218759
Caspase-8 Inhibitor II
≥98% (HPLC), powder, Caspase-8 inhibitor, Calbiochem®
Synonym(s):
Caspase-8 Inhibitor II, Z-IE(OMe)TD(OMe)-FMK, Granzyme B Inhibitor III
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About This Item
Empirical Formula (Hill Notation):
C30H43FN4O11
Molecular Weight:
654.68
UNSPSC Code:
12352200
NACRES:
NA.77
Recommended Products
product name
Caspase-8 Inhibitor II, The Caspase-8 Inhibitor II controls the biological activity of Caspase-8. This small molecule/inhibitor is primarily used for Cancer applications.
Quality Level
form
powder
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze
desiccated
color
white to yellow
solubility
DMSO: 10 mM
shipped in
ambient
storage temp.
−20°C
General description
A potent, cell-permeable, and irreversible inhibitor of caspase-8 (MACH, FLICE, Mch5). Also inhibits granzyme B.
A potent, cell-permeable, and irreversible inhibitor of caspase-8 and granzyme B. Effectively inhibits influenza virus-induced apoptosis in HeLa cells. Also inhibits granzyme B. When using with purified native or recombinant enzyme, pretreatment with an esterase is required. A 5 mM (250 µg/76 µl) solution of Z-IETD-FMK (Cat. No. 218840) in DMSO is also available.
Biochem/physiol Actions
Cell permeable: yes
Primary Target
caspase-8
caspase-8
Product does not compete with ATP.
Reversible: no
Warning
Toxicity: Standard Handling (A)
Sequence
Z-Ile-Glu(OMe)-Thr-Asp(OMe)-CH₂F*
Reconstitution
Following reconstitution aliquot and freeze (-20°C). Stock solutions are stable for up to 8 months at -20°C.
Analysis Note
≥98% (HPLC)
Other Notes
Takizawa, T., et al. 1999. Microbiol. Immunol.43, 245.
Martin, D.A., et al. 1998. J. Biol. Chem.273, 4345.
Sweeney, E.A., et al. 1998. FEBS Lett.425, 61.
Thornberry, N.A., and Lazebnik, Y. 1998. Science281, 1312.
Martin, D.A., et al. 1998. J. Biol. Chem.273, 4345.
Sweeney, E.A., et al. 1998. FEBS Lett.425, 61.
Thornberry, N.A., and Lazebnik, Y. 1998. Science281, 1312.
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
Storage Class Code
11 - Combustible Solids
WGK
WGK 1
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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María Segovia et al.
Journal of phycology, 45(5), 1116-1126 (2009-10-01)
When the chlorophyte alga Dunaliella tertiolecta Butcher is placed in darkness, a form of programmed cell death with many similarities to apoptosis is induced, including the induction of caspase-like proteases. Many uncertainties about the regulation and mediators that participate in
Zahara L Chaudhry et al.
Brain sciences, 12(4) (2022-04-22)
The outbreak of COVID-19 caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) signifies a serious worldwide concern to public health. Both transcriptome and proteome of SARS-CoV-2-infected cells synergize the progression of infection in host, which may exacerbate symptoms and/or
W D Thomas et al.
Journal of immunology (Baltimore, Md. : 1950), 165(10), 5612-5620 (2000-11-09)
Past studies have shown that TNF-related apoptosis-inducing ligand (TRAIL) induced apoptosis in a high proportion of cultured melanoma by caspase-dependent mechanisms. In the present studies we have examined whether TRAIL-induced apoptosis of melanoma was mediated by direct activation of effector
Gurdeep Marwarha et al.
Biomedicines, 10(1) (2022-01-22)
Apoptotic cell death of cardiomyocytes is a characteristic hallmark of ischemia-reperfusion (I/R) injury. The master hypoxamiR, microRNA-210 (miR-210), is considered the primary driver of the cellular response to hypoxic stress. However, to date, no consensus has emerged with regards to
Marco Buscetta et al.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 34(1), 1819-1832 (2020-01-10)
The NLRP3 inflammasome is formed by the sensor NLRP3, the adaptor ASC, and pro-caspase-1. Assembly and activation of the inflammasome trigger caspase-1-dependent cleavage of pro-IL-1β and pro-IL-18 into their secreted forms. Cigarette smoke is a risk factor for chronic inflammatory
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