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D3821

Sigma-Aldrich

Devazepide

≥98% (HPLC), powder

Synonym(s):

(S)-N-(2,3-Dihydro-1-methyl-2-oxo-5-phenyl-1H-1,4-benzodiazepin-3-yl)indole-2-carboxamide, L-364,718, MK 329

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About This Item

Empirical Formula (Hill Notation):
C25H20N4O2
CAS Number:
103420-77-5
Molecular Weight:
408.45
MDL number:
MFCD00864500
UNSPSC Code:
12352200
PubChem Substance ID:
329798778
NACRES:
NA.77

Quality Level

100

Assay

≥98% (HPLC)

form

powder

storage condition

desiccated

color

white to off-white

solubility

DMSO: >5 mg/mL

originator

Merck & Co., Inc., Kenilworth, NJ, U.S.

storage temp.

2-8°C

SMILES string

CN1C(=O)[C@@H](NC(=O)c2cc3ccccc3[nH]2)N=C(c4ccccc4)c5ccccc15

InChI

1S/C25H20N4O2/c1-29-21-14-8-6-12-18(21)22(16-9-3-2-4-10-16)27-23(25(29)31)28-24(30)20-15-17-11-5-7-13-19(17)26-20/h2-15,23,26H,1H3,(H,28,30)/t23-/m1/s1

InChI key

NFHRQQKPEBFUJK-HSZRJFAPSA-N

General description

Devazepide is derived from asperlicin by chemical modification and has the benzodiazepine backbone.

Application

Devazepide has been used as a cholecystokinin receptor 1 (CCK1R) antagonist in human embryonic kidney 293T cells and in human pancreatic slices.

Biochem/physiol Actions

Devazepide is a CCK1 (CCK-A) receptor antagonist and a CCK8 antagonist.
Devazepide is a cholecystokinin octapeptide (CCK1) (CCK-A) receptor antagonist. It inhibits CCK binding to peripheral-type receptor (CCK-A). Devazepide reverses the cholecystokinin octapeptide (CCK-8) based antagonism towards morphine.

Features and Benefits

This compound was developed by Merck & Co., Inc., Kenilworth, NJ, U.S.. To browse the list of other pharma-developed compounds and Approved Drugs/Drug Candidates, click here.

Pictograms

Skull and crossbones
GHS06

Signal Word

Danger

Hazard Statements

H300

Hazard Classifications

Acute Tox. 1 Oral

Storage Class Code

6.1A - Combustible acute toxic Cat. 1 and 2 / very toxic hazardous materials

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Regulatory Listings

Regulatory Listings are mainly provided for chemical products. Only limited information can be provided here for non-chemical products. No entry means none of the components are listed. It is the user’s obligation to ensure the safe and legal use of the product.

JAN Code

D3821-IP:
D3821-5MG:
D3821-BULK:
D3821-VAR:
D3821-25MG:

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Development of a CCK1R-membrane nanoparticle as a fish-out tool for bioactive peptides
Staljanssens D, et al.
Peptides, 68, 219-227 (2015)
Kaleeckal G Harikumar et al.
Assay and drug development technologies, 9(4), 394-402 (2011-03-15)
The success in screening for drug candidates is highly dependent on the power of the strategy implemented. In this work, we report and characterize a novel fluorescent benzodiazepine antagonist of the type 1 cholecystokinin receptor (3-(3-(7-fluoro-1-(2-isopropyl(4-methoxyphenyl)amino)-2-oxoethyl)-2,4-dioxo-5-phenyl-2,3,4,5-tetrahydro-1H-benzo[b][1,4]-diazepin-3-yl)ureido)benzoic acid) that can be
X-M Wu et al.
Journal of animal physiology and animal nutrition, 96(2), 214-219 (2011-03-29)
Total parenteral nutrition (TPN) results in atrophy of the pancreas, while cholecystokinin (CCK) can significantly stimulate the exocrine pancreas in rodents. This study was designed to examine whether CCK may improve the atrophy of the pancreas in rats on TPN
Clémence Blouet et al.
PloS one, 7(12), e51898-e51898 (2012-12-20)
Previous evidence indicates that duodenal lipid sensing engages gut-brain neurocircuits to determine food intake and hepatic glucose production, but a potential role for gut-brain communication in the control of energy expenditure remains to be determined. Here, we tested the hypothesis
Wenya Chen et al.
Bioscience, biotechnology, and biochemistry, 76(6), 1104-1109 (2012-07-14)
We have recently reported that oral gavage of a potato extract (Potein®) suppressed the food intake in rats. The satiating effect of the potato extract was compared in the present study to other protein sources, and the involvement of endogenous
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