Fig. 12

DMOCPTL could inhibit TNBC and prolong survival life of mice in vivo and had no obvious toxicity. a Compound 13 was injected to SD rats by intravenous administration at a dose of 1 mg/kg. Then, the blood sampling from jugular sinus of rats were collected at 2 min, 5mins, 15mins, 30mins, 1 h, 2 h, 3 h, 4 h, 6 h and 8 h after administration. The samples were treated and analyzed by LC/MS. The pharmacodynamics of 13 on SD rats was calculated by DAS 3.3. b The body weight of mice after intravenous administration of 13 at a dose of 50 mg/kg compared with vehicle group. c The body weight of mice after treatment of 13 at a dose of 7.5 mg/kg compared with vehicle group. d The statistical results of tumor volume after treatment of 13 at a dose of 7.5 mg/kg. e The picture of tumors after administration of 13 compared with vehicle group. f The weight of tumors after the treatment of compound 13 compared with vehicle group. g The levels of GPX4 and EGR1 protein expression in tumors by western blot assay. h The statistical results of GPX4 and EGR1 protein expression in tumors. i The IHC assay of GPX4, EGR1, and mitochondria-mediated apoptosis related proteins Bax and Bcl-2 in tumors. PBS instead of primary antibody was used as negative control. Breast cancer marker MUC16 was used as positive control. j The statistical results of GPX4, Bax (k), EGR1 (l) and Bcl-2 (m) by IHC assay after 13 treatment. n The body weight of mice after oral administration of 13 at a dose of 500 mg/kg. o The body weight of mice during treatment of 13 at a dose of 50 mg/kg every other day compared with vehicle group. p The statistical results of survival life after treatment of 13 at a dose of 50 mg/kg and clinically used drug ADR as a positive control by intraperitoneal administration at a dose of 2 mg/kg every 2 days. Analysis results represented mean ± SD, *P < 0.05, **P < 0.01