Sennidin A, has two hydroxyanthraquinone-like moieties, exerts inhibition on NS3 helicase with IC50 values of 0.8 μM.

Here, we exploited the avidity of the Sennidin A (SA) tracer and radioiodinated SA (131I-SA) to necrotic tumors in order to further empower TNT. We showed high uptake and prolonged retention of SA in necrotic tumors and a quick clearance in other non-targeted tissues including the liver. On SPECT-CT images, tumor mass appeared persistently as a hotspot. Based on the prominent targetability of 131I-SA to the tumor necrosis, we designed a combinational theragnostic modality. The vascular disrupting agent (VDA) combretastatin A4 phosphate (CA4P) was used to cause massive tumor necrosis, which formed the target of 131I-SA that subsequently killed the residual tumor cells by cross-fire irradiation of beta particles. Consequently, 131I-SA combined with CA4P significantly inhibited tumor growth, extended tumor doubling time and prolonged mean animal survival[1]