218759
Caspase-8 Inhibitor II
≥98% (HPLC), powder, Caspase-8 inhibitor, Calbiochem®
Synonyme(s) :
Caspase-8 Inhibitor II, Z-IE(OMe)TD(OMe)-FMK, Granzyme B Inhibitor III
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About This Item
Formule empirique (notation de Hill):
C30H43FN4O11
Poids moléculaire :
654.68
Code UNSPSC :
12352200
Nomenclature NACRES :
NA.77
Produits recommandés
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.
Niveau de qualité
Forme
powder
Fabricant/nom de marque
Calbiochem®
Conditions de stockage
OK to freeze
desiccated
Couleur
white to yellow
Solubilité
DMSO: 10 mM
Conditions d'expédition
ambient
Température de stockage
−20°C
Description générale
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.
Actions biochimiques/physiologiques
Cell permeable: yes
Primary Target
caspase-8
caspase-8
Product does not compete with ATP.
Reversible: no
Avertissement
Toxicity: Standard Handling (A)
Séquence
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.
Remarque sur l'analyse
≥98% (HPLC)
Autres remarques
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.
Informations légales
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
Code de la classe de stockage
11 - Combustible Solids
Classe de danger pour l'eau (WGK)
WGK 1
Point d'éclair (°F)
Not applicable
Point d'éclair (°C)
Not applicable
Certificats d'analyse (COA)
Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "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
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
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
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