产品
编 号：F517581
分子式：C12H11N3O
分子量：213.24
分子式：C12H11N3O
分子量：213.24
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
询价
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5mg
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10mg
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50mg
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结构图
CAS No: 91396-88-2
产品详情
生物活性：
PluriSIn 1 (NSC 14613) is an inhibitor of stearoyl-coA desaturase (SCD), and is a pluripotent cell-specific inhibitor.
体外研究：
PluriSIn 1, a small-molecule inhibitor of stearoyl-coA desaturase (SCD), on induced pluripotent stem cells (iPS)-derived cardiomyocytes (CM). PluriSIn 1 treatment significantly decreases the mRNA and protein level of Nanog, a marker for both cell pluripotency and tumor progression; importantly, we provide evidence that PluriSIn 1 treatment at 20 μM for 1 day significantly induces the apoptosis of Nanog-positive iPS derivates (iPSD). In addition, PluriSIn 1 treatment at 20 μM for 4 days diminished Nanog-positive stem cells in cultured iPSD while not increasing apoptosis of iPS-derived CM. To investigate whether PluriSIn 1 treatment prevents tumorigenicity of iPSD after cell transplantation, we intramyocardially injected PluriSIn 1- or DMSO-treated iPSD in a mouse model of myocardial infarction (MI). DMSO-treated iPSD readily formed Nanog-expressing tumors 2 weeks after injection, which is prevented by treatment with PluriSIn 1. Moreover, treatment with PluriSIn 1 does not change the expression of cTnI, α-MHC, or MLC-2v, markers of cardiac differentiation (P>0.05, n=4). Importantly, PluriSIn 1-treated iPS-derived CM exhibits the ability to engraft and survive in the infarcted myocardium.
PluriSIn 1 (NSC 14613) is an inhibitor of stearoyl-coA desaturase (SCD), and is a pluripotent cell-specific inhibitor.
体外研究：
PluriSIn 1, a small-molecule inhibitor of stearoyl-coA desaturase (SCD), on induced pluripotent stem cells (iPS)-derived cardiomyocytes (CM). PluriSIn 1 treatment significantly decreases the mRNA and protein level of Nanog, a marker for both cell pluripotency and tumor progression; importantly, we provide evidence that PluriSIn 1 treatment at 20 μM for 1 day significantly induces the apoptosis of Nanog-positive iPS derivates (iPSD). In addition, PluriSIn 1 treatment at 20 μM for 4 days diminished Nanog-positive stem cells in cultured iPSD while not increasing apoptosis of iPS-derived CM. To investigate whether PluriSIn 1 treatment prevents tumorigenicity of iPSD after cell transplantation, we intramyocardially injected PluriSIn 1- or DMSO-treated iPSD in a mouse model of myocardial infarction (MI). DMSO-treated iPSD readily formed Nanog-expressing tumors 2 weeks after injection, which is prevented by treatment with PluriSIn 1. Moreover, treatment with PluriSIn 1 does not change the expression of cTnI, α-MHC, or MLC-2v, markers of cardiac differentiation (P>0.05, n=4). Importantly, PluriSIn 1-treated iPS-derived CM exhibits the ability to engraft and survive in the infarcted myocardium.
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