# Revolution Medicines, Inc. (RVMD)

Informational only - not investment advice.

CIK: 0001628171
SIC: 2836 Biological Products, (No Diagnostic Substances)
SIC breadcrumb: [Manufacturing](/division/D/) > [Chemicals And Allied Products](/major-group/28/) > [SIC 2836 Biological Products, (No Diagnostic Substances)](/industry/2836/)
Latest 10-K filed: 2026-02-25
SEC page: https://www.sec.gov/edgar/browse/?CIK=1628171
Filing source: https://www.sec.gov/Archives/edgar/data/1628171/000119312526071563/rvmd-20251231.htm

## At a glance

No standardized annual SEC companyfacts metrics were extracted for this company; the at-a-glance panel is omitted rather than estimated.

No market price, no rating, no forecast on this site. Not investment advice.

### Peer percentile fingerprint

| Ratio | RVMD | Peer median | Percentile | N |
| --- | ---: | ---: | ---: | ---: |
| ROE | -69.3% | -38.7% | 25 | 60 |
| ROA | -48.0% | -30.4% | 25 | 66 |
| Liabilities / equity | 0.44 | 0.38 | 62 | 62 |
| Current ratio | 7.14 | 5.52 | 62 | 66 |

Percentile = share of the N covered peers reporting that ratio whose value is lower (ties counted half); computed among grepcent-covered companies in SIC industry 2836 Biological Products, (No Diagnostic Substances), not the whole market. A higher percentile means a higher value of the ratio, not a better company. Ratios with fewer than 8 reporting peers are omitted. Latest reported values per company; fiscal periods may differ. Descriptive arithmetic - not a score, rating, or ranking.

## Selected Fundamentals
| Metric | Value | Unit | FY | Filed |
| --- | ---: | --- | ---: | --- |
| Net income | -1131301000 | USD | 2025 | 2026-02-25 |
| Assets | 2354508000 | USD | 2025 | 2026-02-25 |

## Financials

Annual standardized facts from SEC companyfacts as of latest extracted filing date 2026-02-25. Source: https://data.sec.gov/api/xbrl/companyfacts/CIK0001628171.json. Derived margins, ratios, and free cash flow are computed from the extracted annual SEC facts.

| Metric | 2017 | 2018 | 2019 | 2020 | 2021 | 2022 | 2023 | 2024 | 2025 |
| --- | ---: | ---: | ---: | ---: | ---: | ---: | ---: | ---: | ---: |
| Net income |  | -41,789,000 | -47,664,000 | -108,159,000 | -187,091,000 | -248,705,000 | -436,367,000 | -600,093,000 | -1,131,301,000 |
| Operating income |  | -40,329,000 | -54,120,000 | -110,697,000 | -188,008,000 | -258,279,000 | -487,185,000 | -689,524,000 | -1,182,369,000 |
| Diluted EPS |  |  |  | -2.01 | -2.57 | -3.08 | -3.86 | -3.58 | -5.95 |
| Operating cash flow |  | 1,213,000 | -49,616,000 | -100,064,000 | -147,180,000 | -224,401,000 | -350,572,000 | -557,436,000 | -897,741,000 |
| Capital expenditures |  | 1,499,000 | 2,589,000 | 2,933,000 | 6,528,000 | 10,816,000 | 7,729,000 | 10,308,000 | 15,990,000 |
| Assets |  |  | 220,529,000 | 567,401,000 | 737,988,000 | 811,930,000 | 2,061,705,000 | 2,558,301,000 | 2,354,508,000 |
| Liabilities |  |  | 67,994,000 | 92,725,000 | 135,420,000 | 126,742,000 | 235,511,000 | 293,097,000 | 723,211,000 |
| Stockholders' equity | -67,717,000 | -108,422,000 | -152,574,000 | 474,676,000 | 602,568,000 | 685,188,000 | 1,826,194,000 | 2,265,204,000 | 1,631,297,000 |
| Cash and cash equivalents |  | 69,586,000 | 16,659,000 | 104,268,000 | 108,497,000 | 161,412,000 | 696,148,000 | 543,064,000 | 383,745,000 |
| Free cash flow |  | -286,000 | -52,205,000 | -102,997,000 | -153,708,000 | -235,217,000 | -358,301,000 | -567,744,000 | -913,731,000 |

### Ratios

ROE and ROA use period-end equity/assets. Liabilities / equity uses total liabilities divided by stockholders' equity. Current ratio uses current assets divided by current liabilities when both are reported.

| Metric | 2017 | 2018 | 2019 | 2020 | 2021 | 2022 | 2023 | 2024 | 2025 |
| --- | ---: | ---: | ---: | ---: | ---: | ---: | ---: | ---: | ---: |
| Return on equity |  |  |  | -22.79% | -31.05% | -36.30% | -23.89% | -26.49% | -69.35% |
| Return on assets |  |  | -21.61% | -19.06% | -25.35% | -30.63% | -21.17% | -23.46% | -48.05% |
| Liabilities / equity |  |  |  | 0.20 | 0.22 | 0.18 | 0.13 | 0.13 | 0.44 |
| Current ratio |  |  | 3.11 | 9.63 | 9.77 | 10.65 | 13.06 | 14.20 | 7.14 |

## As-reported value updates

No tracked differences above grepcent's stated thresholds and capped precision rule were found between the earliest XBRL-filed value and the value currently on file for the standardized annual metrics grepcent tracks.


## Quarterly

Quarterly standardized facts from SEC companyfacts as of latest extracted filing date 2026-08-05. Source: https://data.sec.gov/api/xbrl/companyfacts/CIK0001628171.json.

Flow metrics use discrete quarter-length periods from 10-Q/10-Q/A filings. Q4 revenue and net income are derived only when annual FY and nine-month YTD facts exist for the same fiscal year; derived Q4 values are labeled. EPS Q4 is not derived.

| Quarter | End date | Revenue | Net income | Diluted EPS | Method |
| --- | --- | ---: | ---: | ---: | --- |
| 2021-Q3 | 2021-09-30 |  | -52,940,000 |  | reported discrete quarter |
| 2021-Q4 | 2021-12-31 | 9,460,000 | -52,676,000 |  | derived Q4 = FY annual - nine-month YTD |
| 2022-Q1 | 2022-03-31 | 7,578,000 |  |  | reported discrete quarter |
| 2022-Q2 | 2022-06-30 | 9,116,000 |  | -0.82 | reported discrete quarter |
| 2022-Q3 | 2022-09-30 | 3,356,000 |  | -0.87 | reported discrete quarter |
| 2022-Q4 | 2022-12-31 | 15,330,000 |  |  | derived Q4 = FY annual - nine-month YTD |
| 2023-Q1 | 2023-06-30 | 3,824,000 |  | -0.92 | reported discrete quarter |
| 2023-Q3 | 2023-09-30 | 0.00 |  | -0.99 | reported discrete quarter |
| 2023-Q4 | 2023-12-31 | 742,000 |  |  | derived Q4 = FY annual - nine-month YTD |
| 2024-Q1 | 2024-03-31 | 0.00 | -116,003,000 | -0.70 | reported discrete quarter |
| 2024-Q2 | 2024-03-31 |  |  | -0.81 | reported discrete quarter |
| 2024-Q2 | 2024-06-30 | 0.00 | -133,233,000 |  | reported discrete quarter |
| 2024-Q3 | 2024-09-30 | 0.00 | -156,288,000 | -0.94 | reported discrete quarter |
| 2024-Q4 | 2024-12-31 | 0.00 | -194,569,000 |  | derived Q4 = FY annual - nine-month YTD |
| 2025-Q1 | 2025-03-31 |  | -213,416,000 | -1.13 | reported discrete quarter |
| 2025-Q2 | 2025-06-30 |  | -247,787,000 | -1.31 | reported discrete quarter |
| 2025-Q3 | 2025-09-30 |  | -305,206,000 | -1.61 | reported discrete quarter |
| 2025-Q4 | 2025-12-31 |  | -364,892,000 |  | derived Q4 = FY annual - nine-month YTD |
| 2026-Q1 | 2026-03-31 |  | -453,816,000 | -2.29 | reported discrete quarter |
| 2026-Q2 | 2026-06-30 |  | -644,371,000 | -3.06 | reported discrete quarter |

## Filed narrative (10-K & 10-Q)

## Business

Verbatim Item 1 Business section from RVMD's latest 10-K: [/company/RVMD/business/](/company/RVMD/business/).

## Risk Factors

Verbatim Item 1A Risk Factors from RVMD's latest 10-K: [/company/RVMD/risk-factors/](/company/RVMD/risk-factors/).

## Latest quarter (10-Q)

Latest 10-Q source: https://www.sec.gov/Archives/edgar/data/1628171/000119312526335104/rvmd-20260630.htm

Extracted structurally from real Item 2 body heading to real Item 3/4 boundary. Published MD&A gate trimmed front/tail over-capture.
Confidence: high
Filing date: 2026-08-05
Report date: 2026-06-30

Item 2. Management’s Discussion and Analysis of Financial Condition and Results of Operations.

You should read the following discussion and analysis of our financial condition and results of operations in conjunction with the unaudited condensed consolidated financial statements and the related notes included elsewhere in this Quarterly Report on Form 10-Q. In addition to historical financial information, this discussion contains forward-looking statements based upon current expectations that involve risks and uncertainties. As a result of many factors, including those factors set forth in the “Risk Factors” section of this Quarterly Report on Form 10-Q, our actual results could differ materially from the results described or implied by the forward-looking statements contained in the following discussion and analysis.

Overview

We are a late-stage clinical oncology company developing novel targeted therapies for patients with RAS-addicted cancers. We possess sophisticated structure-based drug discovery capabilities built upon deep chemical biology and cancer pharmacology know-how and innovative, proprietary technologies that enable the creation of small molecules tailored to unconventional binding sites. Guided by our understanding of genetic drivers and adaptive resistance mechanisms in cancer, we deploy precision medicine approaches to inform innovative monotherapy and combination regimens. Our research and development pipeline comprises inhibitors that bind directly to RAS variants (RAS(ON) Inhibitors) that are designed to be used as monotherapy, in combination with other RAS(ON) Inhibitors and/or other therapeutic agents.

RAS(ON) Inhibitors

We are advancing a deep pipeline of RAS(ON) Inhibitors, including daraxonrasib (RMC-6236), our multi-selective inhibitor, zoldonrasib (RMC-9805), our G12D-selective inhibitor, elironrasib (RMC-6291), our G12C-selective inhibitor, and RMC-5127, our G12V-selective inhibitor. We also have other preclinical-stage RAS(ON) Inhibitor clinical development opportunities, including the RAS(ON) mutant-selective inhibitors RMC-0708 (Q61H) and RMC-8839 (G13C) and additional novel targeted approaches for patients with RAS-addicted cancers.

Daraxonrasib

Daraxonrasib, our RAS(ON) multi-selective inhibitor, is designed as an oral, tri-complex inhibitor of multiple RAS(ON) variants containing cancer driver mutations at all three of the major RAS mutation hotspot positions, G12, G13, and Q61. Daraxonrasib inhibits all three major RAS isoforms, suppressing the mutant cancer driver and cooperating wild-type RAS proteins. Daraxonrasib has been granted a non-transferable voucher for daraxonrasib in pancreatic adenocarcinoma (PDAC) under the Commissioner’s National Priority Voucher (CNPV) pilot program, Orphan Drug Designation (ODD) by the FDA and European Medicines Agency (EMA) for the treatment of pancreatic cancer, and Breakthrough Therapy Designation from the FDA for patients with previously treated metastatic PDAC with KRAS G12 mutations and patients with NSCLC with KRAS mutations other than G12C who have received prior platinum-based chemotherapy and anti-PD-(L)1 therapy.

Zoldonrasib

Zoldonrasib is designed as an oral RAS(ON) G12D-selective tri-complex inhibitor. It is designed to exhibit low nanomolar potency for suppressing RAS pathway signaling and growth of RAS G12D-bearing cancer cells and is engineered to covalently inactivate RAS G12D irreversibly. Zoldonrasib has received Breakthrough Therapy Designation from the FDA for the treatment of adult patients with KRAS G12D-mutated locally advanced or metastatic NSCLC who have been previously treated with anti-PD-1/PD-L1 therapy and platinum-based chemotherapy.

Elironrasib

Elironrasib is designed as an oral RAS(ON) G12C-selective tri-complex inhibitor. It is designed to exhibit subnanomolar potency for suppressing RAS pathway signaling and growth of RAS G12C-bearing cancer cells and is engineered to be highly selective for RAS G12C over wild-type RAS and other cellular targets. Elironrasib is designed to be differentiated from first-generation KRAS(OFF) G12C inhibitors, which sequester the KRAS(OFF) G12C form, by its mechanism of directly inhibiting the RAS(ON) G12C form. Elironrasib has received Breakthrough Therapy Designation from the FDA for the treatment of adult patients with KRAS G12C-mutated locally advanced or metastatic NSCLC who have received prior chemotherapy and immunotherapy but have not been previously treated with a KRAS G12C inhibitor.

RMC-5127

RMC-5127 is designed as an oral RAS(ON) G12V-selective tri-complex inhibitor. It is designed to exhibit picomolar potency for suppressing RAS pathway signaling and growth of RAS G12V-bearing cancer cells and is engineered for selective inhibition of RAS G12V over other RAS isoforms via non-covalent binding interactions. A first-in-human dose escalation clinical trial of RMC-5127 is

20

ongoing. We currently expect to identify a recommended Phase 2 dose for RMC-5127 during the second half of 2026 and to share initial clinical data in 2027.

New Class of RAS(ON) Inhibitors

We have designed a new class of tri-complex RAS(ON) Inhibitors in order to overcome RAS-driven drug resistance and thereby extend the clinical benefit of RAS(ON) Inhibitors. We currently expect to initiate a first-in-human clinical trial from this class of RAS(ON) Inhibitors in the fourth quarter of 2026.

Other Development Opportunities

RMC-0708

RMC-0708 is designed as an oral RAS(ON) Q61H-selective tri-complex inhibitor. It is designed to exhibit picomolar potency for suppressing RAS pathway signaling and growth of RAS Q61H-bearing cancer cells and is engineered for selective inhibition of RAS Q61H over other RAS isoforms via non-covalent binding interactions. Clinical development of RMC-0708 is subject to our continuing assessment of portfolio priorities.

RMC-8839

RMC-8839 is designed as an oral RAS(ON) G13C-selective tri-complex inhibitor. It is designed to exhibit picomolar potency for suppressing RAS pathway signaling and growth of KRAS G13C-bearing cancer cells and is engineered to covalently inactivate KRAS G13C for irreversible inhibition. Clinical development of RMC-8839 is subject to our continuing assessment of portfolio priorities.

Clinical Development

RAS Mutant Epidemiology in the United States

Variants in RAS proteins are among the most common oncogenic drivers of cancer. Based on tumor mutation frequencies from Foundation Medicine data, scaled to estimated patient numbers using cancer incidence from the American Cancer Society Cancer Facts and Figures, there are an estimated more than 190,000 new RAS mutant cancer diagnoses each year in the U.S. These include approximately 60,000 patients with NSCLC, representing approximately 30% of NSCLC diagnoses, approximately 75,000 patients with colorectal cancer (CRC), representing approximately 50% of CRC diagnoses, and approximately 56,000 patients with PDAC, representing more than 90% of PDAC diagnoses.

Pancreatic Cancer

Pancreatic cancer is one of the most common and difficult-to-treat cancers and patients have historically had limited treatment options. Because of this unmet need and the prevalence of RAS as a driver of PDAC, we believe that pancreatic cancer represents a particularly compelling opportunity for RAS-targeted therapies.

In May 2026, we presented results from our randomized Phase 3 registration study RASolute 302 comparing daraxonrasib against chemotherapy in patients with second line (2L) PDAC. In this study, daraxonrasib taken orally once daily demonstrated statistically significant and clinically meaningful improvements in progression-free survival (PFS) and overall survival (OS) compared to standard of care cytotoxic chemotherapy delivered intravenously. In the overall (intent-to-treat) study population, daraxonrasib demonstrated a median OS of 13.2 months versus 6.7 months for chemotherapy, with a hazard ratio of 0.40 (p 0.0001). Daraxonrasib was generally well tolerated, with a manageable safety profile and with no new safety signals. Based on the results from this first interim analysis, all PFS and OS endpoint results are considered final. The FDA has accepted for review our New Drug Application (NDA) for daraxonrasib for previously treated metastatic pancreatic cancer and the EMA initiated a phased review of daraxonrasib under its Cancer Medicines Pathfinder project.

21

Based on encouraging early-stage clinical results, we are evaluating daraxonrasib and zoldonrasib in the following global, randomized Phase 3 registrational studies in PDAC:

•
RASolute 303: comparing daraxonrasib with and without chemotherapy against chemotherapy in patients with first-line (1L) metastatic PDAC;

•
RASolute 304: evaluating daraxonrasib as an adjuvant therapy in patients with resectable PDAC who have received surgery and chemotherapy;

•
RASolute 305: evaluating zoldonrasib in combination with the investigator’s choice of chemotherapies in patients with 1L metastatic PDAC in a placebo-controlled study; and

•
RASolute 309: comparing daraxonrasib with zoldonrasib against chemotherapy in 1L patients with RAS G12D PDAC.

In April 2026, we presented updated Phase 1 clinical data for daraxonrasib in patients with 1L PDAC across monotherapy and combination cohorts at the American Association for Cancer Research (AACR) Annual Meeting.

In July 2026 at the European Society for Medical Oncology’s Gastrointestinal Cancers Congress, we presented data for (i) zoldonrasib in combination with chemotherapy in patients with 1L RAS G12D PDAC; and (ii) zoldonrasib in combination with daraxonrasib in patients with previously treated RAS G12D PDAC. We believe these data showed that zoldonrasib in combination with chemotherapy and zoldonrasib in combination with daraxonrasib were generally well tolerated and demonstrated encouraging antitumor activity that supported our initiation of RASolute 305 and RASolute 309, respectively.

Non-Small Cell Lung Cancer

NSCLC is another major cancer type in which RAS mutations are common. While advances in immunotherapy and chemotherapy have improved outcomes for some individuals, many patients with RAS mutant NSCLC continue to experience disease progression, highlighting the need for new targeted approaches. Importantly, RAS mutations in NSCLC extend beyond a single subtype, leaving a significant portion of patients without broadly effective targeted treatment options.

Based on encouraging early-stage clinical results, we are evaluating daraxonrasib and zoldonrasib in the following global, randomized Phase 3 registrational studies in NSCLC:

•
RASolve 301: comparing daraxonrasib against docetaxel in patients with locally advanced or metastatic RAS mutant NSCLC who have been treated with immunotherapy and platinum-containing chemotherapy. We currently expect to complete enrollment in RASolve 301 in 2026, to enable an expected clinical readout in 2027; and

•
RASolve 308: evaluating zoldonrasib in combination with standard of care in patients with 1L metastatic RAS G12D NSCLC in a placebo-controlled study.

Based on our evaluation of the treatment landscape for NSCLC, we are prioritizing a mutant-selective approach for development in

1L NSCLC; we expect to initiate RASolve 307, a global, randomized Phase 3 registrational trial evaluating elironrasib in combination with standard of care in 1L RAS G12C NSCLC in the fourth quarter of 2026 and plan to continue evaluating daraxonrasib in NSCLC in combination with bispecific antibodies targeting both the PD-1/PD-L1 and VEGF axes.

In August 2026, we reported initial Phase 1 clinical data for (i) zoldonrasib in combination with pembrolizumab and chemotherapy in patients with 1L RAS G12D NSCLC and (ii) elironrasib in combination with pembrolizumab and chemotherapy in patients with 1L RAS G12C NSCLC. We believe these data showed that zoldonrasib and elironrasib were generally well tolerated and demonstrated encouraging an

[Excerpt truncated for page length; source filing is linked above.]

## Latest 10-K MD&A (excerpt)

Latest 10-K Item 7 source: https://www.sec.gov/Archives/edgar/data/1628171/000119312526071563/rvmd-20251231.htm
Complete FY 2025 MD&A: /company/RVMD/mda/fy2025/

Extracted from a substantive MD&A body after the formal Item 7 span was a TOC or reference stub.
Confidence: high
Filing date: 2026-02-25
Report date: 2025-12-31

Overview

We are a clinical-stage precision oncology company developing novel targeted therapies for RAS-addicted cancers. We possess sophisticated structure-based drug discovery capabilities built upon deep chemical biology and cancer pharmacology know-how and innovative, proprietary technologies that enable the creation of small molecules tailored to unconventional binding sites. Guided by our understanding of genetic drivers and adaptive resistance mechanisms in cancer, we deploy precision medicine approaches to inform innovative monotherapy and combination regimens. Our research and development pipeline comprises inhibitors that bind directly to RAS variants (RAS(ON) Inhibitors) that are designed to be used as monotherapy, in combination with other RAS(ON) Inhibitors and/or other therapeutic agents.

RAS(ON) Inhibitors

We are advancing a deep pipeline of RAS(ON) Inhibitors, including daraxonrasib (RMC-6236), our multi-selective inhibitor, zoldonrasib (RMC-9805), our G12D-selective inhibitor, elironrasib (RMC-6291), our G12C-selective inhibitor, and RMC-5127, our G12V-selective inhibitor. We also have other preclinical-stage RAS(ON) Inhibitor clinical development opportunities, including the RAS(ON) mutant-selective inhibitors RMC-0708 (Q61H) and RMC-8839 (G13C) and additional novel targeted approaches for patients with RAS-addicted cancers.

Daraxonrasib

Daraxonrasib, our RAS(ON) multi-selective inhibitor, is designed as an oral, RAS-selective tri-complex inhibitor of multiple RAS(ON) variants containing cancer driver mutations at all three of the major RAS mutation hotspot positions, G12, G13, and Q61. Daraxonrasib inhibits all three major RAS isoforms, suppressing the mutant cancer driver and cooperating wild-type RAS proteins. In October 2025, the U.S. Food and Drug Administration (FDA) granted us a non-transferable voucher for daraxonrasib in pancreatic ductal adenocarcinoma (PDAC) under the Commissioner’s National Priority Voucher (CNPV) pilot program. Also in October 2025, daraxonrasib was granted Orphan Drug Designation by the FDA for the treatment of pancreatic cancer. In June 2025, daraxonrasib received Breakthrough Therapy Designation from the FDA for previously treated metastatic PDAC in patients with KRAS G12 mutations.

Zoldonrasib

Zoldonrasib is designed as a RAS(ON) oral G12D-selective tri-complex inhibitor. It is designed to exhibit low nanomolar potency for suppressing RAS pathway signaling and growth of RAS G12D-bearing cancer cells and is engineered to covalently inactivate RAS G12D irreversibly. In December 2025, zoldonrasib received Breakthrough Therapy Designation from the FDA for the treatment of adult patients with KRAS G12D-mutated locally advanced or metastatic non-small cell lung cancer (NSCLC) who have been previously treated with anti-PD-1/PD-L1 therapy and platinum-based chemotherapy.

Elironrasib

Elironrasib is designed as a RAS(ON) oral G12C-selective tri-complex inhibitor. It is designed to exhibit subnanomolar potency for suppressing RAS pathway signaling and growth of RAS G12C-bearing cancer cells and is engineered to be highly selective for RAS G12C over wild-type RAS and other cellular targets. Elironrasib is designed to be differentiated from first-generation KRAS(OFF) G12C inhibitors, which sequester the KRAS(OFF) G12C form, by its mechanism of directly inhibiting the RAS(ON) G12C form. In July 2025, elironrasib received Breakthrough Therapy Designation from the FDA for the treatment of adult patients with KRAS G12C-mutated locally advanced or metastatic NSCLC who have received prior chemotherapy and immunotherapy but have not been previously treated with a KRAS G12C inhibitor.

78

RMC-5127

RMC-5127 is designed as a RAS(ON) oral G12V-selective tri-complex inhibitor. It is designed to exhibit picomolar potency for suppressing RAS pathway signaling and growth of RAS G12V-bearing cancer cells and is engineered for selective inhibition of RAS G12V over other RAS isoforms via non-covalent binding interactions. A first-in-human dose escalation clinical trial of RMC-5127 is ongoing.

New Class of RAS(ON) Inhibitors

We have designed a new class of RAS(ON) Inhibitors in order to overcome RAS-driven drug resistance and thereby extend the clinical benefit of RAS(ON) Inhibitors. We currently expect to initiate a first-in-human clinical trial from this class of RAS(ON) Inhibitors in the fourth quarter of 2026.

Other Development Opportunities

RMC-0708

RMC-0708 is designed as a RAS(ON) oral Q61H-selective tri-complex inhibitor. It is designed to exhibit picomolar potency for suppressing RAS pathway signaling and growth of RAS Q61H-bearing cancer cells and is engineered for selective inhibition of RAS Q61H over other RAS isoforms via non-covalent binding interactions. Clinical development of RMC-0708 is subject to our continuing assessment of portfolio priorities.

RMC-8839

RMC-8839 is designed as a RAS(ON) oral G13C-selective tri-complex inhibitor. It is designed to exhibit picomolar potency for suppressing RAS pathway signaling and growth of KRAS G13C-bearing cancer cells and is engineered to covalently inactivate KRAS G13C for irreversible inhibition. Clinical development of RMC-8839 is subject to our continuing assessment of portfolio priorities.

Clinical Development

RAS Mutant Epidemiology in the United States

Variants in RAS proteins are among the most common oncogenic drivers of cancer. Based on tumor mutation frequencies from Foundation Medicine data, scaled to estimated patient numbers using cancer incidence from the American Cancer Society Cancer Facts and Figures, there are an estimated more than 190,000 new RAS mutant cancer diagnoses each year in the U.S. These include approximately 60,000 patients with NSCLC, representing approximately 30% of NSCLC diagnoses, approximately 75,000 patients with colorectal cancer (CRC), representing approximately 50% of CRC diagnoses, and approximately 56,000 patients with PDAC, representing more than 90% of PDAC diagnoses.

Pancreatic Cancer

Pancreatic cancer is one of the most common and difficult-to-treat cancers and patients have historically had limited treatment options. Because of this unmet need and the prevalence of RAS as a driver of PDAC, we believe that pancreatic cancer represents a particularly compelling opportunity for RAS-targeted therapies.

Based on encouraging early-stage clinical results, we are evaluating daraxonrasib and zoldonrasib in the following global, randomized Phase 3 registrational studies in PDAC:

•
RASolute 302: comparing daraxonrasib against chemotherapy in patients with second line (2L) PDAC; a clinical readout for this study is currently expected in the first half of 2026;

•
RASolute 303: comparing daraxonrasib with and without chemotherapy against chemotherapy in patients with first line (1L) metastatic PDAC;

•
RASolute 304: evaluating daraxonrasib as an adjuvant therapy in patients with resectable PDAC; and

•
RASolute 305: comparing zoldonrasib in combination with the investigator’s choice of either gemcitabine nab-paclitaxel or modified FOLFIRINOX against the investigator’s choice of the chemotherapies in patients with 1L metastatic PDAC in a placebo-controlled study.

79

In addition, we expect to initiate RASolute 309, a global, randomized Phase 3 registrational trial evaluating the combination of daraxonrasib with zoldonrasib in patients with 1L PDAC in the second half of 2026.

Non-Small Cell Lung Cancer

NSCLC is another major cancer type in which RAS mutations are common. While advances in immunotherapy and chemotherapy have improved outcomes for some individuals, many patients with RAS mutant NSCLC continue to experience disease progression, highlighting the need for new targeted approaches. Importantly, RAS mutations in NSCLC extend beyond a single subtype, leaving a significant portion of patients without broadly effective targeted treatment options.

Based on encouraging early-stage clinical results we are evaluating daraxonrasib in RASolve 301, a global, randomized Phase 3 registrational trial comparing daraxonrasib versus docetaxel in patients with locally advanced or metastatic RAS mutant NSCLC who have been treated with immunotherapy and platinum-containing chemotherapy. We currently expect to substantially complete enrollment in RASolve 301 in 2026.

We also currently expect to initiate RASolve 308, a global, randomized placebo-controlled Phase 3 registrational trial evaluating zoldonrasib in combination with standard of care in patients with 1L metastatic RAS G12D NSCLC in the first half of 2026.

We currently expect to provide an update on our plans for advancing daraxonrasib combination therapy in 1L NSCLC in 2026. We also currently expect to share an update on our registrational strategy for elironrasib in NSCLC in 2026.

Colorectal Cancer

Colorectal cancers are genetically complex and heterogeneous, and patients with RAS mutant disease typically have limited targeted treatment options, particularly after progression on standard therapies. As a result, outcomes remain poor for many patients, underscoring the need for new therapeutic approaches that more effectively address the underlying drivers of the disease.

To address this need, we are pursuing a combination-focused strategy designed to maximize clinical impact in this challenging setting. We believe that our early clinical experience supports continued exploration of these strategies. As data mature, we plan to prioritize registrational opportunities with the goal of improving outcomes and expanding treatment options for patients with RAS mutant colorectal cancer. We currently expect to provide updated combination data in CRC in 2026.

Collaborations

Bristol Myers Squibb Collaboration

In February 2026, we entered into a clinical collaboration with Bristol Myers Squibb (BMS) pursuant to which BMS plans to evaluate its compound navlimetostat, an MTA-cooperative PRMT5 inhibitor, in combination with daraxonrasib in patients with PDAC as part of a BMS-sponsored trial.

Amgen Collaboration

In February 2025, we entered into a clinical collaboration with Amgen Inc. (Amgen) pursuant to which Amgen is evaluating its compound AMG 193, an MTA-cooperative PRMT5 inhibitor, in combination with daraxonrasib in patients with 2L PDAC as part of an Amgen-sponsored trial.

Summit Collaboration

In June 2025, we entered into a clinical collaboration with Summit Therapeutics, Inc. (Summit) pursuant to which we are evaluating the safety and efficacy, in multiple solid tumor settings, of our clinical-stage RAS(ON) Inhibitors, including daraxonrasib, elironrasib and zoldonrasib, in combination with Summit’s ivonescimab, a PD-1/VEGF bispecific antibody. The first patient was recently dosed in this clinical trial.

Iambic Collaboration

In May 2025, we entered into a collaboration with Iambic Therapeutics (Iambic), pursuant to which Iambic uses its artificial intelligence capabilities to generate customized models through training with our proprietary data. Our aim in this collaboration is to enhance our lead discovery and optimization processes directed against both current and new drug targets to enable continued development of our pipeline.

Tango Collaboration

80

In November 2024, we entered into a clinical collaboration with Tango Therapeutics, Inc. (Tango) pursuant to which Tango is evaluating its compound vopimetostat (TNG462), an MTA-cooperative PRMT5 inhibitor, in combination with daraxonrasib or zoldonrasib in patients with MTAP-depleted, RAS mutant PDAC or lung cancer as part of a Tango-sponsored trial.

Break Through Cancer Collaboration

In November 2024, we entered into a collaboration with Break Through Cancer. The collaboration is designed to assess biopsy samples taken from patients receiving daraxonrasib in the investigational setting, with the goal of identifying biomarkers that could predict tumor response and how cancer cells adapt to the therapy. We believe this ap

[Excerpt truncated for page length; the complete text is on the linked full-MD&A page.]

Read the full FY 2025 MD&A: /company/RVMD/mda/fy2025/
All MD&A years: /company/RVMD/mda/


## MD&A history

Prior-year 10-K MD&A spans are extracted from SEC filings with the same bounded parser used for the latest filing. Each year's full verbatim text is on its own sub-page.

- [FY 2024 MD&A](/company/RVMD/mda/fy2024/): filed 2025-02-26; accession 0000950170-25-027736 (https://www.sec.gov/Archives/edgar/data/1628171/000095017025027736/rvmd-20241231.htm)
- [FY 2023 MD&A](/company/RVMD/mda/fy2023/): filed 2024-02-26; accession 0000950170-24-020145 (https://www.sec.gov/Archives/edgar/data/1628171/000095017024020145/rvmd-20231231.htm)
- [FY 2022 MD&A](/company/RVMD/mda/fy2022/): filed 2023-02-27; accession 0000950170-23-004645 (https://www.sec.gov/Archives/edgar/data/1628171/000095017023004645/rvmd-20221231.htm)
- [FY 2021 MD&A](/company/RVMD/mda/fy2021/): filed 2022-02-28; accession 0000950170-22-002297 (https://www.sec.gov/Archives/edgar/data/1628171/000095017022002297/rvmd-20211231.htm)


## FDA-approved drug applications

Applications listed under this company's exact-matched sponsor name. Approved applications only.

No resolved FDA applications were found for this company under the exact-unique, approved-only publish rule.

Sponsor as listed in Drugs@FDA at retrieval (2026-08-07); FDA sponsor listings can lag ownership transfers.

This list covers FDA applications whose listed sponsor name maps to this company by an exact-unique match; applications listed under sponsor names not mapped to this company (subsidiaries, name variants, joint ventures) are absent.


## Macro cross-references

Indicators mapped to this company's SIC classification (industry 2836 Biological Products, (No Diagnostic Substances)) by grepcent's deterministic macro-sector crosswalk. A navigational mapping, not a statistical or causal claim.

- [INDPRO](/indicator/INDPRO/): Industrial Production: Total Index
- [TCU](/indicator/TCU/): Capacity Utilization: Total Index
- [PPIACO](/indicator/PPIACO/): Producer Price Index by Commodity: All Commodities
- [GDPC1](/indicator/GDPC1/): Real Gross Domestic Product
- [DGS10](/indicator/DGS10/): Market Yield on U.S. Treasury Securities at 10-Year Constant Maturity
- [FEDFUNDS](/indicator/FEDFUNDS/): Federal Funds Effective Rate
- [CES0500000003](/indicator/CES0500000003/): Average Hourly Earnings of All Employees, Total Private
- [PAYEMS](/indicator/PAYEMS/): All Employees, Total Nonfarm

Macro-to-micro threads including this sector: [Inflation (CPI / PCE / PPI)](/thread/inflation-cpi-pce-ppi/), [US labor market](/thread/us-labor-market/), [Growth & output](/thread/growth-output/), [Money & trade](/thread/money-trade/), [Government finances](/thread/government-finances/), [Sector employment](/thread/sector-employment/), [Industrial orders & inventories](/thread/industrial-orders/), [Trade & external](/thread/trade-external/).

All macro indicators: /indicators/


## For LLMs & downloads

Markdown twin: /company/RVMD.md · JSON record: /company/RVMD.json · verified financials: /company/RVMD/financials.json / /company/RVMD/financials.csv · machine TOC for the whole site: /llms.txt