Adagrasib in Non–Small-Cell Lung Cancer Harboring a KRAS G12C Mutation
Open accessAbstract
BACKGROUND: , locking it in its inactive state. Adagrasib showed clinical activity and had an acceptable adverse-event profile in the phase 1-1b part of the KRYSTAL-1 phase 1-2 study. METHODS: -mutated non-small-cell lung cancer (NSCLC) previously treated with platinum-based chemotherapy and anti-programmed death 1 or programmed death ligand 1 therapy. The primary end point was objective response assessed by blinded independent central review. Secondary end points included the duration of response, progression-free survival, overall survival, and safety. RESULTS: -mutated NSCLC had been treated (median follow-up, 12.9 months); 98.3% had previously received both chemotherapy and immunotherapy. Of 112 patients with measurable disease at baseline, 48 (42.9%) had a confirmed objective response. The median duration of response was 8.5 months (95% confidence interval [CI], 6.2 to 13.8), and the median progression-free survival was 6.5 months (95% CI, 4.7 to 8.4). As of January 15, 2022 (median follow-up, 15.6 months), the median overall survival was 12.6 months (95% CI, 9.2 to 19.2). Among 33 patients with previously treated, stable central nervous system metastases, the intracranial confirmed objective response rate was 33.3% (95% CI, 18.0 to 51.8). Treatment-related adverse events occurred in 97.4% of the patients - grade 1 or 2 in 52.6% and grade 3 or higher in 44.8% (including two grade 5 events) - and resulted in drug discontinuation in 6.9% of patients. CONCLUSIONS: -mutated NSCLC, adagrasib showed clinical efficacy without new safety signals. (Funded by Mirati Therapeutics; ClinicalTrials.gov number, NCT03785249.).
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The clinical response data indicate rapid development of acquired resistance to KRAS G12C inhibitors.
“These results indicate the rapid development of acquired resistance to KRAS G12C inhibitors [18, 26, 27, 49].”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [27]
The Secondary Efficacy End Points report a median response duration of 8.5 months and median progression-free survival of 6.5 months, consistent with relatively short-lived benefit from adagrasib. The paper does not establish that progression was caused by acquired resistance, or show that the finding applies to KRAS G12C inhibitors generally. Page numbers were not provided for these passages. (LLM, conf=0.82)
Experimental — accuracy not yet measuredThe data from CodeBreak 100 for sotorasib and KRYSTAL-1 for adagrasib led to the approval of these inhibitors to treat G12C-mutant NSCLC.
“The data from both CodeBreak 100 for sotorasib and KRYSTAL-1 for adagrasib led to the approval of these inhibitors to treat G12C-mutant NSCLC [51,53,94].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [94]
The Discussion reports that sotorasib had been approved for metastatic KRAS G12C-mutated NSCLC on the basis of response data. The Abstract identifies this paper as reporting a registrational KRYSTAL-1 cohort for adagrasib, but the paper does not state that those data led to adagrasib’s approval or identify CodeBreaK 100 by name. (LLM, conf=0.88)
Experimental — accuracy not yet measuredInactive-state KRASG12C inhibitors adagrasib and sotorasib achieve anti-tumor response rates of 37-43% in NSCLC patients, with most patients experiencing disease progression 6-12 months after starting therapy.
“In clinical trials, the inactive-state KRASG12C mutant-specific inhibitors adagrasib (MRTX849) and sotorasib (AMG510) achieved 37–43% anti-tumor response rates in NSCLC patients with most experiencing disease progression 6–12 months after initiation of therapy7–9.”
From Combined inhibition of KRASG12C and mTORC1 kinase is synergistic in non-small cell lung cancer (2024) · cites this paper as [8]
The Discussion reports objective response rates of 37.1% for sotorasib and 42.9% for adagrasib; the Abstract says adagrasib locks KRAS G12C in its inactive state. The Secondary Efficacy End Points section reports median progression-free survival of 6.5 months for adagrasib, but the paper does not establish that most patients receiving either drug experienced disease progression specifically 6–12 months after starting therapy. Page numbers are unavailable in our copy. (LLM, conf=0.84)
Experimental — accuracy not yet measuredSTK11/LKB1 loss and KEAP1 mutations may contribute to lack of response to different therapies including anti-PD-(L)1 immune checkpoint inhibitors and KRASG12C inhibitors.
“STK11/LKB1 loss and KEAP1 mutations may contribute to lack of response to different therapies including anti-PD-(L)1 immune checkpoint inhibitors9,10 and KRASG12C inhibitors3,4.”
From LKB1 regulates JNK-dependent stress signaling and apoptotic dependency of KRAS-mutant lung cancers (2025) · cites this paper as [3]
The Exploratory Biomarker Analyses (page not specified) report a lower response rate to adagrasib in patients with a KEAP1 co-mutation and wild-type STK11. They do not show a comparable lack of response associated with STK11 alterations; responses occurred across the STK11/KEAP1-defined groups. Citations 9 and 10, not this source, are attached to the checkpoint-inhibitor portion of the sentence. (LLM, conf=0.84)
Experimental — accuracy not yet measuredFor adagrasib, an overall response rate was 23.0% in CRC, compared to 42.8% in NSCLC.
“For adagrasib, an ORR was 23.0% in CRC, compared to 42.8% in NSCLC (Table 1) [27, 48].”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [27]
The Primary End Point section reports a 42.9% objective response rate in patients with NSCLC, close to but not the stated 42.8%. The paper does not report the claimed 23.0% response rate in colorectal cancer, so it does not support the full comparison. (LLM, conf=0.88)
Experimental — accuracy not yet measured
Colorectal cancer has a markedly lower response rate to KRAS G12C inhibitors compared to non-small cell lung cancer.
“Colorectal cancer, in particular, has a markedly lower response rate to KRAS G12C inhibitors compared to non-small cell lung cancer.”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [27]
The Discussion reports a 42.9% objective response rate with adagrasib in KRAS G12C-mutated non-small-cell lung cancer. The introductory text mentions clinical activity in colorectal cancer but gives no colorectal response rate or comparison between the cancers, so it does not establish the claimed difference. (LLM, conf=0.82)
Experimental — accuracy not yet measuredThe therapeutic response to KRAS G12C inhibition was short-lived, with quick emergence of acquired resistance.
“Furthermore, the therapeutic response to KRAS G12C inhibition was short-lived, with quick emergence of acquired resistance.”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [27]
The Secondary Efficacy End Points section (page not provided) reports a median response duration of 8.5 months and median progression-free survival of 6.5 months, supporting the claim that benefit was limited in duration. The paper reports progression but does not establish that acquired resistance emerged quickly or caused it. (LLM, conf=0.84)
Experimental — accuracy not yet measuredEven in NSCLC patients, the response to KRAS G12C inhibitors was often short-lived, with a DOR of 10.9-11.1 months and PFS of 6.3-6.8 months for sotorasib, and a DOR of 8.5 months and PFS of 6.5 months for adagrasib.
“Even in NSCLC patients, the response to KRAS G12C inhibitors was often short-lived, with a DOR of 10.9–11.1 months and PFS of 6.3–6.8 months for sotorasib, and a DOR of 8.5 months and PFS of 6.5 months for adagrasib (Table 1).”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [27]
The Secondary Efficacy End Points section reports a median duration of response of 8.5 months and median progression-free survival of 6.5 months for adagrasib in previously treated KRAS G12C-mutated NSCLC. The paper does not provide the claimed sotorasib duration-of-response or progression-free-survival figures. Page numbers were not supplied for these passages. (LLM, conf=0.88)
Experimental — accuracy not yet measuredSotorasib, adagrasib, and divarasib monotherapies have demonstrated objective response rates ranging from 7.1% to 53.4% and median progression-free survival of 4.0-13.1 months.
“For example, sotorasib, adagrasib, and divarasib monotherapies have demonstrated objective response rates ranging from 7.1% to 53.4% and median progression-free survival of 4.0-13.1 months, 13-20”
From Anti-tumor efficacy of HRS-4642 and its potential combination with proteasome inhibition in KRAS G12D-mutant cancer (2024) · cites this paper as [18]
Table 2 reports a 42.9% objective response rate and 6.5-month median progression-free survival for adagrasib, both within the cited ranges. The Discussion also reports a 37.1% response rate for sotorasib, but our copy does not establish the stated range endpoints or the divarasib results. (LLM, conf=0.87)
Experimental — accuracy not yet measuredThe overall response rate of inactive-state KRASG12C inhibitors sotorasib and adagrasib in patients with KRASG12C mutant NSCLC is 37-43%.
“The overall response rate of inactive-state KRASG12C inhibitors sotorasib and adagrasib in patients with KRASG12C mutant NSCLC is 37-43%, a major advance albeit with significant room for improvement7,8.”
From Combined inhibition of KRASG12C and mTORC1 kinase is synergistic in non-small cell lung cancer (2024) · cites this paper as [8]
In patients with non-small cell lung cancer, divarasib had a numerically higher ORR (56.4%) than sotorasib (37% in a phase 2 trial and 28% in a phase 3 trial) and adagrasib (43% in a phase 2 trial).
“This is further supported by a numerically higher ORR seen with divarasib in patients with non-small cell lung cancer (56.4%) compared with sotorasib (37% in a phase 2 trial and 28% in a phase 3 trial) and adagrasib (43% in a phase 2 trial)11,23–25.”
From Divarasib plus cetuximab in KRAS G12C-positive colorectal cancer: a phase 1b trial (2024) · cites this paper as [24]
Many patients with KRAS G12C cancers did not respond to sotorasib and adagrasib.
“Clinical studies have shown that many patients with KRAS G12C cancers did not respond to sotorasib and adagrasib.”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [27]
Because KRAS mutations are often clonal founder events, mutant KRAS ctDNA can serve as a highly informative molecular marker for tumor burden, treatment response, minimal residual disease, and emergence of resistance.
“Because KRAS mutations are often clonal founder events, mutant KRAS ctDNA can serve as a highly informative molecular marker for tumor burden, treatment response, minimal residual disease, and emergence of resistance [29,47,77,78].”
From Precision Targeting of KRAS-Mutant Cancers: Beyond G12C Toward G12D and Pan-RAS Therapeutic Strategies (2026) · cites this paper as [29]
The Exploratory Biomarker Analyses section describes testing tumor tissue or blood for candidate biomarkers associated with response, but does not identify mutant KRAS ctDNA as a marker. Searches for ctDNA, clonal founder events, and minimal residual disease found no passage addressing the claimed uses for tumor burden, response, residual disease, or resistance. (LLM, conf=0.76)
Experimental — accuracy not yet measuredAdagrasib has a long half-life of 23 hours.
“Adagrasib is a selective, irreversible inhibitor of KRASG12C and has favorable properties, including long half-life (23 hours), dose-dependent pharmacokinetics, and central nervous system penetration (3–5).”
From Efficacy and Safety of Adagrasib plus Cetuximab in Patients with <i>KRAS</i> G12C-Mutated Metastatic Colorectal Cancer (2024) · cites this paper as [4]
Adagrasib is a selective, irreversible inhibitor of KRASG12C.
“Adagrasib is a selective, irreversible inhibitor of KRASG12C and has favorable properties, including long half-life (23 hours), dose-dependent pharmacokinetics, and central nervous system penetration (3–5).”
From Efficacy and Safety of Adagrasib plus Cetuximab in Patients with <i>KRAS</i> G12C-Mutated Metastatic Colorectal Cancer (2024) · cites this paper as [4]
Adagrasib has dose-dependent pharmacokinetics.
“Adagrasib is a selective, irreversible inhibitor of KRASG12C and has favorable properties, including long half-life (23 hours), dose-dependent pharmacokinetics, and central nervous system penetration (3–5).”
From Efficacy and Safety of Adagrasib plus Cetuximab in Patients with <i>KRAS</i> G12C-Mutated Metastatic Colorectal Cancer (2024) · cites this paper as [4]
Adagrasib has central nervous system penetration.
“Adagrasib is a selective, irreversible inhibitor of KRASG12C and has favorable properties, including long half-life (23 hours), dose-dependent pharmacokinetics, and central nervous system penetration (3–5).”
From Efficacy and Safety of Adagrasib plus Cetuximab in Patients with <i>KRAS</i> G12C-Mutated Metastatic Colorectal Cancer (2024) · cites this paper as [4]
Adagrasib is an oral small molecule that selectively and irreversibly inhibits mutant KRAS G12C, and the FDA recently approved it for NSCLC after at least one prior systemic therapy.
“Adagrasib is a selective and irreversible oral small-molecule inhibitor of the mutant KRAS G12C protein18 and was recently approved by the FDA for treatment of NSCLC who have received at least 1 prior systemic therapy19.”
From Early Changes in Circulating Cell-Free <i>KRAS</i> G12C Predict Response to Adagrasib in KRAS Mutant Non–Small Cell Lung Cancer Patients (2023) · cites this paper as [19]
Among Cohort A, the subset evaluable for longitudinal KRAS G12C ctDNA response had a slightly higher ORR (56.4%, 22/39) than the overall cohort (50.5%, 48/95).
“This subset of patients that were evaluable for longitudinal KRASG12C ctDNA response in Cohort A exhibited a slightly higher ORR (56.4%, 22/39 cycle ctDNA response evaluable) compared to Cohort A overall (50.5%, 48/95 RECIST 1.1 evaluable patients)19”
From Early Changes in Circulating Cell-Free <i>KRAS</i> G12C Predict Response to Adagrasib in KRAS Mutant Non–Small Cell Lung Cancer Patients (2023) · cites this paper as [19]
Updated KRYSTAL-1 data from 116 previously treated NSCLC patients showed an ORR of 42.9%, DCR of 79.5%, median DoR of 8.5 months, median PFS of 6.5 months, median OS of 12.6 months and estimated 1-year OS of 50.8% with adagrasib.
“Updated data from 116 patients with previously treated NSCLC included in a registrational phase II cohort of KRYSTAL-1 showed an ORR of 42.9%, a DCR of 79.5%, median DoR of 8.5 months, median PFS of 6.5 months, median OS of 12.6 months and estimated 1-year OS of 50.8% with adagrasib83.”
From The current state of the art and future trends in RAS-targeted cancer therapies (2022) · cites this paper as [83]
In NSCLC, G12C inhibitors produce overall response rates of 30-40%, disease control around 60%, and median duration under one year.
“While these drugs clearly have clinical activity, overall response rates (30-40%) and disease control (~60%) in NSCLC are modest and transient, with median duration less than one year (9,10).”
From Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRASG12C Inhibitor Efficacy (2023) · cites this paper as [10]
Multiple intrinsic and acquired resistance mechanisms to G12C inhibitors are known, and drug combinations will likely be required to maximize their clinical efficacy in NSCLC and other diseases.
“Multiple mechanisms of intrinsic and acquired resistance (10,12,13), have been identified; hence, drug combinations will likely be needed to maximize the clinical efficacy of G12Cis (and probably other, emerging KRAS inhibitors) in NSCLC and other diseases.”
From Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRASG12C Inhibitor Efficacy (2023) · cites this paper as [10]
In the phase II portion of KRYSTAL-2, adagrasib 600 mg bid in 116 patients with KRAS G12C NSCLC produced an ORR of 42.9% with median follow-up 12.9 months.
“The phase II portion of KRYSTAL-2 included 116 patients with KRAS G12C NSCLC treated with adagrasib 600 mg bid [100]. All patients had prior platinum-doublet chemotherapy and 98.3% had received both chemotherapy and checkpoint inhibitor therapy. With a median follow-up of 12.9 months, the ORR was 42.9%.”
From Drugging KRAS: Current perspectives and state-of-art review (2022) · cites this paper as [100]
Among 33 patients with previously treated, stable CNS metastases, adagrasib produced an intracranial confirmed ORR of 33.3% (95% CI 18.0-51.8).
“Among 33 patients with previously treated, stable central nervous system metastases, the intracranial confirmed objective response rate was 33.3% (95% CI, 18.0–51.8) [100].”
From Drugging KRAS: Current perspectives and state-of-art review (2022) · cites this paper as [100]
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“KRAS G12C amplification was a consistent resistance mechanism that increased in frequency over the duration of the treatment of CRC patients and cell lines treated with combinations of KRAS and EGFR inhibitors [101].”
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Targeting Ras-, Rho-, and Rab-family GTPases via a conserved cryptic pocket
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KRAS: the Achilles’ heel of pancreas cancer biology
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KRAS Mutation Subtypes and Their Association with Other Driver Mutations in Oncogenic Pathways
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- Authors
- Jänne, P. A., Riely, G. J., Gadgeel, S. M., Heist, R. S., Ou, S.-H. I., Pacheco, J. M., Johnson, M. L., Sabari, J. K., Leventakos, K., Yau, E., Bazhenova, L., Negrao, M. V., Pennell, N. A., Zhang, J., Anderes, K., Der-Torossian, H., Kheoh, T., Velastegui, K., Yan, X., Christensen, J. G., Chao, R. C., & Spira, A. I.
- Affiliations
- From the Lowe Center for Thoracic Oncology, Dana–Farber Cancer Institute (P.A.J.), and Massachusetts General Hospital (R.S.H.) — both in Boston; the Thoracic Oncology Service, Division of Solid Tumor Oncology, Department of Medicine, Memorial Sloan Kettering Cancer Center, and Weill Cornell Medical College (G.J.R.), and Perlmutter Cancer Center, New York University Langone Health (J.K.S.), New York, and the Department of Medicine, Roswell Park Comprehensive Cancer Center, Buffalo (E.Y.) — all in New York; the Henry Ford Cancer Institute, Detroit (S.M.G.); the University of California Irvine School of Medicine, Chao Family Comprehensive Cancer Center, Orange (S.-H.I.O.), the University of California San Diego Moores Cancer Center, La Jolla (L.B.), and Mirati Therapeutics, San Diego (K.A., H.D.-T., T.K., K.V., X.Y., J.G.C., R.C.C.) — all in California; the Division of Medical Oncology, Department of Medicine, University of Colorado Anschutz Medical Campus, Aurora (J.M.P.); Sarah Cannon Research Institute at...
- Roswell Park Comprehensive Cancer Center (US)
- ORCID
- Riely, Gregory J.
- Gadgeel, Shirish M.
- Heist, Rebecca S.
- Ou, Sai-Hong I.
- Johnson, Melissa L.
- Sabari, Joshua K.
- Leventakos, Konstantinos
- Yau, Edwin
- Bazhenova, Lyudmila
- Negrao, Marcelo V.
- Pennell, Nathan A.
- Zhang, Jun
- Anderes, Kenna
- Kheoh, Thian
- Velastegui, Karen
- Christensen, James G.
- Chao, Richard C.
- Spira, Alexander I.
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 2022-07-14
- Volume
- 387
- Issue
- 2
- Pages
- 120-131
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- OpenAlex
- W4281650778
- Cited by
- 1,061
- References
- 27
- Citations by year
- 2026: 247 · 2025: 270 · 2024: 285 · 2023: 203 · 2022: 56
- FWCI
- 131.68
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Mirati Therapeutics, Inc.
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Diagnosis and Treatment
- Health Sciences › Medicine › Oncology › Lung Cancer Research Studies
- Keywords
- adagrasib, KRAS G12C mutation, non-small cell lung cancer, KRAS inhibitors, objective response rate, progression-free survival, overall survival, central nervous system metastasis, treatment-related adverse events, previously treated patients
- MeSH terms
- Acetonitriles, Antineoplastic Agents, Carcinoma, Non-Small-Cell Lung, Humans, Lung Neoplasms, Mutation, Piperazines, Pyrimidines, Proto-Oncogene Proteins p21(ras)
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