SML2146
SR-18292 Maleate
≥98% (HPLC), hepatic gluconeogenesis inhibitor, powder
Synonym(s):
SR-18292 Maleate, 1-[(1,1-Dimethylethyl)[(4-methylphenyl)methyl]amino]-3-(1H-indol-4-yloxy)-2-propanol maleate, SR 18292, SR 18292 maleate
Sign In to View Organizational & Contract Pricing.
Select a Size
About This Item
Empirical Formula (Hill Notation):
C23H30N2O2 · C4H4O4
CAS Number:
Molecular Weight:
482.57
UNSPSC Code:
12352200
NACRES:
NA.77
Product Name
SR-18292 Maleate, ≥98% (HPLC)
InChI key
CMTOYDGVFTZNSM-BTJKTKAUSA-N
SMILES string
CC(C)(C)N(CC(O)COC1=CC=CC2=C1C=CN2)CC3=CC=C(C)C=C3.O=C(O)/C=C\C(O)=O
assay
≥98% (HPLC)
form
powder
color
white to beige
solubility
DMSO: 2 mg/mL, clear
storage temp.
2-8°C
Related Categories
Application
SR-18292 Maleate has been used as a peroxisome proliferator-activated receptor γ coactivator 1 α (PGC1α) inhibitor to study the protective effects of pioglitazone on demyelinated axons.
Biochem/physiol Actions
SR-18292 is a potent and specific inhibitor of hepatic gluconeogenesis via increased acetylation of PGC-1α and suppression of gluconeogenic gene expression. SR-18292 reduces blood glucose and increases hepatic insulin sensitivity in mouse models of T2D.
inhibitor of hepatic gluconeogenesis via increased acetylation of PGC-1α; anti-diabetic
Storage Class
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Choose from one of the most recent versions:
Already Own This Product?
Find documentation for the products that you have recently purchased in the Document Library.
Simon Licht-Mayer et al.
Acta neuropathologica, 140(2), 143-167 (2020-06-24)
Axonal loss is the key pathological substrate of neurological disability in demyelinating disorders, including multiple sclerosis (MS). However, the consequences of demyelination on neuronal and axonal biology are poorly understood. The abundance of mitochondria in demyelinated axons in MS raises
Kfir Sharabi et al.
Cell, 169(1), 148-160 (2017-03-25)
Type 2 diabetes (T2D) is a worldwide epidemic with a medical need for additional targeted therapies. Suppression of hepatic glucose production (HGP) effectively ameliorates diabetes and can be exploited for its treatment. We hypothesized that targeting PGC-1α acetylation in the liver
Rama Krishna Nimmakayala et al.
Clinical cancer research : an official journal of the American Association for Cancer Research, 27(19), 5415-5429 (2021-06-27)
Metabolic reprogramming and cancer stem cells drive the aggressiveness of pancreatic ductal adenocarcinoma (PDAC). However, the metabolic and stemness programs of pancreatic precursor lesions (PPL), considered early PDAC development events, have not been thoroughly explored. Meta-analyses using gene expression profile
Prakash P Praharaj et al.
Autophagy, 20(6), 1359-1382 (2024-03-07)
Mitophagy involves the selective elimination of defective mitochondria during chemotherapeutic stress to maintain mitochondrial homeostasis and sustain cancer growth. Here, we showed that CLU (clusterin) is localized to mitochondria to induce mitophagy controlling mitochondrial damage in oral cancer cells. Moreover
Our team of scientists has experience in all areas of research including Life Science, Material Science, Chemical Synthesis, Chromatography, Analytical and many others.
Contact Technical Service