IC50: ~0.2 μM (Telomerase)[1]
G-quadruplex[1]
IC50: ~2.5 μM (Taq DNA polymerase)[1]
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[1][2].
BMVC (0.5 μM; 0-18 days; H1299 cells) treatment markedly increases the percentage of sub-G1-phase cells after 18 days[1].
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[1].
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[1].
BMVC also suppresses the tumor-related properties of cancer cells, including cell migration, colony-forming ability, and anchorage-independent growth[1].
Cell Cycle Analysis[1]
| Cell Line: | H1299 cells |
| Concentration: | 0.5 μM |
| Incubation Time: | 0 day, 6 days, 12 days, 18 days |
| Result: | The percentage of sub-G1-phase cells was markedly increased after 18 days. |
Apoptosis Analysis[1]
| Cell Line: | H1299 cells |
| Concentration: | 0.5 μM |
| Incubation Time: | 0 day, 6 days, 12 days, 18 days |
| Result: | Increased apoptotic cells. |
BMVC (1 mg/kg; intraperitoneal injection; every 3 day; BALB/cAnN.Cg-Foxn1nu/CrlNarl mice) treatment delays tumorigenic potential of cancer cells in vivo[1].
| Animal Model: | BALB/cAnN.Cg-Foxn1nu/CrlNarl mice injected with H1299 cells[1] |
| 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. |
[1]. Huang FC, et al. G-quadruplex stabilizer 3,6-bis(1-methyl-4-vinylpyridinium)carbazole diiodide induces accelerated senescence and inhibits tumorigenic properties in cancer cells. Mol Cancer Res. 2008 Jun;6(6):955-64.
[2]. Jen-Fei Chu, et al. A Novel Method for Screening G-quadruplex Stabilizers to Human Telomeres. Journal of the Chinese Chemical Society, 2011, 58, 296-300.