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关于此项目
经验公式(希尔记法):
C20H14O2S2
化学文摘社编号:
分子量:
350.45
UNSPSC Code:
12352200
NACRES:
NA.77
MDL number:
产品名称
p21-Activated Kinase Inhibitor III, IPA-3, The p21-Activated Kinase Inhibitor III, IPA-3, also referenced under CAS 42521-82-4, controls the biological activity of p21-Activated Kinase. This small molecule/inhibitor is primarily used for Phosphorylation & Dephosphorylation applications.
SMILES string
S(Sc3c4c(ccc3O)cccc4)c1c2c(ccc1O)cccc2
InChI
1S/C20H14O2S2/c21-17-11-9-13-5-1-3-7-15(13)19(17)23-24-20-16-8-4-2-6-14(16)10-12-18(20)22/h1-12,21-22H
InChI key
RFAXLXKIAKIUDT-UHFFFAOYSA-N
assay
≥97% (HPLC)
form
solid
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze
protect from light
color
yellow
solubility
DMSO: 10 mg/mL
ethanol: 2 mg/mL
shipped in
wet ice
storage temp.
−20°C
Quality Level
Disclaimer
Toxicity: Irritant (B)
General description
A cell-permeable symmetrical disulfide allosteric inhibitor that selectively targets the autoregulatory domain of group I, but not group II, PAKs (p21-activated kinases) and prevents the activation of PAK1/2/3 (% inhibition= 95, 70, and 60, respectively, with 10 µM inhibitor; IC50 = 2.5 µM for PAK1). Specificity test shows ≥ 50% inhibition, in the presence of 10 µM ATP and inhibitor, against 9 of 214 non-PAK human kinases. Shown to effectively suppress both basal and PDGF-induced PAK activation at 30 µM in mouse embryonic fibroblasts. IPA-3 does not inhibit the enzymatic activity of preactivated PAKs and reduction of the intramolecular disulfide bond of IPA-3 by DTT renders it inactive.
Other Notes
Deacon, S.W., et al. 2008. Chem. Biol.15, 322.
Packaging
Packaged under inert gas
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
signalword
Danger
hcodes
Hazard Classifications
Aquatic Acute 1 - Aquatic Chronic 1 - Eye Dam. 1
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Abinaya Raghavan et al.
iScience, 27(8), 110565-110565 (2024-08-26)
Astroglia play crucial neuroprotective roles by internalizing pathogenic aggregates and facilitating their degradation. Here, we show that α-SYN protofibril-induced organelle toxicities and reactive oxygen species (ROS) cause premature cellular senescence in astrocytes and astrocyte-derived cancer cells, resulting in a transient
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