BMVC is a potentG-quadruplex(G4)stabilizer and a selectivetelomeraseinhibitor with anIC₅₀of ~0.2 μM. BMVC inhibits Taq DNA polymerase with anIC₅₀of ~2.5 μM. BMVC increases the melting temperature ofG4structure of telomere and accelerates telomere length shortening. Anticancer activities^[1][2].

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

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].

BMVC (1 mg/kg; intraperitoneal injection; every 3 day; BALB/cAnN.Cg-Foxn1^nu/CrlNarl mice) treatment delays tumorigenic potential of cancer cells in vivo^[1].

657.33

Solid

C₂₈H₂₅I₂N₃

627810-06-4

Room temperature in continental US; may vary elsewhere.