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Inhibitor of p53; reversibly blocks p53-dependent transcriptional activation and apoptosis. Protects against neuronal death in models of stroke and neurodegenerative disorders. Active in vivo; protects mice from the side-effects of cancer therapy associated with p53 induction. Supresses self-renewal of embryonic stem cells. Also aryl hydrocarbon receptor (AHR) agonist, causes upregulation of AHR target gene CYP1A1 (EC50 = 1.1 μM). Cyclic analog available (Cat. No. 3843).
|Storage||Desiccate at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 367.3. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||2.72 mL||13.61 mL||27.23 mL|
|5 mM||0.54 mL||2.72 mL||5.45 mL|
|10 mM||0.27 mL||1.36 mL||2.72 mL|
|50 mM||0.05 mL||0.27 mL||0.54 mL|
References are publications that support the biological activity of the product.
Culmsee et al (2001) A synthetic inhibitor of p53 protects neurons against death induced by ischemic and excitotoxic insults, and amyloid β-peptide. J.Neurochem. 77 220 PMID: 11279278
Hoagland et al (2005) The p53 inhibitor pifithrin-α is a potent agonist of the aryl hydrocarbon receptor. J.Pharmacol.Exp.Ther. 314 603 PMID: 15843497
Komarov et al (1999) A chemical inhibitor of p53 that protects mice from the side effects of cancer therapy. Science 285 1733 PMID: 10481009
Komarova and Gudkov (2000) Suppression of p53: a new approach to overcome side effects of antitumor therapy. Biochemistry 65 41 PMID: 10702639
Abdelalim and Tooyama (2012) The p53 inhibitor, pifithrin-α, suppresses self-renewal of embryonic stem cells. Biochem.Biophys.Res.Comm. 420 605 PMID: 22445757
If you know of a relevant reference for Pifithrin-α hydrobromide, please let us know.
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Keywords: Pifithrin-a hydrobromide, Pifithrin-a hydrobromide supplier, p53, inhibitors, inhibits, aryl, hydrocarbon, receptors, agonists, AHR, Transcription, Factors, Pifithrin-alpha, hydrobromide, Aryl, Hydrocarbon, Receptors, Stem, Cell, Signaling, Autophagy, 1267, Tocris Bioscience
4 Citations for Pifithrin-α hydrobromide
Citations are publications that use Tocris products. Selected citations for Pifithrin-α hydrobromide include:
Li et al (2018) Zinc deficiency causes neural tube defects through attenuation of p53 ubiquitylation. Development 145 PMID: 30545932
Norlin et al (2018) The ATPase activity of Asna1/TRC40 is required for pancreatic progenitor cell survival. Development 145 PMID: 29180572
Fraser et al (2006) Regulation of p53 and suppression of apoptosis by the soluble guanylyl cyclase/cGMP pathway in human ovarian cancer cells. Cell Commun Signal 25 2203 PMID: 16288207
Guha et al (2015) Novel Pactamycin Analogs Induce p53 Dependent Cell-Cycle Arrest at S-Phase in Human Head and Neck Squamous Cell Carcinoma (HNSCC) Cells. PLoS One 10 e0125322 PMID: 25938491
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Reviews for Pifithrin-α hydrobromide
Average Rating: 5 (Based on 2 Reviews.)
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Pifithrin-alpha were dissolved in DMSO and used at a final concentration of 40 µM for pifithrin-alpha according to previous studies in which 3-100 µM pifithrin-alpha.
We used the p53 inhibitor in order to tackle the p53 protein in-vitro for some cellular proliferation assays,
We are happy with the quality of the product and the assistance from the Tocris technical department. All our questions about the use of the product where answered within a few hours.
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Cell Cycle & DNA Damage Repair Poster
In normal cells, each stage of the cell cycle is tightly regulated, however in cancer cells many genes and proteins that are involved in the regulation of the cell cycle are mutated or over expressed. Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the stages of the cell cycle and DNA repair. It also highlights strategies for enhancing replicative stress in cancer cells to force mitotic catastrophe and cell death.