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Biological Activity for Emricasan
Emricasan is a potent caspase inhibitor (IC50 values are 0.3, 0.4, 2, 4, 6, 6 and 20 nM for caspase-9, -1, -3, -6, -7, -8, and -2, respectively). Emricasan is antiapoptotic by inhibiting caspase 8. It also preserves cell viability after infection with several strains of Zika. Emricasan promotes survival of pluripotent stem cells in culture when used in combination with Chroman-1 (Cat. No. 7163), trans-ISRIB (Cat. No. 5284) and Polyamine Supplement x1000 (lyophilized) (Cat. No. 7739), a combination known as CEPT. When used as part of the CEPT cocktail, Emricasan improves survival of differentiated cells following cryopreservation. The compound also reduces hepatic inflammation in an animal model of liver injury. Orally bioavailable.
Compound Libraries for Emricasan
Technical Data for Emricasan
|Storage||Store 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 Emricasan
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions for Emricasan
The following data is based on the product molecular weight 569.51. 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||1.76 mL||8.78 mL||17.56 mL|
|5 mM||0.35 mL||1.76 mL||3.51 mL|
|10 mM||0.18 mL||0.88 mL||1.76 mL|
|50 mM||0.04 mL||0.18 mL||0.35 mL|
References for Emricasan
References are publications that support the biological activity of the product.
Chen et al (2021) A versatile polypharmacology platform promotes cytoprotection and viability of human pluripotent and differentiated cells. Nat.Methods 18 528 PMID: 33941937
Canbay et al (2004) The caspase inhibitor IDN-6556 attenuates hepatic injury and fibrosis in the bile duct ligated mouse. J.Pharmacol.Exp.Ther. 308 1191 PMID: 14617689
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Citations for Emricasan
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Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
Cell Cycle and DNA Damage Research Product Guide
This product guide provides a review of the cell cycle and DNA damage research area and lists over 170 products, including research tools for:
- Cell Cycle and Mitosis
- DNA Damage Repair
- Targeted Protein Degradation
- Ubiquitin Proteasome Pathway
- Chemotherapy Targets
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.
Huntington's Disease Poster
Huntington's disease (HD) is a severe monogenic neurodegenerative disorder, which is characterized by the prevalent loss of GABAergic medium spiny neurons (MSN) in the striatum. This poster summarizes the effects of mutant huntingtin aggregation implicated in the pathology of HD, as well as highlighting the use of iPSCs for HD modeling.
Parkinson's Disease Poster
Parkinson's disease (PD) causes chronic disability and is the second most common neurodegenerative condition. This poster outlines the neurobiology of the disease, as well as highlighting current therapeutic treatments for symptomatic PD, and emerging therapeutic strategies to delay PD onset and progression.
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.