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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 summarizes selected highlights from STAT’s AACR popup newsletter, intended as a rapid guide to items presented at the American Association for Cancer Research annual meeting.
The source is a concluding edition of the newsletter and notes promotional information about STAT+ subscriptions.
No systematic methods, trial protocols, or full datasets are provided in the source.
Revolution Medicines attracted substantial attendee interest at AACR.
The company presented multiple items, including data on daraxonrasib in frontline pancreatic cancer (which drew most media attention) and initial information about a new investigational compound designated RM-055.
Revolution Medicines’ CEO characterized RM-055 as belonging to a proposed class of “catalytic inhibitors.” The company’s description indicates RM-055 can remove a phosphate group from GTP-bound RAS (the active, “on” state), thereby converting RAS to an inactive state.
That mechanistic description was presented by company leadership at the meeting.
The newsletter summarized the rationale for interest in RM-055: cancers can develop resistance to RAS-targeted therapies by increasing mutant RAS expression, which may overcome conventional inhibitors.
A catalytic mechanism that inactivates multiple RAS molecules could, in principle, address resistance driven by elevated mutant RAS levels; this conceptual rationale was advanced in the company presentation.
The source did not provide clinical trial design, quantitative efficacy or safety data for RM-055, nor independent validation of the catalytic mechanism.
No patient-level outcomes, dosing, or developmental timeline were reported in the excerpt.