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Boc-D-FMK

Pan-caspase inhibitor CAS# 187389-53-3,634911-80-1

Boc-D-FMK

Catalog No. BCC1128----Order now to get a substantial discount!

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Chemical structure

Boc-D-FMK

3D structure

Chemical Properties of Boc-D-FMK

Cas No. 187389-53-3,634911-80-1 SDF Download SDF
PubChem ID 16760348 Appearance Powder
Formula C11H18FNO5 M.Wt 263.26
Type of Compound N/A Storage Desiccate at -20°C
Solubility >11.65mg/mL in DMSO
Chemical Name methyl 5-fluoro-3-[(2-methylpropan-2-yl)oxycarbonylamino]-4-oxopentanoate
SMILES CC(C)(C)OC(=O)NC(CC(=O)OC)C(=O)CF
Standard InChIKey MXOOUCRHWJYCAL-UHFFFAOYSA-N
Standard InChI 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)
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of Boc-D-FMK

DescriptionBOC-D-FMK is a Novel inhibitor of Caspase-3.
TargetsCaspase    

Boc-D-FMK Dilution Calculator

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Boc-D-FMK Molarity Calculator

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Preparing Stock Solutions of Boc-D-FMK

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.7985 mL 18.9926 mL 37.9853 mL 75.9705 mL 94.9632 mL
5 mM 0.7597 mL 3.7985 mL 7.5971 mL 15.1941 mL 18.9926 mL
10 mM 0.3799 mL 1.8993 mL 3.7985 mL 7.5971 mL 9.4963 mL
50 mM 0.076 mL 0.3799 mL 0.7597 mL 1.5194 mL 1.8993 mL
100 mM 0.038 mL 0.1899 mL 0.3799 mL 0.7597 mL 0.9496 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

Research Update of Boc-D-FMK

1. Effect of Boc-D-Fmk on hepatocyte apoptosis after bile duct ligation in rat and survival rate after endotoxin challenge. J Gastroenterol Hepatol. 2008 Aug;23(8 Pt 1):1276-9. doi: 10.1111/j.1440-1746.2008.05368.x. Epub 2008 Mar 27.
Abstract
Boc-D-FMK, a caspase inhibitor, was evaluated for its effect on hepatocyte apoptosis and on survival rate after bile duct ligation in rats.

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Background on Boc-D-FMK

Boc-D-FMK is a cell-permeable broad-spectrum caspase inhibitor that fully inhibits the pro-apoptotic effect of tumor necrosis factor-α (TNFα) with the half maximal inhibition concentration IC50 value of 39 μM [1].

Boc-D-FMK has been found to reduce the activation of nuclear factor kappa light chain enhancer of activated B cells (NF-kB), suppress the phosphorylation of subunit nuclear factor kappa light polypeptide gene enhancer in B cells inhibitor α (IkBα) and inhibits TNF-induced expression of intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) [2].

Moreover, Boc-D-FMK has also effectively attenuated the hepatocyte apoptosis in bile duct-ligated rats potentially improving the survival rates [3].

References:
[1] Cowburn AS, White JF, Deighton J, Walmsley SR, Chilvers ER. z-VAD-fmk augmentation of TNF alpha-stimulated neutrophil apoptosis is compound specific and does not involve the generation of reactive oxygen species. Blood. 2005 Apr 1;105(7):2970-2. Epub 2004 Nov 30.
[2] Wu X, Guo R, Chen P, Wang Q, Cunningham PN. TNF induces caspase-dependent inflammation in renal endothelial cells through a Rho- and myosin light chain kinase-dependent mechanism. Am J Physiol Renal Physiol. 2009 Aug;297(2):F316-26. doi: 10.1152/ajprenal.00089.2009. Epub 2009 May 6.
[3] Sheen-Chen SM, Hung KS, Eng HL. Effect of Boc-D-Fmk on hepatocyte apoptosis after bile duct ligation in rat and survival rate after endotoxin challenge. J Gastroenterol Hepatol. 2008 Aug;23(8 Pt 1):1276-9. doi: 10.1111/j.1440-1746.2008.05368.x. Epub 2008 Mar 27.

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References on Boc-D-FMK

Effect of Boc-D-Fmk on hepatocyte apoptosis after bile duct ligation in rat and survival rate after endotoxin challenge.[Pubmed:18373562]

J Gastroenterol Hepatol. 2008 Aug;23(8 Pt 1):1276-9.

BACKGROUND AND AIM: Retention and accumulation of toxic hydrophobic bile salts within hepatocytes may cause hepatocyte toxicity by inducing apoptosis. Apoptosis is a pathway of cell death orchestrated by a family of proteases called caspases. Boc-D-FMK is a cell-permeable irreversible inhibitor of caspase and recent data suggest that it might block the processing of many caspases. The purpose of the present study was to evaluate the possible effect of Boc-D-FMK on hepatocyte apoptosis and on survival rate after bile duct ligation in the rat. METHODS: Male Sprague-Dawley rats, weighing 280-300 g were randomized to three groups of eight rats each. Group 1 (OBBOC-D) underwent common bile duct ligation and simultaneous treatment with Boc-D-FMK-fmk (dissolved in dimethylsulfoxide [DMSO]). Group 2 (OBZFA) underwent common bile duct ligation and simultaneous treatment with ZFA-fmk (dissolved in DMSO). Group 3 (SHAM) underwent sham operation and simultaneous treatment with the same amount of dimethylsulfoxide (DMSO, n = 4) or the same amount of normal saline (n = 4). After 3 days, liver tissue was harvested for histopathological analysis and measurements of apoptosis. Survival rates were measured in a separate experiment in which animals underwent the same protocol. The animals received endotoxin (15 mg/kg) in the afternoon of the third postoperative day. Animals were observed for 48 h and the survival rates were recorded. RESULTS: When compared with sham operation, common bile duct ligation with ZFA-fmk (placebo) significantly increased hepatocyte apoptosis (P < 0.001). When compared with the OBZFA group, Boc-D-FMK significantly diminished the increased hepatocyte apoptosis in the OBBOC-D group (P < 0.001). There is no difference in hepatocyte apoptosis (P = 0.05) between OBBOC-D and SHAM groups. After endotoxin challenge, the 48 h survival rates were 100%, 87.5% and 62.5% for the SHAM, OBBOC-D and OBZFA groups, respectively. CONCLUSIONS: Boc-D-FMK-fmk effectively attenuated the hepatocyte apoptosis in bile duct-ligated rats and may improve the survival rates after endotoxin challenge.

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