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Biological Activity for 10-DEBC hydrochloride
10-DEBC hydrochloride is a selective inhibitor of Akt/PKB. Inhibits IGF-1-stimulated phosphorylation and activation of Akt (complete inhibition at 2.5 μM), suppressing downstream activation of mTOR, p70 S6 kinase and S6 ribosomal protein. Shows no activity at PDK1, SGK1 or PI 3-kinase. Inhibits cell growth (IC50 ~ 2-6 μM) and induces apoptosis in rhabdomyosarcoma cells.
Compound Libraries for 10-DEBC hydrochloride
10-DEBC hydrochloride is also offered as part of the Tocriscreen 2.0 Max, Tocriscreen Kinase Inhibitor Library and Tocriscreen Antiviral Library. Find out more about compound libraries available from Tocris.
Technical Data for 10-DEBC hydrochloride
|Storage||Desiccate at +4°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 10-DEBC hydrochloride
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions for 10-DEBC hydrochloride
The following data is based on the product molecular weight 381.34. 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||2.62 mL||13.11 mL||26.22 mL|
|5 mM||0.52 mL||2.62 mL||5.24 mL|
|10 mM||0.26 mL||1.31 mL||2.62 mL|
|50 mM||0.05 mL||0.26 mL||0.52 mL|
Product Datasheets for 10-DEBC hydrochloride
References for 10-DEBC hydrochloride
References are publications that support the biological activity of the product.
Thimmaiah et al (1992) Synthesis and chemical characterization of N-substituted phenoxazines directed toward reversing vinca alkaloid resistance in multidrug-resistant cancer cells. J.Med.Chem. 35 3358 PMID: 1527786
Thimmaiah et al (2005) Identification of N10-substituted phenoxazines as potent and specific inhibitors of Akt signaling. J.Biol.Chem. 36 31924
If you know of a relevant reference for 10-DEBC hydrochloride, please let us know.
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Keywords: 10-DEBC hydrochloride, 10-DEBC hydrochloride supplier, Selective, Akt, PKB, inhibitors, inhibits, Protein, Kinase, B, Kinases, Inhibitor, X, (Protein, B), B/Akt, 2558, Tocris Bioscience
6 Citations for 10-DEBC hydrochloride
Citations are publications that use Tocris products. Selected citations for 10-DEBC hydrochloride include:
Gangoiti et al (2012) Ceramide 1-phosphate stimulates proliferation of C2C12 myoblasts. Biochimie 94 597 PMID: 21945811
Goodnough et al (2012) Inhibition of hepcidin transcription by growth factors. Hepatology 56 291 PMID: 22278715
Waltero et al (2019) TOR as a Regulatory Target in Rhipicephalus microplus Embryogenesis. Front Physiol 10 965 PMID: 31417424
Sokołowska et al (2014) Orexins protect neuronal cell cultures against hypoxic stress: an involvement of Akt signaling. PLoS One 52 48 PMID: 24243084
Ali et al (2017) Isolation and characterization of a new naturally immortalized human breast carcinoma cell line, KAIMRC1. BMC Cancer 17 803 PMID: 29187162
Liddell et al (2016) Pyrrolidine dithiocarbamate activates the Nrf2 pathway in astrocytes. J Neuroinflammation 13 49 PMID: 26920699
Do you know of a great paper that uses 10-DEBC hydrochloride from Tocris? Please let us know.
Reviews for 10-DEBC hydrochloride
Average Rating: 5 (Based on 1 Review.)
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As part of our current study, we investigated the role of AKT pathway on the LPA induced inflammatory phenotype in microglia (downstream signaling). BV2 cells were incubated for different time points with LPA (1µM) in the presence or absence of AKT X (5µM). AKT inhibition totally decreased the expression of 2 pro-inflammatory transcription factors (pSTAT1 and pp65). The inhibitor was diluted in water.
Literature in this Area
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Schizophrenia is a debilitating psychiatric disorder that affects 1% of the worldwide population. This poster describes the neurobiology of Schizophrenia, as well as highlighting the genetic and environmental factors that play a fundamental role in the etiology of the disease. The current and emerging drug targets are also discussed.