218776
Caspase-9 Inhibitor II, Cell-Permeable
The Caspase-9 Inhibitor II, Cell-Permeable controls the biological activity of Caspase-9. This small molecule/inhibitor is primarily used for Cancer applications.
Sinónimos:
Caspase-9 Inhibitor II, Cell-Permeable, LEHD-CHO, Cell-permeable
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About This Item
Fórmula empírica (notación de Hill):
C97H162N22O25
Peso molecular:
2036.46
UNSPSC Code:
12352200
NACRES:
NA.54
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Quality Level
assay
≥95% (HPLC)
form
lyophilized solid
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze
desiccated (hygroscopic)
color
white
solubility
DMSO: 5 mg/mL
shipped in
ambient
storage temp.
−20°C
General description
A potent, cell-permeable and reversible inhibitor or caspase-9.
A potent, cell-permeable, and reversible inhibitor of caspase-9. May also inhibit caspase-4 and caspase-5. The N-terminal sequence (amino acids 1-16) corresponds to the hydrophobic region of the signal peptide of Kaposi fibroblast growth factor and confers cell permeability to the peptide.
Biochem/physiol Actions
Cell permeable: yes
Product does not compete with ATP.
Reversible: yes
Warning
Toxicity: Standard Handling (A)
Sequence
Ac-Ala-Ala-Val-Ala-Leu-Leu-Pro-Ala-Val-Leu-Leu-Ala-Leu-Leu-Ala-Pro-Leu-Glu-His-Asp-CHO
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
Storage Class
11 - Combustible Solids
wgk_germany
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
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Aditi A Kapasi et al.
Immunology, 108(3), 313-320 (2003-02-27)
Clinical reports suggest that acute ethanol intoxication is often associated with lymphopenia. Previously, ethanol was reported to invoke thymocyte apoptosis. We studied the effect of ethanol on T cell apoptosis. In addition, we evaluated the molecular mechanism of ethanol-induced T
Kamila Říhová et al.
Journal of proteome research, 23(8), 2999-3011 (2024-03-19)
Caspase-9 is traditionally considered the initiator caspase of the intrinsic apoptotic pathway. In the past decade, however, other functions beyond initiation/execution of cell death have been described including cell type-dependent regulation of proliferation, differentiation/maturation, mitochondrial, and endosomal/lysosomal homeostasis. As previous
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