SML1343
3PO
≥98% (HPLC)
Synonyme(s) :
(2E)-3-(3-Pyridinyl)-1-(4-pyridinyl)-2-propen-1-one, 3PO (inhibitor of glucose metabolism)
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About This Item
Formule empirique (notation de Hill):
C13H10N2O
Numéro CAS:
Poids moléculaire :
210.23
Numéro MDL:
Code UNSPSC :
12352200
ID de substance PubChem :
Nomenclature NACRES :
NA.77
Produits recommandés
Niveau de qualité
Pureté
≥98% (HPLC)
Forme
powder
Couleur
white to beige
Solubilité
DMSO: 5 mg/mL, clear (warmed)
Température de stockage
2-8°C
Chaîne SMILES
O=C(C1=CC=NC=C1)/C=C/C2=CN=CC=C2
InChI
1S/C13H10N2O/c16-13(12-5-8-14-9-6-12)4-3-11-2-1-7-15-10-11/h1-10H/b4-3+
Clé InChI
UOWGYMNWMDNSTL-ONEGZZNKSA-N
Application
3PO has been used as a 6-Phosphofructo-2-kinase/fructose-2,6-bisphosphatase isoform 3(PFKFB3) inhibitor to study its effect on cell viability loss, apoptosis, and necroptosis in colorectal cancer cells. It has also been used as a PFKFB3 inhibitor to inhibit glycolysis and study its effects on cell viability and reactive oxygen species (ROS) production in trabectedin (TRB) and lurbinectedin (LUR) treated human macrophages (hMFs).
Actions biochimiques/physiologiques
3PO is a potent and selective inhibitor of PFKFB3 (6-Phosphofructo-2-kinase/fructose-2,6-bisphosphatase) that reduces glycolytic flux and suppresses glucose uptake. 3PO is selectively cytostatic to transformed cells and suppresses the growth of established tumor in mice.
Inhibition of glycolysis by PFKFB3 blockade mediated by 3PO reduced pathological angiogenesis in cancer and inflammation. 3PO aids in the regulation of endothelial proliferation and migration. It also reduces pro-inflammatory activation of endothelial cells and experimental inflammation in vivo. Therefore, it may be a potential therapeutic for treating chronic inflammation. Its anti-inflammatory activity in human endothelial cells is independent of its target PFKFB3.
Code de la classe de stockage
11 - Combustible Solids
Classe de danger pour l'eau (WGK)
WGK 3
Point d'éclair (°F)
Not applicable
Point d'éclair (°C)
Not applicable
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Recent studies indicate that many developing tissues modify glycolysis to favor lactate synthesis (Agathocleous et al., 2012; Bulusu et al., 2017; Gu et al., 2016; Oginuma et al., 2017; Sá et al., 2017; Wang et al., 2014; Zheng et al.
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