When administered orally at doses of 75 mg/kg or 100 mg/kg twice daily for 25 days, HhAntag significantly delayed tumor growth in certain colorectal cancer cell line xenograft models, with no effect observed on the growth of DLD-1 xenografts^[1].

HhAntag (2-30 µM; 72 hours) demonstrates to be 10-times more potent than the natural product SMO antagonist, cyclopamine, at inhibiting Hh pathway activity and it inhibits Hh signalling pathway sensitivitive cells with IC50 values ranging from 2 µM to >30 µM^[1].

HhAntag inhibits AsPC-1, BXPC-3, CFPAC, HPAC, HPAF-II, KP4, Panc 03.27, PA-TU-8902, PSN-1, SU.86.86 cells with IC50 values of 30 µM, 5.4 µM, 5.8 µM, 2.7 µM, 6.2 µM,10.3 µM, 2.5 µM, 2.9 µM, 5.8 µM and 2.7 µM, respectively^[1].

HhAntag required a concentration of 100 nM to fully block Hh signaling in a specific mesenchymal cell line, showcasing an IC50 for this effect that is substantially lower than the concentration needed to inhibit cancer cell growth by 50% in the most sensitive line tested (1.9 µM)^[1].