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SML2022

Sigma-Aldrich

UCSF924

≥98% (HPLC)

Synonym(s):

6-Methyl-2-((3-phenoxypropylamino)methyl)quinolin-4(1H)-one, ZINC000091726127

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About This Item

Empirical Formula (Hill Notation):
C20H22N2O2
CAS Number:
Molecular Weight:
322.40
UNSPSC Code:
12352200
NACRES:
NA.77

Assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 2 mg/mL, clear

storage temp.

−20°C

SMILES string

CC1=CC=C(NC(CNCCCOC2=CC=CC=C2)=CC3=O)C3=C1

Biochem/physiol Actions

UCSF924 (Compound 9-6-24; ZINC000091726127) is a selective, high-affinity dopamine D4 receptor (DRD4) partial agonist (Ki = 3 nM for human D4) with a 7.4-fold bias toward arrestin recruitment over Gαi (Gαi/0; Gi/G0) signaling activation with respect to quinpirole. UCSF924 exhibits no detectable affinity for D2, D3 or the F261V/L328F D4 mutant and no agonist activity toward a panel of 320 nonolfactory GPCRs even at a high concentration of 1 μM. The UCSF924 structure analog UCSF924NC (Comound 9-6-16; ZINC000091707446) is the recommended negative control compound with a 1/2500-fold reduced D4 affinity.

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


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Sheng Wang et al.
Science (New York, N.Y.), 358(6361), 381-386 (2017-10-21)
Dopamine receptors are implicated in the pathogenesis and treatment of nearly every neuropsychiatric disorder. Although thousands of drugs interact with these receptors, our molecular understanding of dopaminergic drug selectivity and design remains clouded. To illuminate dopamine receptor structure, function, and
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Neurobiology of disease, 103, 11-23 (2017-04-01)
Neurogenesis impairment is considered a major determinant of the intellectual disability that characterizes Down syndrome (DS), a genetic condition caused by triplication of chromosome 21. Previous evidence obtained in the Ts65Dn mouse model of DS showed that the triplicated gene
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Acta neuropathologica, 132(2), 257-276 (2016-05-04)
Endosomal-autophagic-lysosomal (EAL) dysfunction is an early and prominent neuropathological feature of Alzheimers's disease, yet the exact molecular mechanisms contributing to this pathology remain undefined. By combined biochemical, immunohistochemical and ultrastructural approaches, we demonstrate a link between EAL pathology and the
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Journal of Alzheimer's disease : JAD, 55(4), 1549-1570 (2016-12-03)
Alteration of mitochondria-associated membranes (MAMs) has been proposed to contribute to the pathogenesis of Alzheimer's disease (AD). We studied herein the subcellular distribution, the processing, and the protein interactome of the amyloid-β protein precursor (AβPP) and its proteolytic products in

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