506154
Pifithrin-α, p-Nitro, Cyclic
A cell-permeable p53 inhibitor that exhibits 10-fold higher potency and 50% longer half-life than Pifithrin-α.
别名:
Pifithrin-α, p-Nitro, Cyclic, 2-(4-Nitrophenyl)imidazo[2,1-b]-5,6,7,8-tetrahydrobenzothiazole
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关于此项目
经验公式（希尔记法）:
C15H13N3O2S
化学文摘社编号:
分子量:
299.35
MDL number:
UNSPSC Code:
12352200
NACRES:
NA.77
产品名称
Pifithrin-α, p-Nitro, Cyclic, A cell-permeable p53 inhibitor that exhibits 10-fold higher potency and 50% longer half-life than Pifithrin-α.
InChI key
XMFNSEDROOHGBY-UHFFFAOYSA-N
InChI
1S/C15H13N3O2S/c19-18(20)11-7-5-10(6-8-11)12-9-17-13-3-1-2-4-14(13)21-15(17)16-12/h5-9H,1-4H2
SMILES string
[s]1c2[n](c4c1CCCC4)cc(n2)c3ccc(cc3)[N+](=O)[O-]
assay
≥95% (HPLC)
form
solid
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze
protect from light
color
yellow
solubility
DMSO: 2.5 mg/mL
ethanol: 250 μg/mL
shipped in
ambient
storage temp.
−20°C
Quality Level
Biochem/physiol Actions
Cell permeable: yes
ED50 = 30 nM in protecting etoposide-induced cortical neuron death
Primary Target
p53
p53
Product does not compete with ATP.
Reversible: no
Disclaimer
Toxicity: Standard Handling (A)
General description
A cell-permeable p53 inhibitor that exhibits 10-fold higher potency (ED50 = 30 nM in protecting etoposide-induced cortical neuron death) and 50% longer half-life (t1/2 = 6h in neuron culture medium at 37°C) than Pifithrin-α (Cat. No. 506132). However, despite its in vitro efficacy, this inhibitor is not effective when adminstered in rats in vivo. For in vivo applications, please consider Pifithrin-α, p-Nitro (Cat. No. 506152).
Other Notes
Pietrancosta, N., et al. 2006. J. Med. Chem.49, 3645.
Packaging
Packaged under inert gas
Preparation Note
Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
存储类别
11 - Combustible Solids
wgk
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
Richard A Zager et al.
American journal of physiology. Renal physiology, 316(4), F674-F681 (2019-01-31)
The cyclin kinase inhibitor p21 is acutely upregulated during acute kidney injury (AKI) and exerts cytoprotective effects. A proposed mechanism is oxidant stress-induced activation of p53, the dominant p21 transcription factor. Glycerol-induced rhabdomyolysis induces profound renal oxidant stress. Hence, we
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