153088-73-4

153088-73-4 structure

Name: Z-Asp-CH2-DCB
Chemical Name: z-asp-2,6-dichlorobenzoyloxymethylketone
CAS Number: 153088-73-4
Molecular Formula: C₂₀H₁₇Cl₂NO₇
Molecular Weight: 454.258
Catalog: Signaling Pathways Apoptosis Caspase
Create Date: 2018-10-18 08:33:14
Modify Date: 2024-01-13 19:14:48
Z-Asp-CH2-DCB is an irreversible broad spectrum caspase inhibitor. Z-Asp-CH2-DCB also inhibits proteases with caspase-like activity. Z-D-CH2-DCB blocks the production of IL-1β, TNF-α, IL-6, and IFN-γ in staphylococcal enterotoxin B (SEB)-stimulated peripheral blood mononuclear cells (PBMC), and reduces SEB-1-stimulated T-cell proliferation in a dose-dependent manner. Z-Asp-CH2-DCB prevents SU5416-induced septal cell apoptosis and emphysema development[1][2][3].

Name	z-asp-2,6-dichlorobenzoyloxymethylketone
Synonyms	pase-1 inhibitor v ice inhibitor vi (3S)-3-{[(Benzyloxy)carbonyl]amino}-5-[(2,6-dichlorobenzoyl)oxy]-4-oxopentanoic acid Benzoic acid, 2,6-dichloro-, (3S)-4-carboxy-2-oxo-3-[[(phenylmethoxy)carbonyl]amino]butyl ester pase-1 inhibitor iii z-d-ch2-dcb z-asp-ch2-dcb ice inhibitor v

Description	Z-Asp-CH2-DCB is an irreversible broad spectrum caspase inhibitor. Z-Asp-CH2-DCB also inhibits proteases with caspase-like activity. Z-D-CH2-DCB blocks the production of IL-1β, TNF-α, IL-6, and IFN-γ in staphylococcal enterotoxin B (SEB)-stimulated peripheral blood mononuclear cells (PBMC), and reduces SEB-1-stimulated T-cell proliferation in a dose-dependent manner. Z-Asp-CH2-DCB prevents SU5416-induced septal cell apoptosis and emphysema development[1][2][3].
Related Catalog	Signaling Pathways >> Apoptosis >> Caspase Research Areas >> Inflammation/Immunology
In Vitro	Z-Asp-CH2-DCB (10-100 μM) blocks the production of IL-1β, TNF-α, IL-6, and IFN-γ in SEB-stimulated (200 ng; 16 hours) PBMC in a dose-dependent manner. The production of the chemokines MCP-1, MIP-1α, and MIP-1β was also suppresses. The inhibitory effect of Z-Asp-CH2-DCB on TSST-1-activated PBMC is similar, reducing IL-1β, IL-6, TNF-α, IFN-γ, MCP-1, MIP-1α, and MIP-1β to 10, 36, 25, 10, 11, 25, and 30%, respectively, of levels in untreated cells[1]. Z-Asp-CH2-DCB (10-100 μM; 48 hours) inhibits T-cell proliferation in PBMC stimulated with 200 ng of SEB/ml [1]. Cell Viability Assay[1] Cell Line: Human peripheral blood mononuclear cells Concentration: 10, 50, 100 μM Incubation Time: 48 hours Result: Inhibited T-cell proliferation in PBMC stimulated with SEB.
In Vivo	Z-Asp-CH2-DCB (1 mg; i.p.; every day for 3 weeks) prevents SU5416-induced septal cell apoptosis[1]. Animal Model: Male Sprague-Dawley rats (SU5416+ Z-Asp-CH2-DCB group)[1] Dosage: 1 mg Administration: Intraperitoneal injection; every day for 3 weeks Result: The caspase 3-like activity in SU5416-treated rat lungs is significantly higher, whereas lungs from rats treated with SU5416+Z-Asp-CH2-DCB showed no increase in apoptotic activity.
References	[1]. Krakauer T, et al. Caspase inhibitors attenuate superantigen-induced inflammatory cytokines, chemokines, and T-cell proliferation. Clin Diagn Lab Immunol. 2004 May;11(3):621-4. [2]. Kasahara Y, et al. Inhibition of VEGF receptors causes lung cell apoptosis and emphysema. J Clin Invest. 2000 Dec;106(11):1311-9. [3]. Twumasi P, et al. Caspase inhibitors affect the kinetics and dimensions of tracheary elements in xylogenic Zinnia (Zinnia elegans) cell cultures. BMC Plant Biol. 2010 Aug 6;10:162.

Density	1.4±0.1 g/cm3
Boiling Point	674.2±55.0 °C at 760 mmHg
Molecular Formula	C₂₀H₁₇Cl₂NO₇
Molecular Weight	454.258
Flash Point	361.6±31.5 °C
Exact Mass	453.038208
PSA	119.00000
LogP	5.29
Vapour Pressure	0.0±2.2 mmHg at 25°C
Index of Refraction	1.594

WGK Germany	3

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