产品
编 号：F612012
分子式：C28H25I2N3
分子量：657.33
分子式：C28H25I2N3
分子量：657.33
产品类型
规格
价格
是否有货
1mg
询价
询价
5mg
询价
询价
10mg
询价
询价
25mg
询价
询价
结构图
CAS No: 627810-06-4
产品详情
生物活性：
BMVC is a potent G-quadruplex (G4) stabilizer and a selective telomerase inhibitor with an IC50 of ~0.2 μM. BMVC inhibits Taq DNA polymerase with an IC50 of ~2.5 μM. BMVC increases the melting temperature of G4 structure of telomere and accelerates telomere length shortening. Anticancer activities.
体内研究：
BMVC (1 mg/kg; intraperitoneal injection; every 3 day; BALB/cAnN.Cg-Foxn1nu/CrlNarl mice) treatment delays tumorigenic potential of cancer cells in vivo.Animal Model:BALB/cAnN.Cg-Foxn1nu/CrlNarl mice injected with H1299 cells
Dosage:1 mg/kg
Administration:Intraperitoneal injection; every 3 day
Result:The growth rates of tumors in animals were significantly slower than that of control animals. The tumor cells of the mice were indeed entering apoptosis.
体外研究：
BMVC (0.5 μM; 0-18 days; H1299 cells) treatment markedly increases the percentage of sub-G1-phase cells after 18 days.BMVC (0.5 μM; 0-18 days; H1299 cells) long-term treatment leads to ceasing of cell growth and eventually cell death through apoptosis. The long-term BMVC treatment induces senescence program in H1299 cells.In BMVC-treated cancer cells, hallmarks of senescence, including morphologic changes, detection of senescence-associated β-galactosidase activity, and decreasesd bromodeoxyuridine incorporation, are detected. The BMVC-induced senescence phenotype is accompanied by progressive telomere shortening and detection of the DNA damage foci, indicating that BMVC caused telomere uncapping after long-term treatments.BMVC also suppresses the tumor-related properties of cancer cells, including cell migration, colony-forming ability, and anchorage-independent growth.
BMVC is a potent G-quadruplex (G4) stabilizer and a selective telomerase inhibitor with an IC50 of ~0.2 μM. BMVC inhibits Taq DNA polymerase with an IC50 of ~2.5 μM. BMVC increases the melting temperature of G4 structure of telomere and accelerates telomere length shortening. Anticancer activities.
体内研究：
BMVC (1 mg/kg; intraperitoneal injection; every 3 day; BALB/cAnN.Cg-Foxn1nu/CrlNarl mice) treatment delays tumorigenic potential of cancer cells in vivo.Animal Model:BALB/cAnN.Cg-Foxn1nu/CrlNarl mice injected with H1299 cells
Dosage:1 mg/kg
Administration:Intraperitoneal injection; every 3 day
Result:The growth rates of tumors in animals were significantly slower than that of control animals. The tumor cells of the mice were indeed entering apoptosis.
体外研究：
BMVC (0.5 μM; 0-18 days; H1299 cells) treatment markedly increases the percentage of sub-G1-phase cells after 18 days.BMVC (0.5 μM; 0-18 days; H1299 cells) long-term treatment leads to ceasing of cell growth and eventually cell death through apoptosis. The long-term BMVC treatment induces senescence program in H1299 cells.In BMVC-treated cancer cells, hallmarks of senescence, including morphologic changes, detection of senescence-associated β-galactosidase activity, and decreasesd bromodeoxyuridine incorporation, are detected. The BMVC-induced senescence phenotype is accompanied by progressive telomere shortening and detection of the DNA damage foci, indicating that BMVC caused telomere uncapping after long-term treatments.BMVC also suppresses the tumor-related properties of cancer cells, including cell migration, colony-forming ability, and anchorage-independent growth.
产品资料
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