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Merck

324890

E-64 Protease Inhibitor

The E-64 Protease Inhibitor, also referenced under CAS 66701-25-5, controls the biological activity of E-64 Protease. This small molecule/inhibitor is primarily used for Protease Inhibitors applications.

Synonyme(s) :

E-64 Protease Inhibitor, (2 R,3 R)-3-(( S)-1-(4-Guanidinobutylamino)-4-methyl-1-oxopentan-2-ylcarbamoyl)oxirane-2-carboxylic acid, trans-Epoxysuccinyl-L-​leucylamido(4-​guanidino)​butane, L- trans-​3-​Carboxyoxira, (2R,3R)-3-((S)-1-(4-Guanidinobutylamino)-4-methyl-1-oxopentan-2-ylcarbamoyl)oxirane-2-carboxylic acid, trans-Epoxysuccinyl-L-​leucylamido(4-​guanidino)​butane, L-trans-​3-​Carboxyoxiran-R

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A propos de cet article

Formule empirique (notation de Hill) :
C15H27N5O5
Numéro CAS:
66701-25-5
Poids moléculaire :
357.41
UNSPSC Code:
12352200
NACRES:
NA.77
MDL number:
MFCD00080261

Principaux documents

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SMILES string

N([C@@H](CC(C)C)C(=O)NCCCCN\C(=N/[H])\N)C(=O)[C@@H]1O[C@H]1C(=O)O

InChI

1S/C15H27N5O5/c1-8(2)7-9(20-13(22)10-11(25-10)14(23)24)12(21)18-5-3-4-6-19-15(16)17/h8-11H,3-7H2,1-2H3,(H,18,21)(H,20,22)(H,23,24)(H4,16,17,19)/t9-,10+,11+/m0/s1

InChI key

LTLYEAJONXGNFG-HBNTYKKESA-N

description

RTECS - RR0390000

assay

≥98% (HPLC)

form

solid

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze

color

white

solubility

water: 20 mg/mL, DMSO: 25 mg/mL

shipped in

ambient

storage temp.

−20°C

Quality Level

200

General description

Irreversible inhibitor of cysteine proteases. Interacts with the Sn subsites of proteases. Has no action on cysteine residues in other proteins. Inhibits activation-induced programmed cell death and restores defective immune responses in HIV+ donors. Specific active site titrant.

Biochem/physiol Actions

Cell permeable: no
Primary Target
cysteine proteases
Product does not compete with ATP.
Reversible: no

Preparation Note

Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 4 months at -20°C.

Other Notes

Matsumoto, K., et al. 1999. Biopolymers51, 99.
Sarin, A., et al. 1994. J. Immunol.153, 862.
Sarin, A., et al. 1993. J. Exp. Med. 178, 1693.
Barrett, A.J. 1982. Biochem. J.201, 189.

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Disclaimer

Toxicity: Standard Handling (A)

Classe de stockage

11 - Combustible Solids

flash_point_f

Not applicable

flash_point_c

Not applicable

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Michael Anthony Jensen et al.
Biochemistry, 63(1), 9-18 (2023-11-28)
Here we report preliminary data demonstrating that some patients with myalgic encephalomyelitis/chronic fatiguesyndrome (ME/CFS) may have catalytic autoantibodies that cause the breakdown of myelin basic protein (MBP). We propose that these MBP-degradative antibodies are important to the pathophysiology of ME/CFS
Judith Bockstiegel et al.
Cell communication and signaling : CCS, 21(1), 335-335 (2023-11-24)
The purinergic receptor P2X7 plays a crucial role in infection, inflammation, and cell death. It is thought that P2X7 receptor stimulation triggers processing and release of the pro-inflammatory cytokine interleukin (IL)-1β by activation of the NLRP3 inflammasome; however, the underlying
Dana Bohan et al.
PLoS pathogens, 17(11), e1009743-e1009743 (2021-11-20)
Phosphatidylserine (PS) receptors enhance infection of many enveloped viruses through virion-associated PS binding that is termed apoptotic mimicry. Here we show that this broadly shared uptake mechanism is utilized by SARS-CoV-2 in cells that express low surface levels of ACE2.
Thomas Macleod et al.
Cell reports, 33(11), 108515-108515 (2020-12-17)
Epithelial tissues represent vital interfaces between organisms and their environment. As they are constantly exposed to harmful pathogens, innocuous commensals, and environmental microbes, it is essential they sense and elicit appropriate responses toward these different types of microbes. Here, we
Mehdi Benlarbi et al.
iScience, 25(11), 105316-105316 (2022-10-19)
The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) spike glycoprotein (S) binds to angiotensin-converting enzyme 2 (ACE2) to mediate membrane fusion via two distinct pathways: 1) a surface, serine protease-dependent or 2) an endosomal, cysteine protease-dependent pathway. In this study, we found
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