For decades, one of the most stubborn targets in cancer research has been a cellular communication pathway that acts like a stuck growth switch. That pathway, known as RAS/MAPK, is now yielding to a new generation of experimental medicines being developed by the San Diego-based biotechnology company Erasca.
The company’s pipeline is built entirely around this signaling chain, and its strategy is to attack it from multiple angles at once, a tactic designed to stay ahead of cancer cells’ ability to develop resistance. The RAS/MAPK pathway stands for mitogen-activated protein kinase. In plain terms, it functions as the cell’s growth-control system.
When operating normally, a chain of proteins carries signals from a receptor on the cell’s surface all the way to the nucleus. Those signals instruct the cell to produce proteins that trigger division or growth.
When the pathway breaks, the switch gets stuck in the “on” position, and cells divide uncontrollably. Mutations in key genes along this pathway — particularly the RAS genes known as KRAS, NRAS, and HRAS — appear in roughly 30% of all human cancers. The numbers are especially stark in certain malignancies: over 90% of pancreatic cancers carry KRAS mutations, about 40% of colorectal cancers do, and approximately 30% of non-small cell lung cancers harbor these mutations.
A Pathway Deemed Undruggable
For many years, drug developers considered RAS essentially undruggable. The proteins that make up the pathway lacked the structural nooks, crannies, and deep pockets that drug molecules typically need to bind to and shut down a target.
Researchers struggled to create compounds that could interfere with the signals. Progress remained slow for decades. That picture began to change in May 2021, when the U.S. Food and Drug Administration approved sotorasib, sold under the brand name Lumakras, for the treatment of non-small cell lung cancer.
Sotorasib was the first inhibitor of the KRAS G12C mutation to reach patients. Its approval marked a critical breakthrough, proving that even the most challenging parts of this pathway could be tackled with well-designed drugs.
The significance of targeting the RAS/MAPK pathway goes beyond one mutation. Because these cellular switches malfunction in a large portion of human cancers — especially pancreatic, colorectal, and lung cancers — finding ways to shut down the signals offers a method to stop tumor growth in patients who previously had few options. When the pathway stays active, cells grow without control.
Blocking those signals can halt progression.
Erasca’s Multi-Pronged Approach
Erasca is building on the 2021 breakthrough with a pipeline of experimental medicines that hit the pathway at several distinct points. The company’s lead candidates include ERAS-007, a RAF dimer inhibitor designed to block the RAF proteins — ARAF, BRAF, and CRAF — that signal downstream of RAS.
Another drug, ERAS-601, is an SHP2 inhibitor that targets a protein sitting upstream of RAS, interfering with signals before they even reach the RAS proteins. A third candidate, ERAS-0015, is a RAS(ON) inhibitor aimed at multiple RAS mutations at once, broadening the attack beyond a single genetic variant. The practical upshot is that cancer cells are crafty.
They frequently develop resistance to drugs that hit only one target by finding workarounds along the pathway. By blocking the signaling chain at several points simultaneously, Erasca aims to make it harder for resistance to emerge.
The company’s entire research and development effort is centered on the RAS/MAPK pathway, a focused strategy that reflects both the difficulty and the promise of this area of oncology. Each drug in the pipeline targets a different link in the chain, and together they represent a coordinated attempt to shut down one of cancer’s most fundamental drivers.
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