BMVC

Modify Date: 2024-01-02 01:46:15

BMVC Structure
BMVC structure
Common Name BMVC
CAS Number 627810-06-4 Molecular Weight 657.33
Density N/A Boiling Point N/A
Molecular Formula C28H25I2N3 Melting Point N/A
MSDS N/A Flash Point N/A

 Use of BMVC


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].

 Names

Name BMVC

 BMVC Biological Activity

Description 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].
Related Catalog
Target

IC50: ~0.2 μM (Telomerase)[1] G-quadruplex[1] IC50: ~2.5 μM (Taq DNA polymerase)[1]

In Vitro 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.
In Vivo 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.
References

[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.

 Chemical & Physical Properties

Molecular Formula C28H25I2N3
Molecular Weight 657.33
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