Betulin

473-98-3

C30H50O2

H2O : < 0.1 mg/mL (insoluble); DMSO : 3.33 mg/mL (7.52 mM; Need ultrasonic)

Apoptosis

Betulin (Trochol), is a sterol regulatory element-binding protein (SREBP) inhibitor with an IC₅₀ of 14.5 uM in K562 cell line. IC50 & Target: IC50: 14.5 uM (SREBP, K562 cell), 74.1 uM (SREBP, HeLa cell), 17.1 uM (SREBP, GOTO cell)^[1], 21.09 uM (SREBP, 181P cell), 20.62 uM (SREBP, HeLa cell)^[2] In Vitro: Betulin (BE) displays a broad spectrum of biological and pharmacological properties, among which the anticancer and chemopreventive activity attract most of the attention. BE has been shown to elicit anticancer properties by inhibiting cancer cells growth. BE has exhibited quite a different range of its antiproliferative activity, depending on cancer cells type, from a weak inhibition of cell proliferation in human erythroleukaemia cell line (K562) to a strong inhibition in human neuroblastoma cells (SK-N-AS), where the effect has been most pronounced. Additionally, BE has also been found to express significant cytotoxicity against primary cancer cells cultures isolated from tumour samples obtained from ovarian, cervical carcinoma, and glioblastoma patients, where the IC₅₀ values have ranged from 2.8 to 3.4 uM, being significantly lower, when compared with established cell lines^[1]. The cytotoxic activity of crude birch bark extract and purified betulin and betulinic acid towards human gastric carcinoma (EPG85-257) and human pancreatic carcinoma (EPP85-181) drug-sensitive and drug-resistant (daunorubicin and mitoxantrone) cell lines are compared. Significant differences in sensitivity between cell lines depending on the compound used are shown, suggesting that both betulin and betulinic acid can be considered as a promising leads in the treatment of cancer^[2]. In Vivo: Betulin could improve glucose intolerance and modify basal learning performance. Treatment with betulin significantly restores SOD activity and decreased MDA content in hippocampus. Betulin also markedly reduces the contents of inflammatory cytokines in serum and hippocampus. Furthermore, administration of BE effectively upregulated the expressions of Nrf2, HO-1 and blocked the phosphorylations of IkappaB, NF-kappaB. In summary, BE might exhibit protective effect on cognitive decline in STZ-induced diabetic rats through HO-1/Nrf-2/ NF-kappaB pathway^[3].