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Merck

SML1343

Sigma-Aldrich

3PO

≥98% (HPLC)

Sinónimos:

(2E)-3-(3-Pyridinyl)-1-(4-pyridinyl)-2-propen-1-one, 3PO (inhibitor of glucose metabolism)

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About This Item

Fórmula empírica (notación de Hill):
C13H10N2O
Número de CAS:
Peso molecular:
210.23
MDL number:
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77

Quality Level

assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 5 mg/mL, clear (warmed)

storage temp.

2-8°C

SMILES string

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+

InChI key

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).

Biochem/physiol Actions

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.

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


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Siyuan Yan et al.
American journal of cancer research, 11(5), 2062-2080 (2021-06-08)
Cancer cells prone to utilize aerobic glycolysis other than oxidative phosphorylation to sustain its continuous cell activity in the stress microenvironment. Meanwhile, cancer cells generally suffer from genome instability, and both radiotherapy and chemotherapy may arouse DNA strand break, a
Wenwen Yang et al.
Redox biology, 67, 102921-102921 (2023-10-20)
Acute kidney injury (AKI) presents a daunting challenge with limited therapeutic options. To explore the contribution of N6-methyladenosine (m6A) in AKI development, we have investigated m6A-modified mRNAs within renal tubular cells subjected to injuries induced by diverse stressors. Notably, while
Yi-Jia Li et al.
Cell reports, 39(9), 110870-110870 (2022-06-02)
Overcoming resistance to chemotherapies remains a major unmet need for cancers, such as triple-negative breast cancer (TNBC). Therefore, mechanistic studies to provide insight for drug development are urgently needed to overcome TNBC therapy resistance. Recently, an important role of fatty
Krzysztof Kotowski et al.
Anticancer research, 40(5), 2613-2625 (2020-05-06)
The occurrence of BRAFV600E mutation causes an up-regulation of the B-raf kinase activity leading to the stabilization of hypoxia-inducible factor 1-alpha (HIF-1α) - the promoter of the 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3) enzyme. The aim of the study was to examine the
Husniye Kantarci et al.
eLife, 9 (2020-04-28)
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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