Cryptotanshinone counteracts ovarian IR and substantially enhances 2-deoxy-D-[1,2-3H]-glucose uptake in tissues from DEX-treated mice, decreases ovulation rate, and lowers plasma E2 and P levels^[2].

Administered to ob/ob mice (C57BL/6J-Lepob) and diet-induced obese (DIO) mice, Cryptotanshinone substantially curtails body weight and food intake in a dose-dependent manner, significantly reduces adipose tissue fat, serum triglycerides, and cholesterol levels, and elevates AMPK activity in skeletal muscles by 2.5- to 3-fold compared to controls. Notably, oral administration at 600 mg/kg/day drastically lowers blood glucose levels in ob/ob (C57BL/6J-Lepob), db/db (C57BL/KsJ-Leprdb) mice, and ZDF rats, with effects commencing after three days and persisting throughout the observation period^[4].

Cryptotanshinone markedly reduces STAT3-dependent luciferase activity, STAT3 Tyr705 phosphorylation, and STAT3 dimerization, unlike tanshinone IIA which shows no effect. At 7 μM, Cryptotanshinone significantly blocks STAT3 Tyr705 phosphorylation in DU145 cells, but not STAT3 Ser727 phosphorylation, and markedly inhibits JAK2 phosphorylation with an IC50 of approximately 5 μM. This suggests a direct inhibition mechanism, possibly through binding to the SH2 domain of STAT3, leading to reduced proliferation in DU145 cells harboring active STAT3^[1].

Cryptotanshinone notably mitigates the hormonal effects of DEX on ovaries, demonstrated by decreased T levels and increased P levels in the culture medium. It also raises the phosphorylation levels of AKT2 and GSK3β in DEX-treated ovaries^[2].

Combined treatment with imatinib and Cryptotanshinone shows significant synergistic cytotoxic effects on both imatinib-sensitive and -resistant CML cell lines, and primary CML cells^[3].