BMVC (0.5 μM; 0-18 days; H1299 cells) treatment markedly increases the percentage of sub-G1-phase cells after 18 days and long-term treatment leads to ceasing cell growth and eventually cell death through apoptosis. The long-term BMVC treatment induces the senescence program in H1299 cells. 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].

The treatment of BMVC (1 mg/kg; i.p.; every 3 day; BALB/cAnN.Cg-Foxn1nu/CrlNarl mice) delays tumorigenic potential of cancer cells in vivo [1].