Sennidin A 是从狭叶番泻分离得到的一种天然产物，能够抑制HCV NS3 解旋酶，其IC50值为0.8 μM。它诱导Akt和葡萄糖转运蛋白4的磷酸化，刺激葡萄糖掺入。

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]

641-12-3

C30H18O10

538.464

(< 1 mg/ml refers to the product slightly soluble or insoluble )
Powder: -20°C for 3 years
In solvent: -80°C for 2 years