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About This Item
Empirical Formula (Hill Notation):
C16H12N3FS
CAS Number:
Molecular Weight:
297.35
NACRES:
NA.77
PubChem Substance ID:
UNSPSC Code:
12352200
MDL number:
InChI
1S/C16H12FN3S/c17-13-3-1-11(2-4-13)14-15(12-5-7-18-8-6-12)20-9-10-21-16(20)19-14/h1-8H,9-10H2
SMILES string
Fc1ccc(cc1)-c2nc3SCCn3c2-c4ccncc4
InChI key
YOELZIQOLWZLQC-UHFFFAOYSA-N
assay
≥98% (HPLC)
form
solid
storage condition
protect from light
color
off-white
mp
189-190 °C (lit.)
solubility
DMSO: soluble >10 mg/mL
storage temp.
2-8°C
Quality Level
Gene Information
human ... IL1B(3553), TNF(7124)
rat ... Alox5(25290)
Related Categories
Biochem/physiol Actions
p38 MAP kinase inhibitor.
Storage Class
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
dust mask type N95 (US), Eyeshields, Gloves
Regulatory Information
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M Pouliot et al.
Journal of immunology (Baltimore, Md. : 1950), 158(10), 4930-4937 (1997-05-15)
Prostaglandin endoperoxide synthase (PGHS; cyclooxygenase), the rate-limiting enzyme in the conversion of arachidonic acid to prostanoids, has two isoforms. PGHS-1 is constitutively expressed and involved in homeostasis, whereas PGHS-2 is inducible in monocytes in response to proinflammatory agents. Using freshly
Maria Tsirigotis et al.
PloS one, 3(5), e2130-e2130 (2008-05-08)
The signaling pathways that may modulate the pathogenesis of diseases induced by expanded polyglutamine proteins are not well understood. Herein we demonstrate that expanded polyglutamine protein cytotoxicity is mediated primarily through activation of p38MAPK and that the atypical PKC iota
B Schnyder et al.
The Biochemical journal, 331 ( Pt 2), 489-495 (1998-06-11)
Intracellular phosphorylations polymorphonuclear neutrophils are mediated by kinases, including mitogen activated-protein (MAP) kinases and phosphatidylinositol 3-kinase. In the present study we demonstrate their effector functions upon both ligation of cell-surface seven-transmembrane-spanning receptors by bacterial peptide formylmethionyl-leucylphenylalanine as well as in
A Sodhi et al.
Cancer research, 60(17), 4873-4880 (2000-09-15)
The elucidation of the molecular mechanisms governing the transition from a nonangiogenic to an angiogenic phenotype is central for understanding and controlling malignancies. Viral oncogenes represent powerful tools for disclosing transforming mechanisms, and they may also afford the possibility of
Javier Hernández Losa et al.
Oncogene, 22(26), 3998-4006 (2003-06-25)
p38 MAPK has been implicated in the response to cancer therapy. To determine whether the activation of p38 MAPK could be specific to cancer therapy, we investigated the activation of p38 MAPK in response to several chemotherapeutic agents, such as
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