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506126

Sigma-Aldrich

p38 MAP Kinase Inhibitor

The p38 MAP Kinase Inhibitor, also referenced under CAS 219138-24-6, controls the biological activity of p38 MAP Kinase. This small molecule/inhibitor is primarily used for Phosphorylation & Dephosphorylation applications.

Synonym(s):

p38 MAP Kinase Inhibitor, 2-(4-Chlorophenyl)-4-(4-fluorophenyl)-5-pyridin-4-yl-1,2-dihydropyrazol-3-one

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About This Item

Empirical Formula (Hill Notation):
C20H13ClFN3O
CAS Number:
219138-24-6
Molecular Weight:
365.79
UNSPSC Code:
12352200

Quality Level

100

Assay

≥95% (HPLC)

form

solid

potency

35 nM IC50

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze
protect from light

color

pale yellow

solubility

DMSO: 25 mg/mL

shipped in

ambient

storage temp.

−20°C

InChI

1S/C20H13ClFN3O/c21-15-3-7-17(8-4-15)25-20(26)18(13-1-5-16(22)6-2-13)19(24-25)14-9-11-23-12-10-14/h1-12,24H

InChI key

DZFBYHUKZSRPHU-UHFFFAOYSA-N

General description

A potent p38 MAP kinase inhibitor (IC50 = 35 nM).

Biochem/physiol Actions

Cell permeable: no
Product does not compete with ATP.
Reversible: no

Packaging

Packaged under inert gas

Warning

Toxicity: Standard Handling (A)

Other Notes

de Laszlo, S.E., et al. 1998. Bioorg. Med. Chem. Lett. 8, 2689.

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Storage Class Code

11 - Combustible Solids

WGK

WGK 1

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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S E de Laszlo et al.
Bioorganic & medicinal chemistry letters, 8(19), 2689-2694 (1999-01-05)
Investigation of furans, pyrroles and pyrazolones identified 3-pyridyl-2,5-diaryl-pyrroles as potent, orally bioavailable inhibitors of p38 kinase. 3-(4-pyridyl-2-(4-fluoro-phenyl)-5-(4-methylsulfinylphenyl)-pyrrol e (L-167307) reduces secondary paw swelling in the rat adjuvant arthritis model: ID50 = 7.4 mg/kg/b.i.d.
Guoqi Zhang et al.
Cancer research, 68(6), 1691-1696 (2008-03-15)
One of the physiologic consequences of excessive UV radiation (UVR) exposure is apoptosis. This critical response serves to eliminate genetically injured cells and arises, in part, from activation of DNA damage and p53 signaling. Other contributory pathways, however, likely exist
Charles B Trelford et al.
Frontiers in cell and developmental biology, 9, 712124-712124 (2021-11-12)
The mechanism(s) in which transforming growth factor beta 1 (TGFβ) modulates autophagy in cancer remain unclear. Here, we characterized the TGFβ signaling pathways that induce autophagy in non-small cell lung cancer cells, using cells lines stably expressing GFP-LC3-RFP-LC3ΔG constructs that

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