Randomized trial evaluates 1,2,3-benzoxathiazine-2,2-dioxides as inhibitors of thioredoxin reductase, suggesting their potential in cancer therapy.
Thioredoxin reductase 1 (TrxR1) is a selenoenzyme central to cellular redox homeostasis. It is frequently upregulated in cancer and represents an attractive therapeutic target for covalent inhibition. 1,2,3‐Benzoxathiazine‐2,2‐dioxides are bioisosteres of coumarin that have been investigated before as cancer‐associated enzyme inhibitors but never as inhibitors of TrxR. In this study, 52 derivatives of 1,2,3‐benzoxathiazine‐2,2‐dioxides were synthesized and evaluated for inhibition of recombinant rat TrxR1 using a DTNB (5,5′‐Dithiobis‐(2‐nitrobenzoic acid)‐based colorimetric assay. Although 4‐methyl substituted derivatives expressed no activity, the TrxR inhibition effect was observed in the case of 4‐unsubstituted 1,2,3‐benzoxathiazine‐2,2‐dioxides, with some derivatives showing micromolar inhibition toward TrxR1. The most potent inhibitors were 8‐aryl analogs 7k and 7l with IC 50 = 19.3 and IC 50 = 14.1, respectively. Compounds 7k and 7l also displayed cytotoxic effects in MDA‐MB‐231, MDA‐MB‐435, PANC‐1, and U‐118 human cancer cell lines after 48 h exposure with IC 50 values ranging 30–62 µM. Covalent docking of 7k to TrxR1 (PDB: 3EAN) suggested binding under the mobile C‐terminal arm and a geometry compatible with Michael addition to Sec498. Together, these results identify 1,2,3‐benzoxathiazine‐2,2‐dioxides as a previously unexplored TrxR1 inhibitor scaffold and provide starting points for further optimization.
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Ivanova et al. (2026) studied this question.
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