Cell-permeable, irreversible inhibitor of caspase-3/CPP32; inhibits tumor cell apoptosis. Neuroprotective in rat hippocampus following seizures in vivo.
(Modifications: Asp-1 = Z-Asp(OMe), Glu-2 = Glu(OMe), Asp-4 = (OMe)-fluoromethylketone)
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
|Solubility||Soluble to 13.37 mg/ml in DMSO|
Preparing Stock Solutions
The following data is based on the product molecular weight 668.67. Batch specific molecular weights may vary from batch to batch due to solvent 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||1.5 mL||7.48 mL||14.96 mL|
|5 mM||0.3 mL||1.5 mL||2.99 mL|
|10 mM||0.15 mL||0.75 mL||1.5 mL|
|50 mM||0.03 mL||0.15 mL||0.3 mL|
The reconstitution calculator allows you to quickly calculate the volume of a reagent to reconstitute your vial. Simply enter the mass of reagent and the target concentration and the calculator will determine the rest.
References are publications that support the products' biological activity.
Brocksted et al (1998) Identification of apoptosis-associated proteins in a human Burkitt lymphoma cell line. J.Biol.Chem. 273 28057 PMID: 9774422
Henshall et al (2000) Involvement of caspase-3-like protease in the mechanism of cell death following focally evoked limbic seizures. J.Neurochem. 74 1215 PMID: 10693954
Kugawa et al (2000) Apoptosis of NG108-15 cells induced by buprenorphine hydrochloride occurs via the caspase-3 pathway. Biol.Pharm.Bull. 23 930 PMID: 10963298
If you know of a relevant reference for Z-DEVD-FMK, please let us know.
View Related Products by Product Action
Keywords: Z-DEVD-FMK, supplier, Cell-permeable, irreversible, caspase-3, inhibitors, inhibits, Caspases, Proteinases, Proteases, Caspases, Tocris Bioscience
4 Citations for Z-DEVD-FMK
Citations are publications that use Tocris products. Selected citations for Z-DEVD-FMK include:
Wu et al (2016) Human genome-wide RNAi screen reveals host factors required for enterovirus 71 replication Nature Communications 7 13150 PMID: 27748395
Bill et al (2015) ANO1 interacts with EGFR and correlates with sensitivity to EGFR-targeting therapy in head and neck cancer. BMB Rep 6 9173 PMID: 25823819
Im-aram et al (2013) The mTORC2 component rictor contributes to cisplatin resistance in human ovarian cancer cells. PLoS One 8 e75455 PMID: 24086535
Woo et al (2012) Calpain-mediated processing of p53-associated parkin-like cytoplasmic protein (PARC) affects chemosensitivity of human ovarian cancer cells by promoting p53 subcellular trafficking. J Biol Chem 287 3963 PMID: 22117079
Do you know of a great paper that uses Z-DEVD-FMK from Tocris? If so please let us know.
Literature in this Area
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 monogenic neurodegenerative disorder, which is characterized by the prevalent loss of GABAergic medium spiny neurons (MSN) in the striatum. This poster summarizes the MSN intracellular signaling pathways implicated in the pathology of HD, as well as highlighting the use of iPSCs for HD modeling.
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.