SML1009
PFK15
≥98% (HPLC)
Synonym(s):
1-(4-Pyridinyl)-3-(2-quinolinyl)-2-propen-1-one
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About This Item
Assay
≥98% (HPLC)
form
powder
color
white to beige
solubility
DMSO: 10 mg/mL, clear
storage temp.
2-8°C
InChI
1S/C17H12N2O/c20-17(14-9-11-18-12-10-14)8-7-15-6-5-13-3-1-2-4-16(13)19-15/h1-12H/b8-7+
InChI key
UJJUKZPBUMCSJZ-BQYQJAHWSA-N
Application
PFK15, a PFKFB3 inhibitor has been used to investigate its effects on the modulation of autophagy and proliferation in rhabdomyosarcoma (RD) cells.
Biochem/physiol Actions
PFK15 is also referred as 1-(4-pyridinyl)-3-(2-quinolinyl)-2-propen-1-one. It prevents autophagy and multiplication in rhabdomyosarcoma cells. PFK15 results in cell death in gastric cancer cells via mitochondrial pathway. It also blocks MKN45 (human gastric cancer cell lines) tumor growth in vivo. PFK15 promotes cell cycle arrest and changes the upregulation of key cell cycle proteins.
PFK15 is potent and selective antagonist of PFKB3 (6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3) that causes a rapid induction of apoptosis in cancer and transformed cells. PFK15 inhibits the growth of LLC xenografts.
Storage Class Code
11 - Combustible Solids
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
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PFK15, a small molecule inhibitor of PFKFB3, induces cell cycle arrest, apoptosis and inhibits invasion in gastric cancer.
PLoS ONE, 11(9), e0163768-e0163768 (2016)
PFK15, a PFKFB3 antagonist, inhibits autophagy and proliferation in rhabdomyosarcoma cells.
International Journal of Molecular Medicine, 42(1), 359-367 (2018)
Oncotarget, 8(46), 80909-80922 (2017-11-09)
6-Phosphofructo-2-kinase/fructose-2,6-bisphosphatase isoform 3 (PFKFB3), is a critical enzyme for glycolysis and highly expressed in cancer cells. It plays an essential role in regulating metabolism, angiogenesis, and inflammation. Although PFKFB3 is involved in modulating autophagy, its regulatory role appears to be
Nature communications, 12(1), 879-879 (2021-02-11)
Salmonella Typhimurium establishes systemic infection by replicating in host macrophages. Here we show that macrophages infected with S. Typhimurium exhibit upregulated glycolysis and decreased serine synthesis, leading to accumulation of glycolytic intermediates. The effects on serine synthesis are mediated by
Cell death & disease, 6, e2005-e2005 (2015-12-04)
Rasfonin is a fungal secondary metabolite with demonstrated antitumor effects. However, the underlying mechanism of the regulatory role in autophagy initiated by rasfonin is largely unknown. Moreover, the function of Akt to positively mediate the induced autophagy remains elusive. In
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