产品
编 号：F406819
分子式：C16H22Cl2N2O2S
分子量：377.33
分子式：C16H22Cl2N2O2S
分子量：377.33
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
询价
询价
5mg
384
In-stock
10mg
608
In-stock
25mg
960
In-stock
50mg
1320
In-stock
100mg
1840
In-stock
结构图
CAS No: 61714-27-0
产品详情
生物活性：
W-7 hydrochloride is a selective calmodulin antagonist. W-7 hydrochloride inhibits the Ca2+-calmodulin-dependent phosphodiesterase and myosin light chain kinase with IC50 values of 28 μM and 51 μM, respectively. W-7 hydrochloride induces apoptosis and has antitumor activity.
体内研究：
W-7 (3 mg/kg; intraperitoneal injection; on 5 consecutive days per week; female BALB/c nu mice) treatment significantly reduces tumor growth in a murine MM model.Animal Model:Female BALB/c nu mice (6-week-old) injected with RPMI 8226 cells
Dosage:3 mg/kg
Administration:Intraperitoneal injection; on 5 consecutive days per week
Result:Significantly reduced tumor growth in a murine MM model.
体外研究：
W-7 is distributed mainly in the cytoplasm, and inhibits proliferation of Chinese hamster ovary K1 (CHO-K1) cells. W-7 selectively blocks the phase of the cell cycle (G1/S boundary phase) in a manner. 25 μM W-7 arrests the growth of the cells at the G1/S boundary phase of the cell cycle.W-7 (100 μM) exhibits a similar extent of antagonism between the contractile responses to carbachol and KCl. The increase in myosin light chain (P-LC) phosphate content in response to 1-min stimulation with 10 μM carbachol is inhibited by W-7. W-7 antagonizes the smooth muscle contraction through the inhibition of the initial increase in the P-LC phosphorylation.Treatment with W-7 results in the dose-dependent inhibition of cell proliferation in various human multiple myeloma cell lines. W-7induces G1 phase cell cycle arrest by downregulating cyclins and upregulating p21cip1. W-7 induces apoptosis via caspase activation; this occurred partly through the elevation of intracellular calcium levels and mitochondrial membrane potential depolarization and through inhibition of the STAT3 phosphorylation and subsequent downregulation of Mcl-1 protein. W-7 competitively inhibits Ca2+/calmodulin-dependent phosphodiesterase with a Ki value of 300 μM.
W-7 hydrochloride is a selective calmodulin antagonist. W-7 hydrochloride inhibits the Ca2+-calmodulin-dependent phosphodiesterase and myosin light chain kinase with IC50 values of 28 μM and 51 μM, respectively. W-7 hydrochloride induces apoptosis and has antitumor activity.
体内研究：
W-7 (3 mg/kg; intraperitoneal injection; on 5 consecutive days per week; female BALB/c nu mice) treatment significantly reduces tumor growth in a murine MM model.Animal Model:Female BALB/c nu mice (6-week-old) injected with RPMI 8226 cells
Dosage:3 mg/kg
Administration:Intraperitoneal injection; on 5 consecutive days per week
Result:Significantly reduced tumor growth in a murine MM model.
体外研究：
W-7 is distributed mainly in the cytoplasm, and inhibits proliferation of Chinese hamster ovary K1 (CHO-K1) cells. W-7 selectively blocks the phase of the cell cycle (G1/S boundary phase) in a manner. 25 μM W-7 arrests the growth of the cells at the G1/S boundary phase of the cell cycle.W-7 (100 μM) exhibits a similar extent of antagonism between the contractile responses to carbachol and KCl. The increase in myosin light chain (P-LC) phosphate content in response to 1-min stimulation with 10 μM carbachol is inhibited by W-7. W-7 antagonizes the smooth muscle contraction through the inhibition of the initial increase in the P-LC phosphorylation.Treatment with W-7 results in the dose-dependent inhibition of cell proliferation in various human multiple myeloma cell lines. W-7induces G1 phase cell cycle arrest by downregulating cyclins and upregulating p21cip1. W-7 induces apoptosis via caspase activation; this occurred partly through the elevation of intracellular calcium levels and mitochondrial membrane potential depolarization and through inhibition of the STAT3 phosphorylation and subsequent downregulation of Mcl-1 protein. W-7 competitively inhibits Ca2+/calmodulin-dependent phosphodiesterase with a Ki value of 300 μM.
产品资料
Copyright©2015-2024 沪ICP备2022026524号-1
沪公网安备