Lonidamine

Lonidamine reduces the oxygen consumption in both normal and neoplastic cells, while it increases the aerobic glycolysis of normal cells but inhibited that of tumor cells. ^[1]

Lonidamine induces the permeabilization of ANT proteoliposomes in a cell-free system, yet has no effect on protein-free liposomes. Lonidamine adds to synthetic planar lipid bilayers containing ANT, eliciting ANT channel activities with clearly distinct conductance levels. ^[2]

Lonidamine provokes a disruption of the mitochondrial transmembrane potential which precedes signs of nuclear apoptosis and cytolysis. Lonidamine causes the dissipation of the mitochondrial inner transmembrane potential and the release of apoptogenic factors capable of inducing nuclear apoptosis in vitro. ^[3]

Lonidamine (50 mg/mL) induces apoptosis in resistant cells (MCF-7 ADR(r) human breast cancer cell line, and LB9 glioblastoma multiform cell line), as demonstrated by sub-G1 peaks in DNA content histograms, condensation of nuclear chromatin, and internucleosomal DNA fragmentation. ^[4]

Lonidamine has a stronger effect on glioblastoma cell proliferation and metabolism in vitro than did either agent used alone. ^[5]

Lonidamine (160 mg/kg) in combination is significantly more effective in reducing glioblastoma tumor growth than either drug alone in mice, this tumor growth retardation is maintained as long as treatment is given. ^[5]

• Animal Models

  Female nu/nu mice

• Dosages

  80 mg/kg

• Administration

  Tail vein