Dewpoint Therapeutics selects groundbreaking MYC development candidate
R&D

Dewpoint Therapeutics selects groundbreaking MYC development candidate

MYC, a master regulator of oncogenic transcription, drives multiple high-burden cancers but has long eluded direct pharmacologic control

  • By IPP Bureau | February 16, 2026
Dewpoint Therapeutics, a biotechnology company at the forefront of condensate-modulating therapeutics, has announced the selection of a Development Candidate (DC) for its MYC program—a potential game-changer in cancer treatment.
 
MYC, a master regulator of oncogenic transcription, drives multiple high-burden cancers but has long eluded direct pharmacologic control. Dewpoint’s MYC DC is a first-in-class small molecule designed to disrupt MYC-driven transcription by targeting aberrant biomolecular condensates that organize gene regulation in cancer cells.
 
“MYC has long been one of the most compelling and most elusive targets in oncology,” said Isaac Klein, Chief Scientific Officer of Dewpoint Therapeutics. 
 
“This milestone underscores the power of Dewpoint’s condensate-modulating platform to tackle foundational drivers of disease that have resisted conventional drug discovery approaches. Advancing a MYC development candidate is a significant step forward for the Company and reinforces our conviction that condensate biology can open entirely new therapeutic frontiers.”
 
The MYC DC was selected based on robust preclinical data showing potent and specific activity in MYC-dependent cellular systems, favorable in vivo pharmacology—including tumor regressions in MYC-dependent models—and tolerability suitable for IND-enabling studies. Dewpoint plans to explore multiple tumor types where MYC dependence drives cancer progression.
 
“What is exciting about this molecule is not just that it impacts MYC, but how it does so,” said Ann Boija, SVP Head of Research at Dewpoint Therapeutics. “By targeting the condensate-level organization of transcription, we are intervening at the level where MYC exerts its function. This provides a mechanistically novel and coherent framework for understanding efficacy, selectivity, and therapeutic window in MYC-driven cancers.”

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