Abstract IA006: Genetic Drivers of Sensitivity or Resistance to RAS(ON) Multi- Selective Inhibitors in NRAS-Mutated Melanoma

Abstract Most patients with advanced BRAF or NRAS-driven melanoma receive front-line immunotherapy. However, if immunotherapy fails, BRAF-mutated patients have effective second-line therapies, whereas NRAS-mutated patients lack pathway-targeted options. Recently, RAS(ON) multi-selective inhibitors like RMC-7977, and the investigational agent daraxonrasib, were described that, in partnership with cyclophilin-A (CYPA), inhibit RAS[GTP] signaling. Both compounds demonstrate potent anti- proliferative activity against NRAS-mutated melanoma cell lines and robust anti-tumor activity against preclinical melanoma models. However, in preclinical models, resistance to RMC-7977 monotherapy arose through mutations in Ppia (encoding CYPA) or Map2k1 (encoding MEK1). Moreover, two clinical case studies in patients with NRAS-mutated melanoma treated with daraxonrasib demonstrated clear anti-tumor activity in one patient, but progressive disease in another with co-occurring NRAS and MAP2K1 mutations at baseline. These findings support the potential for daraxonrasib in treatment of patients with NRAS-mutated melanoma, and reveal candidate mechanisms of monotherapy resistance, underscoring the need for combination therapies to improve outcomes. Citation Format: Mona Foth, Wontak Kim, Kayla O'Toole, Brandon Murphy, Montserrat Justo-Garrido, Sanjana Boggaram, Phaedra Ghazi, Euan Brennan, Isaac Wright, Tate Shepherd, Emilio Cortes-Sanchez, Yingyun Wang, Jennifer Roth, Matthew Rees, Melissa Ronan, Jingjing Jiang, Ursula Wasko, Amanda Jiang, Carly Becker, Dekker Deacon, Siwen Hu-Lieskovan, Conan Kinsey, Jeffery Russell, Aparna Hegde, Ignacio Garrido-Laguna, Matthew Holderfield, Mallika Singh, Martin McMahon. Genetic Drivers of Sensitivity or Resistance to RAS(ON) Multi- Selective Inhibitors in NRAS-Mutated Melanoma [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: RAS Oncogenesis and Therapeutics; 2026 Mar 5-8; Los Angeles, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(5_Suppl_1):Abstract nr IA006.

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Journal
Cancer Research
Published
2026-03-05
DOI
https://doi.org/10.1158/1538-7445.rasoncother26-ia006
Primary Topic
Melanoma and MAPK Pathways
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article
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article

Abstract IA006: Genetic Drivers of Sensitivity or Resistance to RAS(ON) Multi- Selective Inhibitors in NRAS-Mutated Melanoma

Phaedra C. Ghazi, Emilio Cortes-Sanchez, Matthew Holderfield, Montserrat Justo-Garrido et al.
Cancer Research
Melanoma and MAPK Pathways
article

Abstract IA006: Genetic Drivers of Sensitivity or Resistance to RAS(ON) Multi- Selective Inhibitors in NRAS-Mutated Melanoma

Phaedra C. Ghazi, Emilio Cortes-Sanchez, Matthew Holderfield, Montserrat Justo-Garrido, Aparna Hegde, Kayla T. O'Toole, Wontak Kim, Mallika Singh, Dekker C. Deacon, Conan G. Kinsey, Mona Foth, Jeffery S. Russell, Euan Brennan, Tate Shepherd, Ignacio Garrido-Laguna, Siwen Hu-Lieskovan, Amanda Jiang, Carly Becker, Martin McMahon, Ursula Wasko, Jennifer Roth, Brandon Murphy, Isaac Wright, Jingjing Jiang, Melissa Ronan, Sanjana Boggaram
article en

Abstract

Abstract Most patients with advanced BRAF or NRAS-driven melanoma receive front-line immunotherapy. However, if immunotherapy fails, BRAF-mutated patients have effective second-line therapies, whereas NRAS-mutated patients lack pathway-targeted options. Recently, RAS(ON) multi-selective inhibitors like RMC-7977, and the investigational agent daraxonrasib, were described that, in partnership with cyclophilin-A (CYPA), inhibit RAS[GTP] signaling. Both compounds demonstrate potent anti- proliferative activity against NRAS-mutated melanoma cell lines and robust anti-tumor activity against preclinical melanoma models. However, in preclinical models, resistance to RMC-7977 monotherapy arose through mutations in Ppia (encoding CYPA) or Map2k1 (encoding MEK1). Moreover, two clinical case studies in patients with NRAS-mutated melanoma treated with daraxonrasib demonstrated clear anti-tumor activity in one patient, but progressive disease in another with co-occurring NRAS and MAP2K1 mutations at baseline. These findings support the potential for daraxonrasib in treatment of patients with NRAS-mutated melanoma, and reveal candidate mechanisms of monotherapy resistance, underscoring the need for combination therapies to improve outcomes. Citation Format: Mona Foth, Wontak Kim, Kayla O'Toole, Brandon Murphy, Montserrat Justo-Garrido, Sanjana Boggaram, Phaedra Ghazi, Euan Brennan, Isaac Wright, Tate Shepherd, Emilio Cortes-Sanchez, Yingyun Wang, Jennifer Roth, Matthew Rees, Melissa Ronan, Jingjing Jiang, Ursula Wasko, Amanda Jiang, Carly Becker, Dekker Deacon, Siwen Hu-Lieskovan, Conan Kinsey, Jeffery Russell, Aparna Hegde, Ignacio Garrido-Laguna, Matthew Holderfield, Mallika Singh, Martin McMahon. Genetic Drivers of Sensitivity or Resistance to RAS(ON) Multi- Selective Inhibitors in NRAS-Mutated Melanoma [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: RAS Oncogenesis and Therapeutics; 2026 Mar 5-8; Los Angeles, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(5_Suppl_1):Abstract nr IA006.

Cancer ResearchVol. 86(5_Supplement_1)
Broad Institute (US), University of Utah (US), Huntsman Cancer Institute (US), Revolution Medicines (United States) (US)
Partnerships for the goals
Openalex Percentile: Top 33%
Melanoma and MAPK Pathways
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