You’re reading the web version of STAT’s popup newsletter, AACR in 30 seconds, your guide to what’s happening at the American Association of Cancer Researchers’ annual meeting. This is the last edition of our pop-up newsletter.
We hope you’ve learned as much as we have. If you’re not already a STAT+ subscriber, consider it!
There’s currently a  60% off promotion  on annual subscriptions. In the meantime, thanks for joining us.
Overcoming resistance and RevMed’s next drug? In case you missed it, Revolution Medicines’ sessions yesterday were jam-packed with conference attendees.
While most of the media coverage focused on the daraxonrasib in frontline pancreatic cancer data, the company also revealed some activity in a new compound, RM-055. CEO Mark Goldsmith described it as being part of a new class of “catalytic inhibitors,” since it can slice off a phosphate from GTP-RAS, or the “on” form of RAS, and turn the protein off.
This brief derives from STAT’s pop-up newsletter covering highlights from the American Association for Cancer Research annual meeting.
It is the final edition of that newsletter; subscription and promotional details were included in the source but are not central to the scientific content summarized here.
Revolution Medicines presented data and discussion that drew substantial attendee interest.
Coverage concentrated on daraxonrasib in frontline pancreatic cancer, but the company also disclosed activity for a novel agent, RM-055.
RM-055 was described by the company’s CEO as belonging to a purported new category termed “catalytic inhibitors.” The compound was characterized as able to remove a phosphate from GTP-bound RAS (the active form), thereby inactivating the protein.
This mechanistic description was presented by the company as distinct from conventional RAS inhibitors.
The report framed RM-055’s appeal in the context of a recognized resistance mechanism—tumor cells increasing levels of mutant RAS to overcome inhibitors.
Because RM-055 was portrayed as catalytically inactivating multiple RAS molecules rather than binding stoichiometrically, the company suggested it could counteract resistance driven by amplified mutant RAS.
The source provided no primary preclinical or clinical data, quantitative results, study design details, safety information, or timelines for development.
Independent corroboration or peer-reviewed data were not reported in the source.
If the described catalytic mechanism is borne out, it could represent an alternative strategy against RAS-driven resistance.