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SML2546

Sigma-Aldrich

GLX351322

≥98% (HPLC)

Synonym(s):

2-[[2-[4-(2-Furanylcarbonyl)-1-piperazinyl]acetyl]amino]-5,6-dihydro-4H-cyclopenta[b]thiophene-3-carboxylic acid ethyl ester

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5 MG
$100.00
25 MG
$406.00

$100.00

Available to ship onApril 29, 2025Details

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5 MG
$100.00
25 MG
$406.00

About This Item

Empirical Formula (Hill Notation):
C21H25N3O5S
CAS Number:
835598-94-2
Molecular Weight:
431.51
MDL number:
MFCD05123600
UNSPSC Code:
12352200
NACRES:
NA.77

$100.00

Available to ship onApril 29, 2025Details

Request a Bulk Order

assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 2 mg/mL, clear

storage temp.

2-8°C

SMILES string

O=C(C1=C(NC(CN2CCN(C(C3=CC=CO3)=O)CC2)=O)SC4=C1CCC4)OCC

InChI key

KEVHLTCEMHIJTQ-UHFFFAOYSA-N

Biochem/physiol Actions

GLX351322 is a potent and selective inhibitor of NOX4 (NADPH oxidase 4). GLX351322 prevents ROS generation and cellular death, improves pancreatic beta cell function in high-fat diet fed C57Bl/6 mice.
potent and selective inhibitor of NOX4 (NADPH oxidase 4)

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

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Certificates of Analysis (COA)

Lot/Batch Number
0000167924
0000207172

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Qing-Liang Wen et al.
Molecular and cellular endocrinology, 523, 111144-111144 (2021-01-01)
In this study, we aimed to clarify the role of PIM-1 in papillary thyroid carcinoma (PTC) in vitro and investigate the relationship between PIM-1 and redox proteins (NOX4, SOD2, and GPX2) at the tissue and cellular levels. As a PIM-1
E Anvari et al.
Free radical research, 49(11), 1308-1318 (2015-06-30)
In type 2 diabetes, it has been proposed that pancreatic beta-cell dysfunction is promoted by oxidative stress caused by NADPH oxidase (NOX) overactivity. Five different NOX enzymes (NOX1-5) have been characterized, among which NOX1 and NOX2 have been proposed to
Xuan Wang et al.
PloS one, 13(9), e0204271-e0204271 (2018-09-29)
It has been proposed that pancreatic beta-cell dysfunction in type 2 diabetes is promoted by oxidative stress caused by NADPH oxidase (Nox) over-activity. The aim of the present study was to evaluate the efficacy of novel Nox inhibitors as protective

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