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P9248

PD 169316

≥98% (HPLC), solid

Synonym(s):

4-(4-Fluorophenyl)-2-(4-nitrophenyl)-5-(4-pyridyl)-1H-imidazole

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$186.15

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$625.00

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About This Item

Empirical Formula (Hill Notation):
C20H13FN4O2
CAS Number:
152121-53-4
Molecular Weight:
360.34
MDL number:
MFCD12405019
UNSPSC Code:
12352200
PubChem Substance ID:
24278156
NACRES:
NA.77

Key Documents

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assay

≥98% (HPLC)

form

solid

color

faint yellow to dark orange

solubility

DMSO: >10 mg/mL
H2O: insoluble

originator

GlaxoSmithKline

storage temp.

2-8°C

SMILES string

[O-][N+](=O)c1ccc(cc1)-c2nc(-c3ccc(F)cc3)c([nH]2)-c4ccncc4

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)

InChI key

BGIYKDUASORTBB-UHFFFAOYSA-N

Gene Information

human ... MAPK14(1432)

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This Item
S7067513030559388
PD 169316 ≥98% (HPLC), solid

Sigma-Aldrich

P9248

PD 169316

SB 202190 ≥98% (HPLC)

Sigma-Aldrich

S7067

SB 202190

PD 169316 A potent, cell-permeable, reversible, competitive, and selective p38 MAP kinase inhibitor (IC50 = 89 nM).

Sigma-Aldrich

513030

PD 169316

SB 202190 SB 202190, CAS 152121-30-7, is a potent, reversible, competitive inhibitor of p38. Inhibits p38 phosphorylation of myelin basic protein. Blocks the activity of p38β (Ki = 16 nM; IC50 = 350 nM).

Millipore

559388

SB 202190

form

solid

form

powder

form

solid

form

solid

assay

≥98% (HPLC)

assay

≥98% (HPLC)

assay

≥98% (HPLC)

assay

≥98% (HPLC)

Quality Level

100

Quality Level

100

Quality Level

100

Quality Level

100

storage temp.

2-8°C

storage temp.

2-8°C

storage temp.

−20°C

storage temp.

−20°C

solubility

DMSO: >10 mg/mL, H2O: insoluble

solubility

DMSO: 10 mg/mL, clear

solubility

DMSO: 10 mg/mL

solubility

DMSO: 50 mg/mL

originator

GlaxoSmithKline

originator

GlaxoSmithKline

originator

-

originator

-

General description

PD 169316 is a pyridinyl imidazole compound. It is a potential inhibitor of p38 mitogen-activated protein kinases.[1] It also inhibits signalling transforming growth factor β (TGFβ), particularly in human ovarian cancer cells.[2]

Application

PD 169316 has been used for the inhibition of p38 enzyme in human hepatocytes.[3] It has been used in culture media to promote embryoid bodies differentiation.[4]

Biochem/physiol Actions

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

Features and Benefits

This compound was developed by GlaxoSmithKline. To browse the list of other pharma-developed compounds and Approved Drugs/Drug Candidates, click here.

pictograms

Skull and crossbonesCorrosion
GHS06,GHS05

signalword

Danger

Hazard Classifications

Acute Tox. 3 Oral - Eye Dam. 1 - Skin Irrit. 2 - STOT SE 3

target_organs

Respiratory system

Storage Class

6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

dust mask type N95 (US), Eyeshields, Faceshields, Gloves

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Certificates of Analysis (COA)

Lot/Batch Number
099K4609V
099K46091
099K4609
085K4611

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Inhibition of p38 kinase mimics survival signal-linked protection against apoptosis in rat cerebellar granule neurons
Nath R, et al.
Cellular & Molecular Biology Letters, 6(2), 173-184 (2001)
Activation of CD40 with platelet derived CD154 promotes reactive oxygen species dependent death of human hepatocytes during hypoxia and reoxygenation
Bhogal RH, et al.
PLoS ONE, 7(1), e30867-e30867 (2012)
The p38 MAPK inhibitor, PD169316, inhibits transforming growth factor beta-induced Smad signaling in human ovarian cancer cells
Fu Y, et al.
Biochemical and Biophysical Research Communications, 310(2), 391-397 (2003)
A p38MAPK-p53 cascade regulates mesodermal differentiation and neurogenesis of embryonic stem cells
Hadjal Y, et al.
Cell Death & Disease, 4(7), e737-e737 (2013)
Tony E Walshe et al.
Arteriosclerosis, thrombosis, and vascular biology, 29(8), 1185-1192 (2009-05-23)
Motivated by the central roles that vascular endothelial growth factor (VEGF) and transforming growth factor (TGF)-beta play in the assembly and maintenance of the vasculature, we examined the impact of systemic VEGF or TGF-beta signal inhibition on endothelial activation as
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