DTHIB (5 mg/kg; intraperitoneal injection; daily; for 3 weeks) potently inhibits tumor progression in a C4-2 xenograft mouse model ^[1].

C4-2 cells with DTHIB (5 μM; 48 hours) induces cell cycle arrest, leading to accumulation in the G1 phase, and stimulates entry into senescence ^[1].

DTHIB (0.5-5 μM; 48 hours), in C4-2 prostate cancer cells, reduces the steady-state protein levels of molecular chaperones P23, HSP27, HSP70, and HSP90, all of which are bona fide HSF1 targets ^[1].

DTHIB demonstrates dose-dependent reduction in clonal expansion for both C4-2 and PC-3 PCa cells, with EC50 values of 1.2 μM and 3.0 μM, respectively ^[1].

DTHIB (0.5-10 μM) dose-dependently attenuates the robust acute heat shock induction of HSP70 and HSP25 molecular chaperones in mouse embryonic fibroblasts (MEFs). This attenuation occurs by reducing the steady-state transcript abundance of multiple molecular chaperones ^[1].