Researchers at Francis Crick Institute and Vividion Therapeutics have created a compound that blocks RAS-PI3K interaction, stopping tumor growth in mice with RAS or HER2 mutations and sparing healthy cells. This approach avoids side effects of previous drugs and has entered human clinical trials.
October 19, 2025
Source:
SciTechDaily
Breakthrough in Cancer Therapy Targeting RAS-PI3K
Scientists from the Francis Crick Institute and Vividion Therapeutics have reported the discovery of a compound that disrupts a key signaling pathway central to cancer growth, without harming healthy tissues (ScienceDaily). This compound specifically blocks the binding of the cancer-driving RAS gene to the enzyme PI3K, halting tumor progression in preclinical mouse models.
RAS and PI3K: The Target
RAS mutations are found in about 20% of all cancers. The mutated RAS protein perpetually activates growth signals, pushing cells to divide uncontrollably.
PI3K plays a central role in cell growth and also helps regulate blood sugar. Existing drugs that completely block PI3K can cause metabolic issues, like hyperglycemia.
This new targeted approach blocks only the cancer-promoting effect of PI3K, preserving its healthy function in other cellular processes.
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Source:
Science Daily
Preclinical Results and Combination Potential
In animal studies, mice with RAS-mutated lung and HER2-mutated breast tumors received this new compound. Results showed tumor growth stopped, with no signs of elevated blood sugar or major toxicity (News-Medical).
When combined with other targeted cancer drugs, there was even stronger and more durable suppression of tumor activity.
The compound uses new drug design concepts like covalent inhibitors and molecular glues to precisely disrupt cancer-driving protein complexes (SciTechDaily).
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Source:
Medical Xpress
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