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<p>Astatine-211 (<sup>211</sup>At) is a promising α-emitting radionuclide for targeted alpha therapy, yet systematic evaluation of the biological effects of <sup>211</sup>At remains limited. In this study, we examined in vitro cytotoxic effects of free <sup>211</sup>At using both cell viability and proliferation assays across three cancer cell lines (LLC, HeLa, and AD293 cells). Dose- and time-dependent cytotoxic effects were observed, with LD₅₀ values consistently ranging from 0.125–0.25&#xa0;MBq/mL for all cell lines after 72-h exposure. Notably, cell viability in LLC and HeLa cells did not reach zero even at the highest radio-activities tested. Proliferation analysis revealed that <sup>211</sup>At gradually inhibited cell division in a dose-dependent manner, and complete cell cycle arrest occurred in LLC and HeLa cells at 0.25&#xa0;MBq/mL. The correlation between residual viability and division failure indicates that both endpoints exhibit threshold-like responses to <sup>211</sup>At under the present in vitro conditions. These results suggest that the potent antitumor effect of α-irradiation is not simply cell killing but also involves cell proliferation arrest.</p>

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Dose-dependent cytotoxic profiling of astatine-211 for targeted alpha therapy

  • 期刊论文

  • 发表日期：

    2026年1月2日

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  • Jumpei Ueno,
  • Masayuki Takamatsu,
  • Koki Mayusumi,
  • Atsushi Shimoyama,
  • Kazuhiro Ooe,
  • Masashi Murakami,
  • Atsushi Toyoshima,
  • Tadashi Watabe,
  • Sadahiro Naka,
  • Jens Cardinale,
  • Frederik Giesel,
  • Koichi Fukase,
  • Kazuya Kabayama

摘要

Astatine-211 (211At) is a promising α-emitting radionuclide for targeted alpha therapy, yet systematic evaluation of the biological effects of 211At remains limited. In this study, we examined in vitro cytotoxic effects of free 211At using both cell viability and proliferation assays across three cancer cell lines (LLC, HeLa, and AD293 cells). Dose- and time-dependent cytotoxic effects were observed, with LD₅₀ values consistently ranging from 0.125–0.25 MBq/mL for all cell lines after 72-h exposure. Notably, cell viability in LLC and HeLa cells did not reach zero even at the highest radio-activities tested. Proliferation analysis revealed that 211At gradually inhibited cell division in a dose-dependent manner, and complete cell cycle arrest occurred in LLC and HeLa cells at 0.25 MBq/mL. The correlation between residual viability and division failure indicates that both endpoints exhibit threshold-like responses to 211At under the present in vitro conditions. These results suggest that the potent antitumor effect of α-irradiation is not simply cell killing but also involves cell proliferation arrest.