be exploited by pathogens and tumours to establish persistence in the host, warranting a deeper understanding of how to fine-tune immune responses during these chronic diseases. Here, I discuss various features of immune regulatory pathways and what important aspects must be considered in the next generation of therapies to reverse immune exhaustion, understanding that this process is a natural mechanism to prevent the host from destroying itself.

Pd(II)-Catalyzed Direct ortho-C-H Acylation of Aromatic Ketones by Oxidative Decarboxylation of alpha-Oxocarboxylic Acids.[Pubmed:28374587]

Org Lett. 2017 Apr 21;19(8):2082-2085.

A Pd-catalyzed decarboxylative acylation of aromatic ketones with alpha-oxocarboxylic acids was developed, and 1,2-diacylbenzenes were formed in up to 90% yield with excellent ortho-selectivity. This work demonstrates the first successful attempt to direct C-H acylation of aromatic ketones without the need for prederivatization to imines. The acylation reaction was inhibited by radical scavengers such as TEMPO, and 2,2,6,6-tetramethylpiperidin-1-yl benzoate, the adduct of TEMPO and a benzoyl radical, has been isolated and characterized. This finding is compatible with the intermediacy of acyl radicals. A mechanism involving the reaction of the palladacyclic complexes of aryl ketones with acyl radicals is proposed.

Isocyanide insertion across the Pd-C bond of allenyl and propargyl palladium complexes bearing phosphoquinoline as a spectator ligand. Synthesis of a palladium complex bearing a coordinated cyclobutenyl fragment.[Pubmed:28374876]

Dalton Trans. 2017 Apr 19;46(16):5210-5217.

We have studied the insertion of p-toluenesulfonylmethyl isocyanide (TosMIC) on selected allenyl and propargyl complexes of palladium bearing diphenylphosphine quinoline as a spectator ligand. The fast process gives different products depending on the tautomer involved in the reaction. Thus, the unsubstituted allenyl species yields an insertion complex with the isocyanide coordinated between the metal and the first allenyl carbon. On the other hand, a mixture of phenyl substituted allenyl and propargyl palladium complexes yields a novel species characterized by a cyclo-butenyl fragment directly coordinated to palladium. The solid state structure of such a complex together with an exhaustive kinetic study of the whole process is reported.

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.

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