B2682
Boc-Asp(OMe)-fluoromethyl ketone
≥90% (TLC), solid
Synonym(s):
Boc-D-FMK
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About This Item
Recommended Products
Quality Level
Assay
≥90% (TLC)
form
solid
solubility
DMF: soluble
storage temp.
−20°C
SMILES string
COC(=O)C[C@H](NC(=O)OC(C)(C)C)C(=O)CF
InChI
1S/C11H18FNO5/c1-11(2,3)18-10(16)13-7(8(14)6-12)5-9(15)17-4/h7H,5-6H2,1-4H3,(H,13,16)/t7-/m0/s1
InChI key
MXOOUCRHWJYCAL-ZETCQYMHSA-N
Application
Boc-Asp(OMe)-fluoromethyl ketone (Boc-D-fmk) has been used as a caspase inhibitor to study its effects on lactate dehydrogenase (LDH) leakage, apoptosis and virus proliferation in chorion cells , as a component of the transplantation medium for the transplantation of human embryonic stem cells (ESC)-derived medial ganglionic eminence (MGE) cells into hippocampus of mice , as a protease inhibitor to study its effects on cell death in parasites .
Biochem/physiol Actions
Boc-Asp(OMe)-fluoromethyl ketone (Boc-D-fmk) permits cell permeability. It is a caspase inhibitor and suppresses apoptosis induced by various kinds of stimuli. Boc-D-fmk poorly inhibits caspases-2, -5, -6 and -10.
Signal Word
Warning
Hazard Statements
Precautionary Statements
Hazard Classifications
Eye Irrit. 2
Storage Class Code
11 - Combustible Solids
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Personal Protective Equipment
dust mask type N95 (US), Eyeshields, Gloves
Certificates of Analysis (COA)
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Heat-induced programmed cell death in Leishmania infantum is reverted by Bcl-X L expression
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Lactate dehydrogenase leakage as a marker for apoptotic cell degradation induced by influenza virus infection in human fetal membrane cells
Intervirology, 52(3), 164-173 (2009)
Differentiation of human pluripotent stem cells into Medial Ganglionic Eminence vs. Caudal Ganglionic Eminence cells
Methods, 101(3), 103-112 (2016)
Cell biochemistry and biophysics, 70(1), 461-465 (2014-05-06)
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Following ventral root avulsion in neonatal animals, the degeneration of spinal motoneurons occurs by an apoptotic-like morphological pathway. In adult animals, however, the mechanism of degeneration of injured motoneurons is still controversial. Because caspases are important mediators of apoptosis, we
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