787-59-7Relevant academic research and scientific papers
Thienopyrimidinone compound and use thereof
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Paragraph 0122; 0126; 0128; 0134-0137, (2019/01/20)
The invention belongs to the field of chemical medicines and specifically relates to a thienopyrimidinone compound. The thienopyrimidinone compound has a structural formula shown in the description. The novel thienopyrimidinone compound can produce good inhibition effects on Tankyrase, has no obvious toxicity, can obviously inhibit the proliferation of tumor cells after STF3A cell treatment basedon the compound, has the good medicinal potential and provides a novel potential choice for clinical medication. The novel thienopyrimidinone compound can improve the expression level of an axin in the wnt signal pathway, induce the degradation of beta-catenin, thereby inhibiting the proliferation of tumor cells, can be used as a clinical prodrug candidate compound for various tumor cells and hasfurther research and development potential. A preparation method of the thienopyrimidinone compound can produce the compound with a high yield and high biological activity. The thienopyrimidinone compound has significant drug properties and has broad market prospects.
WNT INHIBITORS FOR HUMAN STEM CELL DIFFERENTIATION
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Paragraph 0176, (2013/07/19)
Methods and small molecule compounds for stem cell differentiation and treatment of animals with diseases are provided. One example of a class of compounds that may be used is represented by the compound of Formula I and II: or a pharmaceutically acceptab
Wnt inhibition correlates with human embryonic stem cell cardiomyogenesis: A structure-activity relationship study based on inhibitors for the Wnt response
Lanier, Marion,Schade, Dennis,Willems, Erik,Tsuda, Masanao,Spiering, Sean,Kalisiak, Jaroslaw,Mercola, Mark,Cashman, John R.
, p. 697 - 708 (2012/04/10)
Human embryonic stem cell-based high-content screening of 550 known signal transduction modulators showed that one "lead" (1, a recently described inhibitor of the proteolytic degradation of Axin) stimulated cardiomyogenesis. Because Axin controls canonical Wnt signaling, we conducted an investigation to determine whether the cardiogenic activity of 1 is Wnt-dependent, and we developed a structure-activity relationship to optimize the cardiogenic properties of 1. We prepared analogues with a range of potencies (low nanomolar to inactive) for Wnt/β-catenin inhibition and for cardiogenic induction. Both functional activities correlated positively (r 2 = 0.72). The optimal compounds induced cardiogenesis 1.5-fold greater than 1 at 30-fold lower concentrations. In contrast, no correlation was observed for cardiogenesis and modulation of transforming growth factor β (TGFβ)/Smad signaling that prominently influences cardiogenesis. Taken together, these data show that Wnt signaling inhibition is essential for cardiogenic activity and that the pathway can be targeted for the design of druglike cardiogenic molecules.
