Inhibition of betulinic acid to growth and angiogenesis of human colorectal cancer cell in nude mice

Betulinic acid inhibits endotoxin‐stimulated phosphorylation cascade and pro‐inflammatory prostaglandin E2 production in human peripheral blood mononuclear cells

“…The plant is enriched with many phytochemicals of which betulinic acid (BA), a triterpenoid belonging to lupane series, was recently explored to its topoisomerase inhibitory potential (Chowdhury et al ., 2002). BA has a wide range of other pharmacological properties like anti‐cancer (Ren et al ., 2010), anti‐malarial (Santos et al ., 2009), anti‐retroviral and anti‐inflammatory properties (Chowdhury et al ., 2002). To the best of our admittedly limited knowledge, the effect of BA on inflammation has yet to be elucidated in detail.…”

Mitochondrial Metabolism Inhibitors for Cancer Therapy

“…Bongkrekic acid is also able to prevent mitochondrial permeability transition following the dissociation of HK from VDAC (159). Betulinic acid induces apoptosis of a variety of human cancer cell lines, including doxorubicinresistant neuroblastoma cells (156,158,160), and has antitumor activity in murine melanoma and colorectal cancer models (161,162). The compound was well tolerated in a phase I trial (163) and a phase II trial using betulinic acid as an ointment for the treatment of dysplastic nevi (a mole that has the potential to develop into melanoma) is ongoing (Table I).…”

Betulinic acid shows anticancer activity against equine melanoma cells and permeates isolated equine skin in vitro

“…In some EMM an increased vascularization was observed [26,51], which could lead to a higher and faster elimination of the active compound when topically applied in vivo. On the other hand, BAs' potential to reduce angiogenesis was demonstrated in vitro and in vivo by inhibition of hypoxia-inducible factor 1α and vascular endothelial growth factor and by a negative impact on the normal growth of the capillaries in the chorioallantoic membrane assay [17,18,54]. Reducing the vascularization in the tumor could increase the drug concentration in this area.…”

“…Formation of the mitochondrial permeability transition pore complex leads to cytochrome c and apoptosis-inducing factor release with subsequent caspases activation [12,13]. Further molecular antitumoral mechanisms, such as reactive oxygen species formation [14,15], mitogen-activated protein kinase activation [16], angiogenesis inhibition [17,18] and other controlled cell death mechanisms [19], have been implicated. Moreover, a selective cytotoxicity on human cancer cells compared to normal cells has been described [5,20,21] and might be explained by BA's ability to inhibit the steroyl-CoAdesaturase activity [22].…”