Leah Lawrence

GI Oncology Now

The Kirsten rat sarcoma virus oncogene homolog, more commonly known as KRAS, is one of the most common oncogenic drivers in human cancer. Depending on the tumor type, mutations can occur with different frequencies and in a large variety of subtypes.1 In a study of gastrointestinal (GI) cancers by Wang and colleagues,2 the frequency of KRAS mutations was found to vary by site; KRAS mutations were detected in 85% of pancreas tumors, about 41% of colorectal tumors, and less than 10% of esophageal, stomach, or gallbladder tumors.2,3
“KRAS plays a central role in driving tumor growth through the RAS/MAPK pathway,” explained Anwaar Saeed, MD, chief of the Gastrointestinal Medical Oncology Program at University of Pittsburgh Medical Center (UPMC) Hillman Cancer Center, in a brief interview. “In colorectal and pancreatic cancers in particular, KRAS mutations are among the earliest and most consistent genetic alterations observed.”
Unfortunately, for decades, KRAS was thought to be undruggable.
“Think about KRAS as a shiny ball, and if you try to stick an antibody to it, nothing will stick,” explained Shubham Pant, MD, MBBS, professor in the Department of Gastrointestinal Medical Oncology at the University of Texas MD Anderson Cancer Center. The protein lacks deep binding pockets that traditional small molecules require. “KRAS is constitutively active in the GTP [guanosine triphosphate] phase, meaning that signal is always turned on. That leads to challenges in turning it off.”
An additional complication involved in targeting KRAS is its essential role in multiple normal cellular functions.
<h2>Drugging the Undruggable</h2>
In 2013, Kevan M. Shokat, PhD, and colleagues identified a pocket in which small molecules could bind to KRASG12C; their research showed that the small molecule compounds “rely on the mutant cysteine for binding and therefore do not affect the wild-type protein.”4
“A few years after that discovery, two companies developed, in the clinic, the first KRASG12C inhibitors, sotorasib and adagrasib,” said Ignacio Garrido-Laguna, MD, PhD, MBA, professor of GU oncology at the Huntsman Cancer Institute, exclusively with GI Oncology Now.
The FDA granted sotorasib accelerated approval for KRASG12C non–small cell lung cancer (NSCLC) in 2021, and, in combination with panitumumab, full approval for KRASG12C metastatic colorectal cancer (CRC) in January 2025.5 In 2022, adagrasib received FDA accelerated approval for advanced KRASG12C NSCLC, with an accelerated approval for adagrasib in combination with cetuximab for advanced or metastatic CRC in 2024.6
Dr. Garrido-Laguna also pointed out that there are more G12C inhibitors in development expected to be more potent than sotorasib and adagrasib. These new molecules have “have both increased potency as well as faster target engagement. … In addition, there are new G12C inhibitors that inhibit both ON/OFF forms of KRASG12C that are likely to lead to increased activity.”
Unfortunately, response rates for the approved KRASG12C inhibitors have been more modest in GI tumors than those seen in NSCLC. The single-arm KRYSTAL-1 study demonstrated that adagrasib yielded an overall response rate (ORR) of 34% with a median duration of response of 5.8 months among patients with previously treated locally advanced or metastatic KRASG12C-mutated CRC.7 In the phase 3 CodeBreaK 300 trial, investigators randomly assigned patients with KRASG12C-mutated metastatic CRC to sotorasib 960 mg plus panitumumab, sotorasib 240 mg plus panitumumab, or investigator’s choice. Median progression-free survival (PFS) was more than double with sotorasib plus panitumumab—regardless of dose—compared with standard of care (5.6 vs 2 months).8
This lower response “is partly due to intrinsic resistance mechanisms in the tumor microenvironment,” Dr. Saeed said. “Only a small subset of GI cancer patients harbor the G12C mutation—about 3% to 4% in colorectal cancer and far fewer (less than 1%) in pancreatic cancer—so the overall eligible patient population remains limited.”
“In pancreatic cancer, around 40% of KRAS mutations are G12D, followed by G12V, which occur in about 35% of pancreas cancer, and G12R, which are rare in other GI cancers but occur in about 20% of pancreas cancer,” Dr. Garrido said. “In CRC, the most common are G12D, occurring in about 28% and G12V occurring in about 20%.”
In addition, both primary and acquired resistance to KRASG12C inhibitors represent a growing challenge.
“Tumors can bypass the KRAS blockade by activating alternative pathways such as EGFR, MET, or PI3K,” Dr. Saeed said. “There are also cases of on-target resistance through additional KRAS mutations that prevent drug binding or through amplification of KRAS or downstream effectors.”
<h2>Aiming at Other Targets</h2>
The different KRAS variants are important because they differ in how they activate downstream signaling and respond to therapeutic strategies, Dr. Saeed explained. In recent years, more effort has gone into developing inhibitors targeted either to these other KRAS variants or to all of the variants in codon 12 using so-called pan- or multi-(K)RAS inhibitors.
Unfortunately, targeting each variant has its own challenges. For example, the switch II pocket in G12D does not have the same reactive residue as G12C, making it harder for molecules to bond.9 However, progress is still being made.
RMC-6236 is a multi-selective RAS inhibitor being tested in patients with previously treated pancreatic ductal adenocarcinoma (PDAC).
“This drug is a bit unique because it works as a molecular glue,” said Dr. Garrido-Laguna. “It brings together two proteins that otherwise would not interact.”
The drug first forms a binary complex with cyclophilin, a protein that is ubiquitously expressed in every cell of the body. Then this binary complex binds to activated RAS via a noncovalent manner to form a tricomplex.
“When the drug brings these two proteins together, it alters the configuration of cyclophilin so that it causes steric occlusion of the binding sites of RAS downstream mediators,” Dr. Garrido-Laguna said. “When RAS is activated, it signals downstream through different proteins including RAF. This drug makes it so those downstream mediators cannot bind to RAS, and that means the activated protein is not signaling downstream.”
Dr. Garrido-Laguna presented efficacy and safety results of a phase 1 trial of RMC-6236 in patients with PDAC at the 2025 ASCO Gastrointestinal Cancers Symposium.10 The study included 127 patients with RAS-mutant PDAC. At the recommended phase 2 dose for PDAC (300 mg), the ORR (both confirmed and unconfirmed) was 27%, but among those with KRAS mutations in codon 12, the ORR was 36%.
“Confirmed responses to standard-of-care second-line chemotherapy in pancreatic cancer are in the single digits,” Dr. Garrido-Laguna said.
Median PFS was 8.5 months for those with mutations in KRAS codon 12. Most common toxicities were skin rash, diarrhea, and nausea. These results prompted the phase 3 RASOLUTE study, an ongoing study in the second line evaluating RMC-6236 versus standard of care.11 The results of the study are expected to be published in 2026.
Data from a study of RMC-9805, a RAS(ON) allele–specific G12D inhibitor, were presented in October at the European Organisation for Research and Treatment of Cancer–National Cancer Institute–American Association for Cancer Research (EORTC-NCI-AACR) Symposium on Molecular Targets and Cancer Therapeutics in Barcelona. Among those patients with PDAC treated with the recommended phase 2 dose of 1,200 mg daily (n=40), the objective response rate was 30%.12
“The activity was very similar to 6236 in terms of response but had a significant advantage because the toxicity seemed much better,” Dr. Garrido-Laguna said. He also mentioned some exciting compounds in early trials that target both active and inactive forms of the KRAS protein.
“This is very important because most of the drugs we have in the clinic now that are KRASG12D inhibitors only hit the off form of the protein, and that may lead to limited activity,” Dr. Garrido-Laguna said.
In all though, there are too many compounds under investigation in pancreatic, colorectal, and other cancers to begin to try to summarize them all, he said.
The early results of a study of a first-in-class protein degrader targeting KRASG12D were presented at the European Society of Medical Oncology (ESMO) Congress 2024. 13 Although it showed only modest activity in PDAC, it provided proof of concept of this new mechanism to target KRAS.13
<h2>What Does the Future Hold</h2>
The future definitely holds more progress for targeting KRAS, Dr. Pant said. In addition to inhibitors, another potential treatment strategy is RAS-directed cancer vaccines used in earlier lines of therapy.
Patients with pancreatic cancer who undergo resection and adjuvant chemotherapy still have a high risk for recurrence, Dr. Pant explained. The phase 1 AMPLIFY-1 trial tested cancer vaccine ELI-002 2P in a small group of patients with pancreatic cancer or CRC who were considered to be at high risk for relapse after locoregional treatment. The vaccine induced “considerable T cell responses” and yielded a median recurrence-free survival (RFS) of 16.33 months in the full cohort, whereas the median RFS was not reached in the patients who exhibited above median T-cell responses.14
Increased research into combination therapies will also play an important role. Current approaches under investigation include combining KRAS inhibitors with “SHP2 inhibitors, MEK inhibitors, or immune checkpoint blockade to shut down escape pathways and enhance tumor response,” Dr. Saeed said.
Interest is also growing in indirect KRAS-targeting approaches, such as disrupting upstream regulators (eg, SOS1, SHP2), downstream signaling nodes, or exploiting synthetic lethality, Dr. Saeed added. All of this information points toward the fact that “the field is rapidly evolving toward more personalized and combination-based strategies.”
<h2>References</h2>
<ol>
<li>Huang L, et al. Signal Transduct Target Ther. 2021;6(1):386. doi:<a href="https://pubmed.ncbi.nlm.nih.gov/34776511/" target="_blank" rel="noopener">10.1038/s41392-021-00780-4</a></li>
<li>Wang L, et al. Mod Pathol. 2023;36(2):100014. doi:<a href="https://pubmed.ncbi.nlm.nih.gov/36853786/" target="_blank" rel="noopener">10.1016/j.modpat.2022.100014</a></li>
<li>Varghese AM, et al. Nat Med. 2025;31(2):466-477. doi:<a href="https://pubmed.ncbi.nlm.nih.gov/39753968/" target="_blank" rel="noopener">10.1038/s41591-024-03362-3</a></li>
<li>Ostrem JM, et al. Nature. 2013;503(7477):548-51. doi:<a href="https://pubmed.ncbi.nlm.nih.gov/24256730/" target="_blank" rel="noopener">10.1038/nature12796</a></li>
<li>Drugs.com. Lumakras FDA Approval History. Updated January 18, 2025. Accessed June 26, 2025. <a href="https://www.drugs.com/history/lumakras.html" target="_blank" rel="noopener">https://www.drugs.com/history/lumakras.html</a></li>
<li>Drugs.com. Krazati FDA Approval History. Updated June 24, 2024. Accessed June 26, 2025. <a href="https://www.drugs.com/history/krazati.html%20" target="_blank" rel="noopener">https://www.drugs.com/history/krazati.html</a></li>
<li>Yaeger R, et al. Cancer Discov. 2024;14(6):982-993. doi:<a href="https://pubmed.ncbi.nlm.nih.gov/38587856/" target="_blank" rel="noopener">10.1158/2159-8290.CD-24-0217</a></li>
<li>Fakih MG, et al N Engl J Med. 2023;389:2125-2139. doi:<a href="https://pubmed.ncbi.nlm.nih.gov/37870968/" target="_blank" rel="noopener">10.1056/NEJMoa2308795</a></li>
<li>Bannoura SF, et al. Front Oncol. 2022;12:1013902. doi:<a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC9749787/" target="_blank" rel="noopener">10.3389/fonc.2022.1013902</a></li>
<li>Garrido-Laguna I, et al. J Clin Oncol. 2025;43(4_suppl). doi: <a href="https://ascopubs.org/doi/10.1200/JCO.2025.43.4_suppl.722" target="_blank" rel="noopener">10.1200/JCO.2025.43.4_suppl.722</a></li>
<li>Revolution Medicines. Accessed June 26, 2025. <a href="https://ir.revmed.com/news-releases/news-release-details/revolution-medicines-announces-first-patient-dosed-phase-3-study" target="_blank" rel="noopener">https://ir.revmed.com/news-releases/news-release-details/revolution-medicines-announces-first-patient-dosed-phase-3-study</a></li>
<li>Revolution Medicines. Accessed June 26, 2025. <a href="https://ir.revmed.com/news-releases/news-release-details/revolution-medicines-presents-initial-data-rmc-9805-monotherapy" target="_blank" rel="noopener">https://ir.revmed.com/news-releases/news-release-details/revolution-medicines-presents-initial-data-rmc-9805-monotherapy</a></li>
<li>Park W, et al. <a href="https://www.annalsofoncology.org/article/S0923-7534(24)02194-X/fulltext" target="_blank" rel="noopener">Ann Oncol. 2024;35(2):S486-S487</a>.</li>
<li>Pant S, et al Nat Med. 2024;30(2):531-542. doi: <a href="https://pubmed.ncbi.nlm.nih.gov/38195752/" target="_blank" rel="noopener">10.1038/s41591-023-02760-3</a></li>
</ol>

The Kirsten rat sarcoma virus oncogene homolog, more commonly known as KRAS, is one of the most common oncogenic drivers in human cancer. Depending on the tumor type, mutations can occur with different frequencies and in a large variety of subtypes.1 In a study of gastrointestinal (GI) cancers by Wang and colleagues,2 the frequency of KRAS mutations was found to vary by site; KRAS mutations were detected in 85% of pancreas tumors, about 41% of colorectal tumors, and less than 10% of esophageal, stomach, or gallbladder tumors.2,3“KRAS plays a central role in driving tumor growth through the RAS/MAPK pathway,” explained Anwaar Saeed, MD, chief of the Gastrointestinal Medical Oncology Program at University of Pittsburgh Medical Center (UPMC) Hillman Cancer Center, in a brief interview. “In colorectal and pancreatic cancers in particular, KRAS mutations are among the earliest and most consistent genetic alterations observed.”Unfortunately, for decades, KRAS was thought to be undruggable.“Think about KRAS as a shiny ball, and if you try to stick an antibody to it, nothing will stick,” explained Shubham Pant, MD, MBBS, professor in the Department of Gastrointestinal Medical Oncology at the University of Texas MD Anderson Cancer Center. The protein lacks deep binding pockets that traditional small molecules require. “KRAS is constitutively active in the GTP [guanosine triphosphate] phase, meaning that signal is always turned on. That leads to challenges in turning it off.”An additional complication involved in targeting KRAS is its essential role in multiple normal cellular functions.<h2>Drugging the Undruggable</h2>In 2013, Kevan M. Shokat, PhD, and colleagues identified a pocket in which small molecules could bind to KRASG12C; their research showed that the small molecule compounds “rely on the mutant cysteine for binding and therefore do not affect the wild-type protein.”4“A few years after that discovery, two companies developed, in the clinic, the first KRASG12C inhibitors, sotorasib and adagrasib,” said Ignacio Garrido-Laguna, MD, PhD, MBA, professor of GU oncology at the Huntsman Cancer Institute, exclusively with GI Oncology Now.The FDA granted sotorasib accelerated approval for KRASG12C non–small cell lung cancer (NSCLC) in 2021, and, in combination with panitumumab, full approval for KRASG12C metastatic colorectal cancer (CRC) in January 2025.5 In 2022, adagrasib received FDA accelerated approval for advanced KRASG12C NSCLC, with an accelerated approval for adagrasib in combination with cetuximab for advanced or metastatic CRC in 2024.6Dr. Garrido-Laguna also pointed out that there are more G12C inhibitors in development expected to be more potent than sotorasib and adagrasib. These new molecules have “have both increased potency as well as faster target engagement. … In addition, there are new G12C inhibitors that inhibit both ON/OFF forms of KRASG12C that are likely to lead to increased activity.”Unfortunately, response rates for the approved KRASG12C inhibitors have been more modest in GI tumors than those seen in NSCLC. The single-arm KRYSTAL-1 study demonstrated that adagrasib yielded an overall response rate (ORR) of 34% with a median duration of response of 5.8 months among patients with previously treated locally advanced or metastatic KRASG12C-mutated CRC.7 In the phase 3 CodeBreaK 300 trial, investigators randomly assigned patients with KRASG12C-mutated metastatic CRC to sotorasib 960 mg plus panitumumab, sotorasib 240 mg plus panitumumab, or investigator’s choice. Median progression-free survival (PFS) was more than double with sotorasib plus panitumumab—regardless of dose—compared with standard of care (5.6 vs 2 months).8This lower response “is partly due to intrinsic resistance mechanisms in the tumor microenvironment,” Dr. Saeed said. “Only a small subset of GI cancer patients harbor the G12C mutation—about 3% to 4% in colorectal cancer and far fewer (less than 1%) in pancreatic cancer—so the overall eligible patient population remains limited.”“In pancreatic cancer, around 40% of KRAS mutations are G12D, followed by G12V, which occur in about 35% of pancreas cancer, and G12R, which are rare in other GI cancers but occur in about 20% of pancreas cancer,” Dr. Garrido said. “In CRC, the most common are G12D, occurring in about 28% and G12V occurring in about 20%.”In addition, both primary and acquired resistance to KRASG12C inhibitors represent a growing challenge.“Tumors can bypass the KRAS blockade by activating alternative pathways such as EGFR, MET, or PI3K,” Dr. Saeed said. “There are also cases of on-target resistance through additional KRAS mutations that prevent drug binding or through amplification of KRAS or downstream effectors.”<h2>Aiming at Other Targets</h2>The different KRAS variants are important because they differ in how they activate downstream signaling and respond to therapeutic strategies, Dr. Saeed explained. In recent years, more effort has gone into developing inhibitors targeted either to these other KRAS variants or to all of the variants in codon 12 using so-called pan- or multi-(K)RAS inhibitors.Unfortunately, targeting each variant has its own challenges. For example, the switch II pocket in G12D does not have the same reactive residue as G12C, making it harder for molecules to bond.9 However, progress is still being made.RMC-6236 is a multi-selective RAS inhibitor being tested in patients with previously treated pancreatic ductal adenocarcinoma (PDAC).“This drug is a bit unique because it works as a molecular glue,” said Dr. Garrido-Laguna. “It brings together two proteins that otherwise would not interact.”The drug first forms a binary complex with cyclophilin, a protein that is ubiquitously expressed in every cell of the body. Then this binary complex binds to activated RAS via a noncovalent manner to form a tricomplex.“When the drug brings these two proteins together, it alters the configuration of cyclophilin so that it causes steric occlusion of the binding sites of RAS downstream mediators,” Dr. Garrido-Laguna said. “When RAS is activated, it signals downstream through different proteins including RAF. This drug makes it so those downstream mediators cannot bind to RAS, and that means the activated protein is not signaling downstream.”Dr. Garrido-Laguna presented efficacy and safety results of a phase 1 trial of RMC-6236 in patients with PDAC at the 2025 ASCO Gastrointestinal Cancers Symposium.10 The study included 127 patients with RAS-mutant PDAC. At the recommended phase 2 dose for PDAC (300 mg), the ORR (both confirmed and unconfirmed) was 27%, but among those with KRAS mutations in codon 12, the ORR was 36%.“Confirmed responses to standard-of-care second-line chemotherapy in pancreatic cancer are in the single digits,” Dr. Garrido-Laguna said.Median PFS was 8.5 months for those with mutations in KRAS codon 12. Most common toxicities were skin rash, diarrhea, and nausea. These results prompted the phase 3 RASOLUTE study, an ongoing study in the second line evaluating RMC-6236 versus standard of care.11 The results of the study are expected to be published in 2026.Data from a study of RMC-9805, a RAS(ON) allele–specific G12D inhibitor, were presented in October at the European Organisation for Research and Treatment of Cancer–National Cancer Institute–American Association for Cancer Research (EORTC-NCI-AACR) Symposium on Molecular Targets and Cancer Therapeutics in Barcelona. Among those patients with PDAC treated with the recommended phase 2 dose of 1,200 mg daily (n=40), the objective response rate was 30%.12“The activity was very similar to 6236 in terms of response but had a significant advantage because the toxicity seemed much better,” Dr. Garrido-Laguna said. He also mentioned some exciting compounds in early trials that target both active and inactive forms of the KRAS protein.“This is very important because most of the drugs we have in the clinic now that are KRASG12D inhibitors only hit the off form of the protein, and that may lead to limited activity,” Dr. Garrido-Laguna said.In all though, there are too many compounds under investigation in pancreatic, colorectal, and other cancers to begin to try to summarize them all, he said.The early results of a study of a first-in-class protein degrader targeting KRASG12D were presented at the European Society of Medical Oncology (ESMO) Congress 2024. 13 Although it showed only modest activity in PDAC, it provided proof of concept of this new mechanism to target KRAS.13<h2>What Does the Future Hold</h2>The future definitely holds more progress for targeting KRAS, Dr. Pant said. In addition to inhibitors, another potential treatment strategy is RAS-directed cancer vaccines used in earlier lines of therapy.Patients with pancreatic cancer who undergo resection and adjuvant chemotherapy still have a high risk for recurrence, Dr. Pant explained. The phase 1 AMPLIFY-1 trial tested cancer vaccine ELI-002 2P in a small group of patients with pancreatic cancer or CRC who were considered to be at high risk for relapse after locoregional treatment. The vaccine induced “considerable T cell responses” and yielded a median recurrence-free survival (RFS) of 16.33 months in the full cohort, whereas the median RFS was not reached in the patients who exhibited above median T-cell responses.14Increased research into combination therapies will also play an important role. Current approaches under investigation include combining KRAS inhibitors with “SHP2 inhibitors, MEK inhibitors, or immune checkpoint blockade to shut down escape pathways and enhance tumor response,” Dr. Saeed said.Interest is also growing in indirect KRAS-targeting approaches, such as disrupting upstream regulators (eg, SOS1, SHP2), downstream signaling nodes, or exploiting synthetic lethality, Dr. Saeed added. All of this information points toward the fact that “the field is rapidly evolving toward more personalized and combination-based strategies.”<h2>References</h2><ol>
<li>Huang L, et al. Signal Transduct Target Ther. 2021;6(1):386. doi:<a href="https://pubmed.ncbi.nlm.nih.gov/34776511/" target="_blank" rel="noopener">10.1038/s41392-021-00780-4</a></li>
<li>Wang L, et al. Mod Pathol. 2023;36(2):100014. doi:<a href="https://pubmed.ncbi.nlm.nih.gov/36853786/" target="_blank" rel="noopener">10.1016/j.modpat.2022.100014</a></li>
<li>Varghese AM, et al. Nat Med. 2025;31(2):466-477. doi:<a href="https://pubmed.ncbi.nlm.nih.gov/39753968/" target="_blank" rel="noopener">10.1038/s41591-024-03362-3</a></li>
<li>Ostrem JM, et al. Nature. 2013;503(7477):548-51. doi:<a href="https://pubmed.ncbi.nlm.nih.gov/24256730/" target="_blank" rel="noopener">10.1038/nature12796</a></li>
<li>Drugs.com. Lumakras FDA Approval History. Updated January 18, 2025. Accessed June 26, 2025. <a href="https://www.drugs.com/history/lumakras.html" target="_blank" rel="noopener">https://www.drugs.com/history/lumakras.html</a></li>
<li>Drugs.com. Krazati FDA Approval History. Updated June 24, 2024. Accessed June 26, 2025. <a href="https://www.drugs.com/history/krazati.html%20" target="_blank" rel="noopener">https://www.drugs.com/history/krazati.html</a></li>
<li>Yaeger R, et al. Cancer Discov. 2024;14(6):982-993. doi:<a href="https://pubmed.ncbi.nlm.nih.gov/38587856/" target="_blank" rel="noopener">10.1158/2159-8290.CD-24-0217</a></li>
<li>Fakih MG, et al N Engl J Med. 2023;389:2125-2139. doi:<a href="https://pubmed.ncbi.nlm.nih.gov/37870968/" target="_blank" rel="noopener">10.1056/NEJMoa2308795</a></li>
<li>Bannoura SF, et al. Front Oncol. 2022;12:1013902. doi:<a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC9749787/" target="_blank" rel="noopener">10.3389/fonc.2022.1013902</a></li>
<li>Garrido-Laguna I, et al. J Clin Oncol. 2025;43(4_suppl). doi: <a href="https://ascopubs.org/doi/10.1200/JCO.2025.43.4_suppl.722" target="_blank" rel="noopener">10.1200/JCO.2025.43.4_suppl.722</a></li>
<li>Revolution Medicines. Accessed June 26, 2025. <a href="https://ir.revmed.com/news-releases/news-release-details/revolution-medicines-announces-first-patient-dosed-phase-3-study" target="_blank" rel="noopener">https://ir.revmed.com/news-releases/news-release-details/revolution-medicines-announces-first-patient-dosed-phase-3-study</a></li>
<li>Revolution Medicines. Accessed June 26, 2025. <a href="https://ir.revmed.com/news-releases/news-release-details/revolution-medicines-presents-initial-data-rmc-9805-monotherapy" target="_blank" rel="noopener">https://ir.revmed.com/news-releases/news-release-details/revolution-medicines-presents-initial-data-rmc-9805-monotherapy</a></li>
<li>Park W, et al. <a href="https://www.annalsofoncology.org/article/S0923-7534(24)02194-X/fulltext" target="_blank" rel="noopener">Ann Oncol. 2024;35(2):S486-S487</a>.</li>
<li>Pant S, et al Nat Med. 2024;30(2):531-542. doi: <a href="https://pubmed.ncbi.nlm.nih.gov/38195752/" target="_blank" rel="noopener">10.1038/s41591-023-02760-3</a></li>
</ol>

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