Identification | Back Directory | [Name]
Ac-DEVD-CMK | [CAS]
285570-60-7 | [Synonyms]
AC-DEVD-CMK AC-ASP-GLU-VAL-ASP-CMK CASPASE-3 INHIBITOR III AC-ASP-GLU-VAL-ASP-CMK: AC-DEVD-CMK Ac-Asp-Glu-Val-Asp-chloromethylketone CASPASE-3 INHIBITOR III ; AC-ASP-GLU-VAL-ASP-CMK Ac-Asp-Glu-Val-Asp-chloromethylketone trifluoroacetate salt L-Valinamide, N-acetyl-L-α-aspartyl-L-α-glutamyl-N-[(1S)-1-(carboxymethyl)-3-chloro-2-oxopropyl]- N-Acetyl-L-alpha-aspartyl-L-alpha-glutamyl-N-[(1S)-1-(carboxymethyl)-3-chloro-2-oxopropyl]-L-valinamide | [Molecular Formula]
C21H31ClN4O11 | [MDL Number]
MFCD01323001 | [MOL File]
285570-60-7.mol | [Molecular Weight]
550.94 |
Chemical Properties | Back Directory | [Boiling point ]
1048.1±65.0 °C(Predicted) | [density ]
1.401±0.06 g/cm3(Predicted) | [storage temp. ]
-20°C | [solubility ]
Soluble in DMSO | [form ]
Powder | [pka]
3.93±0.19(Predicted) |
Hazard Information | Back Directory | [Uses]
A potent, cell-permeable, and irreversible inhibitor of caspase-3; also inhibits caspases -6, -7, -8, and -10. Commonly used at concentrations up to 100 M to examine the role of caspase-3-dependent apoptosis | [Uses]
Ac-DEVD-CMK is a cell-permeable, and irreversible inhibitor of caspase-3 as well as caspase-6, -7, -8, and -10. It is commonly used at concentrations up to 100 μM to examine the role of caspase-3-dependent apoptosis in biological systems.
| [Biological Activity]
ac-devd-cmk is a cell-permeable and irreversible caspase-3 inhibitor [1][2][3].apoptosis is a process of programmed cell death that occurs in multicellular organisms. caspase are a family of protease enzymes playing essential roles in programmed cell death (including apoptosis, pyroptosis and necroptosis) and inflammation. caspase activation is a major event in apoptosis. caspase-3 cleaves and activates caspases 6 and 7, and is processed and activated by caspases 8, 9, and 10 [1][2][3].ac-devd-cmk (ac-asp-glu-val-asp-ch2cl) is a cell-permeable, irreversible and specific caspase-3 inhibitor. in coronary occlusion/reperfusion rat isolated hearts, ac-devd-cmk reduced infarct size (the percentage of infarction 27.8+3.3% vs control 38.5+2.6%), suggesting that caspase inhibition during early reperfusion protected myocardium against lethal reperfusion injury [1]. in bl41 cells, ac-devd-cmk partially inhibited mn2+-induced apoptosis and parp cleavage, and partially blocked b cell death by 37% even at 100 μm [2]. ac-devd-cmk significantly blocked neurotoxicity at 24 hr after 1 hr of sin-1 exposure and also protected against neurotoxicity at 24 hr after 90 min of zinc (75 μm) exposure. ac-devd-cmk completely blocked sin-1-induced activation of caspase-3 [3]. | [storage]
Store at -20°C | [References]
[1]. mocanu mm, baxter gf, yellon dm. caspase inhibition and limitation of myocardial infarct size: protection against lethal reperfusion injury. br j pharmacol. 2000 may;130(2):197-200. [2]. schrantz n, blanchard da, mitenne f, et al. manganese induces apoptosis of human b cells: caspase-dependent cell death blocked by bcl-2. cell death differ. 1999 may;6(5):445-53. [3]. zhang y, wang h, li j, et al. peroxynitrite-induced neuronal apoptosis is mediated by intracellular zinc release and 12-lipoxygenase activation. j neurosci. 2004 nov 24;24(47):10616-27. |
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Company Name: |
BOC Sciences
|
Tel: |
16314854226 |
Website: |
www.bocsci.com |
Company Name: |
Alabiotech Inc.
|
Tel: |
001-619-354-5251 |
Website: |
www.alabiotech-e.com |
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