Boc-D-FMK
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Boc-D-FMK

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BOC-D-FMK is a cell-permeable broad-spectrum caspase inhibitor that fully inhibits the pro-apoptotic effect of tumor necrosis factor-α (TNFα). It 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 inhibit TNF-induced expression of intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1). Moreover, it has also effectively attenuated the hepatocyte apoptosis in bile duct-ligated rats potentially improving the survival rates.

Category
Peptide Inhibitors
Catalog number
BAT-010386
CAS number
187389-53-3
Molecular Formula
C11H18FNO5
Molecular Weight
263.26
Boc-D-FMK
Size Price Stock Quantity
100 mg $899 In stock
IUPAC Name
methyl (3S)-5-fluoro-3-[(2-methylpropan-2-yl)oxycarbonylamino]-4-oxopentanoate
Alternative CAS
634911-80-1
Synonyms
Boc-Asp(OMe)-fluoromethyl ketone; Caspase Inhibitor 3; N-Boc-L-aspartic acid 4-methyl ester fluoromethyl ketone; BAF; Boc-D-Fluoromethyl Ketone; Boc-D(OMe)-FMK; 3S-[[(1,1-dimethylethoxy)carbonyl]amino]-5-fluoro-4-oxo-pentanoic acid, methyl ester; Caspase Inhibitor III
Appearance
Off-white crystalline Solid
Purity
95%
Density
1.150±0.06 g/cm3 at 20°C, 760 Torr
Boiling Point
383.5±37.0°C (Predicted)
Storage
Store at -20°C
Solubility
Slightly soluble in DMF, DMSO, Ethanol, PBS
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)/t7-/m0/s1
InChI Key
MXOOUCRHWJYCAL-ZETCQYMHSA-N
Canonical SMILES
CC(C)(C)OC(=O)NC(CC(=O)OC)C(=O)CF
1.p27KIP1 is down-regulated by two different mechanisms in human lymphoid cells undergoing apoptosis.
Frost V;Sinclair AJ Oncogene. 2000 Jun 22;19(27):3115-20.
The cyclin-dependent kinase inhibitor p27KIP1 is a crucial component of the mammalian restriction point, and as such is subject to multiple regulatory mechanisms. It has recently been shown that the abundance of p27KIP1 is also regulated during apoptosis; p27KIP1 is cleaved by a Z-VAD-fmk-sensitive caspase during apoptosis induced by growth factor deprivation in endothelial cells, and also following exposure of myeloid leukaemia cells to etoposide. Here, we investigate p27KIP1 regulation in B- and T-lymphoid cells undergoing apoptosis. We observe that p27KIP1 is down-regulated following exposure to a variety of apoptotic stimuli including an agonistic anti-Fas antibody, cycloheximide and etoposide. Further investigation revealed the existence of two different routes of p27KIP1 regulation in lymphoid cells undergoing apoptosis. The first pathway is utilized by lymphoid cells stimulated through Fas, is abrogated in a caspase-8-deficient T-cell line, and is blocked by the caspase inhibitors Z-VAD-fmk and Boc-D-fmk. In contrast, the loss of p27KIP1 in cells exposed to cycloheximide and etoposide occurs in the absence of caspase-8 or any Z-VAD-fmk- or Boc-D-fmk-sensitive caspase activities.
2.p38 MAPK mediates TNF-induced apoptosis in endothelial cells via phosphorylation and downregulation of Bcl-x(L).
Grethe S;Ares MP;Andersson T;Pörn-Ares MI Exp Cell Res. 2004 Aug 15;298(2):632-42.
The role of p38 mitogen-activated protein kinase (MAPK) in apoptosis is a matter of debate. Here, we investigated the involvement of p38 MAPK in endothelial apoptosis induced by tumor necrosis factor alpha (TNF). We found that activation of p38 MAPK preceded activation of caspase-3, and the early phase of p38 MAPK stimulation did not depend on caspase activity, as shown by pretreatment with the caspase inhibitors z-Val-Ala-Asp(OMe)-fluoromethylketone (zVAD-fmk) and Boc-Asp(OMe)-fluoromethylketone (BAF). The p38 MAPK inhibitor SB203580 significantly attenuated TNF-induced apoptosis in endothelial cells, suggesting that p38 MAPK is essential for apoptotic signaling. Furthermore, we observed a time-dependent increase in active p38 MAPK in the mitochondrial subfraction of cells exposed to TNF. Notably, the level of Bcl-x(L) protein was reduced in cells undergoing TNF-induced apoptosis, and this reduction was prevented by treatment with SB203580. Immunoprecipitation experiments revealed p38 MAPK-dependent serine-threonine phosphorylation of Bcl-x(L) in TNF-treated cells. Exposure to lactacystin prevented both the downregulation of Bcl-x(L) and activation of caspase-3. Taken together, our results suggest that TNF-induced p38 MAPK-mediated phosphorylation of Bcl-x(L) in endothelial cells leads to degradation of Bcl-x(L) in proteasomes and subsequent induction of apoptosis.
3.Selective caspase activation may contribute to neurological dysfunction after experimental spinal cord trauma.
Knoblach SM;Huang X;VanGelderen J;Calva-Cerqueira D;Faden AI J Neurosci Res. 2005 May 1;80(3):369-80.
Caspases are implicated in apoptotic cell death after spinal cord injury (SCI), but the relative contribution of these proteases to the secondary injury process has been only partially described. We examined the activation of caspases 1, 2, 3, 6, 8, and 9 from 1 hr to 7 days after moderate contusion injury induced by a weight-drop method in the rat. Tissue homogenates from a 1-cm segment of cord that contained the site of impact were processed by fluorometric enzymatic activity assays and/or immunoblotting methods. Caspases 3, 8, and 9 were activated from 1 to 72 hr after injury, whereas caspases 1, 2, and 6 were not. Double-label immunohistochemistry utilizing antibodies for CNS cell-type-specific markers and active subunits of caspases 3, 8, or 9 showed that, at 4 and 72 hr after injury, these caspases were primarily activated in neurons and oligodendrocytes, rather than in astrocytes. Active caspase subunits were present in neurons within the necrotic lesion core at 4 hr after injury and in cells more than several segments away at 4 or 72 hr after injury. Intrathecal injection of the pan-caspase inhibitor Boc-Asp (OMe)-fluoromethylketone (Boc-d-fmk) at 15 min after injury improved locomotor function 21 and 28 days later.
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