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Biological Activity for 2,3-DCPE hydrochloride
2,3-DCPE hydrochloride is a selectively induces apoptosis and downregulates Bcl-XL protein expression in various human cancer cells versus normal cells in vitro. IC50 values are 0.89 and 12.6 μM for LoVo human colon cancer cell line and normal human fibroblasts respectively. Induces p21 expression and S-phase arrest in cancer cells via ERK-mediated pathways.
Technical Data for 2,3-DCPE hydrochloride
|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.
Solubility Data for 2,3-DCPE hydrochloride
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions for 2,3-DCPE hydrochloride
The following data is based on the product molecular weight 300.61. 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||3.33 mL||16.63 mL||33.27 mL|
|5 mM||0.67 mL||3.33 mL||6.65 mL|
|10 mM||0.33 mL||1.66 mL||3.33 mL|
|50 mM||0.07 mL||0.33 mL||0.67 mL|
Product Datasheets for 2,3-DCPE hydrochloride
References for 2,3-DCPE hydrochloride
References are publications that support the biological activity of the product.
Wu et al (2004) Induction of apoptosis and down-regulation of Bcl-XL in cancer cells by a novel small molecule, 2[[3-(2,3-Dichlorophenoxy)propyl]amino]ethanol. Cancer Res. 64 1110 PMID: 14871845
Zhu et al (2004) Induction of S-phase arrest and p21 overexpression by a small molecule 2[[3-(2,3-dichlorophenoxy)propyl]amino]ethanol in correlation with activation of ERK. Oncogene 23 4984 PMID: 15122344
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Citations for 2,3-DCPE hydrochloride
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Programmed Cell Death Poster
There are two currently recognized forms of programmed cell death: apoptosis and necroptosis. This poster summarizes the signaling pathways involved in apoptosis, necroptosis and cell survival following death receptor activation, and highlights the influence of the molecular switch, cFLIP, on cell fate.