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HBE-843, a Novel, Potent, and Selective EGFR Targeting PROTAC for the Treatment of Non-Small-Cell Lung Cancer.

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Archiv der Pharmazie 📖 저널 OA 12% 2024: 0/1 OA 2025: 2/10 OA 2026: 1/14 OA 2024~2026 2026 Vol.359(2) p. e70193
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Baig MH, Kim CJ, Dattatraya NS, Seong JY, Bok J, Kim H

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The emergence of the EGFR C797S mutation poses a significant challenge in the treatment of non-small cell lung cancer due to resistance to third-generation EGFR-tyrosine kinase inhibitors.

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APA Baig MH, Kim CJ, et al. (2026). HBE-843, a Novel, Potent, and Selective EGFR Targeting PROTAC for the Treatment of Non-Small-Cell Lung Cancer.. Archiv der Pharmazie, 359(2), e70193. https://doi.org/10.1002/ardp.70193
MLA Baig MH, et al.. "HBE-843, a Novel, Potent, and Selective EGFR Targeting PROTAC for the Treatment of Non-Small-Cell Lung Cancer.." Archiv der Pharmazie, vol. 359, no. 2, 2026, pp. e70193.
PMID 41635121 ↗
DOI 10.1002/ardp.70193

Abstract

The emergence of the EGFR C797S mutation poses a significant challenge in the treatment of non-small cell lung cancer due to resistance to third-generation EGFR-tyrosine kinase inhibitors. This study introduces a novel and highly selective EGFR PROTAC, HBE-843, designed to degrade mutant EGFR while sparing wild-type EGFR. Our degrader not only effectively degrades the L858R but also shows promising activity against exon 19 deletion, T790M, and C797S, where it demonstrated low nanomolar GI (26-103 nM) across all these EGFR mutant-harboring cell lines while sparing the wild-type. HBE-843 effectively reduced EGFR protein levels in mutant cells in a dose-dependent manner, with a DC in the low nanomolar range (1.9-18 nM) and a D above 90%. Mechanistic studies showed that HBE-843 mediates EGFR degradation through the CRBN-associated proteasome pathway, preventing the activation of the ERK downstream signal and hindering cell growth. In vivo studies demonstrated a 112% tumor growth inhibition in L858R-induced cancers. These findings suggest that HBE-843 holds promise as a lead compound for developing new drugs to overcome C797S mutant-mediated resistance in clinical settings.

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