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Merck

506132

Pifithrin-α

≥95% (HPLC), solid, p53 inhibitor, Calbiochem®

Sinónimos:

Pifithrin-α, 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1- p-tolylethanone, HBr

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Acerca de este artículo

Fórmula empírica (notación de Hill):
C16H18N2OS · xHBr
Número CAS:
63208-82-2
Peso molecular:
286.39 (free base basis)
UNSPSC Code:
12352200
NACRES:
NA.77
MDL number:
MFCD00417851
Assay:
≥95% (HPLC)
Form:
solid
Quality level:
100
Storage condition:
OK to freeze, protect from light

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Nombre del producto

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

100

Categorías relacionadas

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
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.

Legal Information

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

Disclaimer

Toxicity: Standard Handling (A)

Clase de almacenamiento

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

Certificados de análisis (COA)

Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»

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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
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
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

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