506132
Pifithrin-α
≥95% (HPLC), solid, p53 inhibitor, Calbiochem®
别名:
Pifithrin-α, 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1- p-tolylethanone, HBr
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关于此项目
经验公式（希尔记法）:
C16H18N2OS · xHBr
化学文摘社编号:
分子量:
286.39 (free base basis)
UNSPSC Code:
12352200
NACRES:
NA.77
MDL number:
Assay:
≥95% (HPLC)
Form:
solid
Quality level:
Storage condition:
OK to freeze, protect from light
产品名称
Pifithrin-α, A cell-permeable chemical inhibitor of p53.
SMILES string
[s]1c2c([n+](c1N)CC(=O)c3ccc(cc3)C)CCCC2.[Br-]
InChI
1S/C16H18N2OS.BrH/c1-11-6-8-12(9-7-11)14(19)10-18-13-4-2-3-5-15(13)20-16(18)17;/h6-9,17H,2-5,10H2,1H3;1H
InChI key
HAGVCKULCLQGRF-UHFFFAOYSA-N
assay
≥95% (HPLC)
form
solid
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze, protect from light
color
off-white
solubility
DMSO: 100 mg/mL
shipped in
ambient
storage temp.
−20°C
Quality Level
General description
A cell-permeable chemical inhibitor of p53. Reversibly inhibits p53-dependent transactivation of p53-responsive genes and reversibly blocks p53-mediated apoptosis. Inhibits p53-dependent growth arrest of human diploid fibroblasts in response to DNA damage but has no effect on p53-deficient fibroblasts. Protects normal tissues from the deleterious side effects of chemotherapy. Has been reported to protect neurons against β-amyloid peptide and glutamate-induced apoptosis.
A reversible inhibitor of p53-dependent transactivation of p53-responsive genes and reversibly blocks p53-mediated apoptosis. Inhibits p53-dependent growth arrest of human diploid fibroblasts in response to DNA damage but has no effect on p53-deficient fibroblasts. Protects mice from lethal genotoxic stress associated with anticancer treatment without promoting tumor formation. Has been reported to protect neurons against β-amyloid and glutamate-induced apoptosis.
Biochem/physiol Actions
Cell permeable: yes
Primary Target
PS3
PS3
Product does not compete with ATP.
Reversible: yes
Packaging
Packaged under inert gas
Preparation Note
Following reconstitution, aliquot into cold tubes and freeze (-20°C). Stock solutions in DMSO are stable for 3 months at -20°C. Unstable in aqueous solutions.
Other Notes
Murphy, P.J.M., et al. 2004. J. Biol. Chem.279, 30195.
Culmsee, C., et al. 2001. J. Neurochem.77, 220.
Komarova, E.A., and Gudkov, A.V. 2000. Biochemistry (Mosc.) 65, 41.
Stadler, P., et al. 2000. Strahlenther Onkol. 176, 98.
Ferber, D. 1999. Science 285, 1651.
Jacquemin-Sablon, A. 1999. Bull. Cancer86, 894.
Komarov, P.G., et al. 1999. Science 285, 1733.
Culmsee, C., et al. 2001. J. Neurochem.77, 220.
Komarova, E.A., and Gudkov, A.V. 2000. Biochemistry (Mosc.) 65, 41.
Stadler, P., et al. 2000. Strahlenther Onkol. 176, 98.
Ferber, D. 1999. Science 285, 1651.
Jacquemin-Sablon, A. 1999. Bull. Cancer86, 894.
Komarov, P.G., et al. 1999. Science 285, 1733.
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
Toxicity: Standard Handling (A)
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Irene Paterniti et al.
Biomedicines, 9(7) (2021-08-07)
Cisplatin is one of the chemotherapeutic drugs used for the management of oral carcinoma, in which combined therapies are estimated to exert superior therapeutic efficacy compared with monotherapy. It is known that poly(ADP-ribosyl)ation is implicated in a multiplicity of cellular
Roberta Gonnella et al.
Biology, 11(1) (2022-01-22)
We have previously shown that Zinc supplementation triggered ER stress/UPR in cancer cells undergoing treatment by genotoxic agents, reactivated wtp53 in cancer cells harboring mutant p53 (mutp53) and potentiated the activity of wtp53 in those carrying wtp53. In this study
Chun-Hao Su et al.
iScience, 24(11), 103368-103368 (2021-11-25)
Thrombocytopenia-absent radius (TAR) syndrome is caused by RBM8A insufficiency. We generated megakaryocyte-specific Rbm8a knockout (Rbm8aKOMK) mice that exhibited marked thrombocytopenia, internal hemorrhage, and splenomegaly, providing evidence that genetic deficiency of Rbm8a causes a disorder of platelet production. Rbm8aKOMK mice accumulated
Amena BenYounès et al.
Autophagy, 7(8), 883-891 (2011-04-05)
Autophagic flux can be measured by determining the declining abundance of autophagic substrates such as sequestosome 1 (SQSTM1, better known as p62), which is sequestered in autophagosomes upon its direct interaction with LC3. However, the total amount of p62 results
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