Pifithrin-Hydrobromide
Pifithrin-α
CAS: 63208-82-2
Molecular Formula: C16H19BrN2OS
Pifithrin-Hydrobromide - Names and Identifiers
Pifithrin-Hydrobromide - Physico-chemical Properties
| Molecular Formula | C16H19BrN2OS |
| Molar Mass | 367.3 |
| Melting Point | 192.1-192.5°C(lit.) |
| Solubility | DMSO: 20mg/mL |
| Appearance | powder |
| Color | off-white |
| pKa | 9.11(at 25℃) |
| Storage Condition | -20°C |
| Stability | Stable for 1 year from date of purchase as supplied. Solutions in DMSO may be stored at -20°C for up to 3 months. |
| In vitro study | Pifithrin-α acts on ConA cells to inhibit p53-dependent transcription of p53 responsive genes. Pififrin-α (10 μm) inhibited Dox, Etoposide, Taxol, and Cytosine arabinoside-induced apoptosis in C8 cells. Pifithrin-α inhibits p53-dependent growth arrest of human diploid fibroblasts formed as a result of DNA damage without any effect on p53-deficient fibroblasts. Pifithrin-α can regulate the nuclear input or output of p53 (or both), and can also reduce the stability of nuclear p53. Pifithrin-α (100-200 nM) acts on hippocampal cells and completely inhibits the increase of p53 DNA binding level and p53 response gene Bax induced by Camptothecin. Pifithrin-α also reduced the level of p53 DNA-binding activity. Pififrin-α (200 nM) protects cultured hippocampal neurons from DNA damaging agent-induced death. Pifithrin-α(200 μm) stabilizes mitochondrial function, inhibits caspase activation, and protects cultured hippocampal neurons from glutamate and β-amyloid peptide-induced death. Pifithrin-α inhibits heat Shock and glucocorticoid receptor signaling, but does not affect NF-κB signaling. Pififrin-α (10 μm) reduces the activation of heat Shock transcription factor (HSF1) and enhances the sensitivity of cells to heat. Pififrin-α (10 μm) acts on HeLa cells, reduces the activation of glucocorticoid receptors, and protects the mouse thymus from dexamethone-induced apoptosis. Pifithrin-α acts on human embryonic kidney cells to inhibit p53-mediated induction of p21/Waf-1. Pifithrin-α shifts the dexamethone dose response curve to the left by increasing the intracellular dexamethone concentration. pifithrin-α acts on ConA cells to inhibit p53-dependent p53 responsive gene transcription. Pififrin-α (10 μm) inhibited Dox, Etoposide, Taxol, and Cytosine arabinoside-induced apoptosis in C8 cells. Pifithrin-α inhibits p53-dependent growth arrest of human diploid fibroblasts formed as a result of DNA damage without any effect on p53-deficient fibroblasts. Pifithrin-α can regulate the nuclear input or output of p53 (or both), and can also reduce the stability of nuclear p53. Pifithrin-α (100-200 nM) acts on hippocampal cells and completely inhibits the increase of p53 DNA binding level and p53 response gene Bax induced by Camptothecin. Pifithrin-α also reduced the level of p53 DNA-binding activity. Pifithrin-α (200 nM) Protection of cultured hippocampal neurons from DNA damaging agent-induced death. Pifithrin-α(200 μm) stabilizes mitochondrial function, inhibits caspase activation, and protects cultured hippocampal neurons from glutamate and β-amyloid peptide-induced death. Pifithrin-α inhibits heat Shock and glucocorticoid receptor signaling, but does not affect NF-κB signaling. Pififrin-α (10 μm) reduces the activation of heat Shock transcription factor (HSF1) and enhances the sensitivity of cells to heat. Pififrin-α (10 μm) acts on HeLa cells, reduces the activation of glucocorticoid receptors, and protects the mouse thymus from dexamethone-induced apoptosis. Pifithrin-α acts on human embryonic kidney cells to inhibit p53-mediated induction of p21/Waf-1. Pifithrin-α shifts the dexamethone dose response curve to the left by increasing the intracellular dexamethone concentration. |
| In vivo study | Mice (C57BL and Balb/c) were intraperitoneally injected with 2.2 mg/kg of pifihrin-α to completely protect mice from 60% gamma irradiation (8 Gy for C57BL mice), balb/c mice were 6 Gy). Mice injected with pifithrin-α lost less weight than irradiated mice treated without pifithrin-α. Whole-body gamma-irradiated mice were treated with pifithrin-α (2.2 mg/kg) to abrogate the p53-dependent regulation of DNA replication. Treatment of mice with middle cerebral artery occlusion with pifithrin-α(2 mg/kg, I. P.) reduced ischemic brain damage and protected hippocampal neurons from toxic damage 30 minutes later. Treatment of mice with pifithrin-α(3.6 μg/kg, I. P.) inhibited Dex-Induced thymic degeneration. Pifithrin-α(2 mg/kg) treatment of rats with transient middle cerebral artery occlusion significantly reduced the extent of dyskinesia compared to the control group. After the onset of stroke, one hour after the administration of pifithrin-α, the animal had decreased dyskinesia and decreased infarction. After 7 days of treatment with pifithrin-α, the dyskinesia score of the rats was significantly reduced compared to the blank control group. By Tunel and caspase 3 staining, it was observed that pifithrin-α significantly reduced apoptosis in rats. pifithrin-α was administered intraperitoneally at a dose of 2.2 mg/kg to mice (C57BL and Balb/c), mice of both strains were completely protected from the killing dose of 60% gamma irradiation (8 Gy for C57BL mice and 6 Gy for Balb/c mice). Mice injected with pifithrin-α lost less weight than irradiated mice treated without pifithrin-α. Whole-body gamma-irradiated mice were treated with pifithrin-α (2.2 mg/kg) to abrogate the p53-dependent regulation of DNA replication. Treatment of mice with middle cerebral artery occlusion with pifithrin-α(2 mg/kg, I. P.) reduced ischemic brain damage and protected hippocampal neurons from toxic damage 30 minutes later. Treatment of mice with pifithrin-α(3.6 μg/kg, I. P.) inhibited Dex-Induced thymic degeneration. Pifithrin-α(2 mg/kg) treatment of rats with transient middle cerebral artery occlusion significantly reduced the extent of dyskinesia compared to the control group. After the onset of stroke, one hour after the administration of pifithrin-α, the animal had decreased dyskinesia and decreased infarction. After 7 days of treatment with pifithrin-α, the dyskinesia score of the rats was significantly reduced compared to the blank control group. By Tunel and caspase 3 staining, it was observed that pifithrin-α significantly reduced apoptosis in rats. |
Pifithrin-Hydrobromide - Risk and Safety
| WGK Germany | 3 |
Pifithrin-Hydrobromide - Preparation solution concentration reference
| 1mg | 5mg | 10mg | |
|---|---|---|---|
| 1 mM | 2.723 ml | 13.613 ml | 27.226 ml |
| 5 mM | 0.545 ml | 2.723 ml | 5.445 ml |
| 10 mM | 0.272 ml | 1.361 ml | 2.723 ml |
| 5 mM | 0.054 ml | 0.272 ml | 0.545 ml |
Last Update：2024-01-02 23:10:35
Pifithrin-Hydrobromide - Reference Information
| biological activity | Pifithrin-α (PFT α) is a p53 inhibitor that inhibits p53-dependent p53 response gene transcription. Pifithrin-α (PFT α) is a p53 inhibitor that inhibits p53-dependent transcription of p53-responsive genes. Pifithrin-α is also an effective stimulant of aryl hydrocarbon receptor (AhR). |
| In vitro study | Pifithrin-α acts on ConA cells to inhibit the transcription of p53-dependent p53 response genes. Pifithrin-α (10 μM) inhibits Dox, Etoposide, Taxol, and Cytosine arabinoside-induced apoptosis of C8 cells. Pifithrin-α inhibited the growth arrest of p53-dependent human diploid fibroblasts formed due to DNA damage without any effect on p53-deficient fibroblasts. Pifithrin-α can regulate nuclear input or output of p53 (or both), and can also reduce the stability of nuclear p53. Pifithrin-α (100-200 nM) acts on hippocampal cells, completely inhibiting the Camptothecin-induced increase in p53 DNA binding levels and the p53-responsive gene Bax. Pifithrin-α also reduced the level of p53 DNA-binding activity. Pifithrin-α (200 nM) protects cultured hippocampal neurons from death induced by DNA damaging agents. Pifithrin-α(200 μM) stabilizes mitochondrial function, inhibits caspase activation, and protects cultured hippocampal neurons from glutamate and β-amyloid peptide-induced death. Pifithrin-α can inhibit heat shock and glucocorticoid receptor signaling, but does not affect NF-κB signaling. Pifithrin-α (10 μM) reduces the activation of heat shock transcription factor (HSF1) and enhances the sensitivity of cells to heat. Pifithrin-α (10 μM) acts on HeLa cells, reduces the activation of glucocorticoid receptor, and protects mouse thymus from Dexamethasone-induced apoptosis. Pifithrin-α acts on human embryonic kidney cells and inhibits p21/Waf-1 induction mediated by p53. Pifithrin-α shifts the Dexamethasone dose-response curve to the left by increasing the intracellular Dexamethasone concentration. Pifithrin-α acts on ConA cells to inhibit the transcription of p53-dependent p53 response genes. Pifithrin-α (10 μM) inhibits Dox, Etoposide, Taxol, and Cytosine arabinoside-induced apoptosis of C8 cells. Pifithrin-α inhibited the growth arrest of p53-dependent human diploid fibroblasts formed due to DNA damage without any effect on p53-deficient fibroblasts. Pifithrin-α can regulate nuclear input or output of p53 (or both), and can also reduce the stability of nuclear p53. Pifithrin-α (100-200 nM) acts on hippocampal cells, completely inhibiting the Camptothecin-induced increase in p53 DNA binding levels and the p53-responsive gene Bax. Pifithrin-α also reduced the level of p53 DNA-binding activity. Pifithrin-α (200 nM) protects cultured hippocampal neurons from death induced by DNA damaging agents. Pifithrin-α(200 μM) stabilizes mitochondrial function, inhibits caspase activation, and protects cultured hippocampal neurons from glutamate and β-amyloid peptide-induced death. Pifithrin-α can inhibit heat shock and glucocorticoid receptor signaling, but does not affect NF-κB signaling. Pifithrin-α (10 μM) reduces the activation of heat shock transcription factor (HSF1) and enhances the sensitivity of cells to heat. Pifithrin-α (10 μM) acts on HeLa cells, reduces the activation of glucocorticoid receptor, and protects mouse thymus from Dexamethasone-induced apoptosis. Pifithrin-α acts on human embryonic kidney cells and inhibits p21/Waf-1 induction mediated by p53. Pifithrin-α shifts the Dexamethasone dose-response curve to the left by increasing the intracellular Dexamethasone concentration. |
| in vivo study | Pifithrin-α was intraperitoneally injected into mice (C57BL and Balb/c) at a dose of 2.2 mg/kg to completely protect the mice of the two strains from the killing dose of 60% gamma rays (8 Gy for C57BL mice and 6 Gy for Balb/c mice). Mice injected with Pifithrin-α lost less weight than irradiated mice not treated with Pifithrin-α. Pifithrin-α (2.2 mg/kg) was treated with whole-body γ-irradiated mice, abolishing p53-dependent regulation of DNA replication. Pifithrin-α(2 mg/kg, intraperitoneal injection) reduced ischemic brain damage and protected hippocampal neurons from toxic damage after 30 minutes in mice with midcerebral artery occlusion. Pifithrin-α(3.6 μg/kg, intraperitoneal injection) treated mice to inhibit Dex-induced thymus degeneration. Pifithrin-α(2 mg/kg) treated rats with transient midcerebral artery occlusion significantly reduced the degree of dyskinesia compared with the control group. After the onset of stroke, one hour after the administration of Pifithrin-α, the animal had decreased dyskinesia and decreased infarction. Compared with the blank control group, Pifithrin-α treatment significantly reduced the dyskinesia score of rats after 7 days. Through Tunel and caspase 3 staining, it was observed that Pifithrin-α significantly reduced apoptosis in rats. Pifithrin-α was injected intraperitoneally into mice (C57BL and Balb/c) at a dose of 2.2 mg/kg, so that the mice of the two strains were completely protected from the killing dose of 60% gamma rays (8 Gy for C57BL mice and 6 Gy for Balb/c mice). Mice injected with Pifithrin-α lost less weight than irradiated mice not treated with Pifithrin-α. Pifithrin-α (2.2 mg/kg) was treated with whole-body γ-irradiated mice, abolishing p53-dependent regulation of DNA replication. Pifithrin-α(2 mg/kg, intraperitoneal injection) reduced ischemic brain damage and protected hippocampal neurons from toxic damage after 30 minutes in mice with midcerebral artery occlusion. Pifithrin-α(3.6 μg/kg, intraperitoneal injection) treated mice to inhibit Dex-induced thymus degeneration. Pifithrin-α(2 mg/kg) treated rats with transient midcerebral artery occlusion significantly reduced the degree of dyskinesia compared with the control group. After the onset of stroke, one hour after the administration of Pifithrin-α, the animal had decreased dyskinesia and decreased infarction. Compared with the blank control group, Pifithrin-α treatment significantly reduced the dyskinesia score of rats after 7 days. Through Tunel and caspase 3 staining, it was observed that Pifithrin-α significantly reduced apoptosis in rats. |
| target | TargetValue p53 |
| Target | Value |
Last Update：2024-04-10 22:29:15
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Product Name: 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanoneHydrobromide Request for quotationCAS: 63208-82-2
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View History
Pifithrin-Hydrobromide
C.I. Direct Red 81 (7CI)
ZBPD
FEC
2-Nitrocinnamic acid
Methyltriethylammonium
FR901465
C.I. Direct Red 81 (7CI)
ZBPD
FEC
2-Nitrocinnamic acid
Methyltriethylammonium
FR901465