The DOI matches its Crossref record; 40 of the 40 references it cites were found in a registry or an index.
KRAS G12C Inhibition with Sotorasib in Advanced Solid Tumors
Open accessAbstract
BACKGROUND: . METHODS: p.G12C mutation. Patients received sotorasib orally once daily. The primary end point was safety. Key secondary end points were pharmacokinetics and objective response, as assessed according to Response Evaluation Criteria in Solid Tumors (RECIST), version 1.1. RESULTS: A total of 129 patients (59 with NSCLC, 42 with colorectal cancer, and 28 with other tumors) were included in dose escalation and expansion cohorts. Patients had received a median of 3 (range, 0 to 11) previous lines of anticancer therapies for metastatic disease. No dose-limiting toxic effects or treatment-related deaths were observed. A total of 73 patients (56.6%) had treatment-related adverse events; 15 patients (11.6%) had grade 3 or 4 events. In the subgroup with NSCLC, 32.2% (19 patients) had a confirmed objective response (complete or partial response) and 88.1% (52 patients) had disease control (objective response or stable disease); the median progression-free survival was 6.3 months (range, 0.0+ to 14.9 [with + indicating that the value includes patient data that were censored at data cutoff]). In the subgroup with colorectal cancer, 7.1% (3 patients) had a confirmed response, and 73.8% (31 patients) had disease control; the median progression-free survival was 4.0 months (range, 0.0+ to 11.1+). Responses were also observed in patients with pancreatic, endometrial, and appendiceal cancers and melanoma. CONCLUSIONS: p.G12C mutation. Grade 3 or 4 treatment-related toxic effects occurred in 11.6% of the patients. (Funded by Amgen and others; CodeBreaK100 ClinicalTrials.gov number, NCT03600883.).
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The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Adagrasib and sotorasib are both selective covalent inhibitors of KRAS G12C, but pharmacologic differences between the two drugs have been reported, including half-life (5 hours for sotorasib and 23 hours for adagrasib), dose-dependent exposure with adagrasib, and potential CNS penetration with adagrasib.22,29”
From Adagrasib with or without Cetuximab in Colorectal Cancer with Mutated KRAS G12C (2023) · cites this paper as [29]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Sotorasib and adagrasib, two prominent members of this class, were effective at halting the growth of G12C-mutant cancer cells in 2-dimensional, 3-dimensional, and xenograft models, clearing the path for clinical trials [48,49,50,51].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [51]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“In 2021, the FDA approved sotorasib for the treatment of adult patients with KRAS G12C-mutated NSCLC, while adagrasib received similar approval the following year [48,50,51,52,53].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [51]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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 [51]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Even in NSCLC, where the compounds were approved, median response rates were in the 6–7 month range before relapse occurred, indicating that the vast majority of tumors develop resistance to single-agent KRAS G12C inhibitors [51,95].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [51]
Experimental — accuracy not yet measured
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“However, neither of these compounds was approved as single agents against colorectal cancer or other types of cancer with KRAS G12C due to subpar objective response rates.”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [51]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Clinical trials of multiple KRASG12C inhibitors have shown promising efficacy in advanced, previously treated non–small cell lung cancer (NSCLC), leading to United States Food and Drug Administration (FDA) accelerated approval of two of these therapies (adagrasib and sotorasib) and many others being investigated in this setting (9–17).”
From Mechanisms of Resistance to Oncogenic KRAS Inhibition in Pancreatic Cancer (2024) · cites this paper as [11]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Clinical studies of other KRAS G12C inhibitors, such as sotorasib and adagrasib, support this hypothesis, with higher response rates observed when used in combination with an EGFR inhibitor compared to when used as single-agent treatment in patients with CRC16–20.”
From Divarasib plus cetuximab in KRAS G12C-positive colorectal cancer: a phase 1b trial (2024) · cites this paper as [18]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“For sotorasib, an overall response rate (ORR) of 7.1–9.7% was observed in patients with advanced CRC, compared to 32.2–37.1% in those with advanced NSCLC (Table 1) [26, 46, 47].”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [46]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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 [46]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“A recent trial with the KRASG12C inhibitor AMG510 (sotorasib) has shown remarkable single-agent activity in KRASG12CMT lung cancer, but efficacy was not encouraging in KRASG12CMT colorectal cancer (10).”
From Bcl-xL Is a Key Mediator of Apoptosis Following KRASG12C Inhibition in KRASG12C -mutant Colorectal Cancer (2023) · cites this paper as [10]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“In early-phase clinical trials, two potent, selective, and irreversible small-molecule KRASG12C inhibitors have shown promising results in non–small-cell lung cancer (NSCLC) and more modest efficacy in colorectal cancer: adagrasib (MRTX849) and sotorasib (AMG510).6,7,10”
From Acquired Resistance to KRAS G12C Inhibition in Cancer (2021) · cites this paper as [10]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Sotorasib was associated with an objective response rate of 37.1% and a median progression-free survival of 6.8 months among patients with NSCLC14 and a response rate of 7.1% among those with colorectal cancer.10”
From Acquired Resistance to KRAS G12C Inhibition in Cancer (2021) · cites this paper as [10]
The cited source says what the claim attributes to it.
In the citing paper
“For instance, AMG510 treatment in patients with KRASG12C-driven NSCLC achieved a response rate of over 30%,18,19”
From Therapeutic targeting of syndecan-1 axis overcomes acquired resistance to KRAS-targeted therapy in gastrointestinal cancers (2025) · cites this paper as [18]
The cited source says what the claim attributes to it.
In the citing paper
“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 [46]
The cited source says what the claim attributes to it.
In the citing paper
“Novel covalent inhibitors of KRASG12C have shown limited response rates in patients with KRASG12C-mutant (MT) colorectal cancer.”
From Bcl-xL Is a Key Mediator of Apoptosis Following KRASG12C Inhibition in KRASG12C -mutant Colorectal Cancer (2023) · cites this paper as [10]
The cited source says what the claim attributes to it.
In the citing paper
“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 [14]
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“The downstream effectors of KRAS signaling that were mutated post-KRAS inhibition included activating lesions in PIK3CA, MEK1, BRAF, and RAF1 [51,68,97,112].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [51]
Experimental — accuracy not yet measuredIn the citing paper
“In addition, the KRAS G12C mutation accounts for only one to three percent of all CRC patients, which largely limits the potential populations who could benefit [2, 11].”
From Genome-wide CRISPR-cas9 knockout screening identifies GRB7 as a driver for MEK inhibitor resistance in KRAS mutant colon cancer (2022) · cites this paper as [11]
In the citing paper
“Single-agent JDQ443 demonstrated antitumor activity in both panels, with deeper responses in NSCLC than colorectal cancer (Fig. 4A vs. 4E; Supplementary Table S7), consistent with reported clinical findings for other single-agent KRASG12C inhibitors in these indications (20, 21, 25, 33).”
In the citing paper
“Despite this success, disease progression occurs in many patients4,5,7, with development of resistance to KRASG12Ci recapitulated in preclinical studies9–11.”
From Co-targeting SOS1 enhances the antitumor effects of KRASG12C inhibitors by addressing intrinsic and acquired resistance (2024) · cites this paper as [4]
In the citing paper
“initial monotherapy response rates for both drugs in colorectal cancer (CRC) are lower than in NSCLC.”
From Expanding the Reach of Precision Oncology by Drugging All KRAS Mutants (2022) · cites this paper as [23]
In the citing paper
“sotorasib (AMG 510) and adagrasib (MRTX849) have demonstrated robust efficacy with objective response rates of 37% and 45%, and disease control rates of 81% and 96%, respectively (20, 23–25).”
From Expanding the Reach of Precision Oncology by Drugging All KRAS Mutants (2022) · cites this paper as [23]
In the citing paper
“In CRC, RTK dependency and signaling rebound kinetics have been identified as potential mechanisms underlying resistance to KRASG12C inhibition (23, 26, 27).”
From Expanding the Reach of Precision Oncology by Drugging All KRAS Mutants (2022) · cites this paper as [23]
In the citing paper
“Learnings from KRASG12C inhibitors have been limited so far with only case reports of responses, since KRASG12D and KRASG12V represent the majority of KRAS mutations occurring in about 65% of all PDAC cases, while G12C mutations are very rare with 1.1% (23, 26).”
From Expanding the Reach of Precision Oncology by Drugging All KRAS Mutants (2022) · cites this paper as [23]
In the citing paper
“In KRASG12C-mutated CRC, sotorasib showed an initial objective response rate of 7% (3 of 42 patients), while treatment with adagrasib yielded a preliminary response rate of 17% (3 of 18 patients) (23, 26).”
From Expanding the Reach of Precision Oncology by Drugging All KRAS Mutants (2022) · cites this paper as [23]
In the citing paper
“28 patients with diagnosed cancers other than NSCLC or colorectal cancer were evaluated, with four reaching PR and 17/28 achieving SD.”
From Selective KRAS G12C inhibitors in non-small cell lung cancer: chemistry, concurrent pathway alterations, and clinical outcomes (2021) · cites this paper as [28]
In the citing paper
“In 2020, updated results of 59 evaluable NSCLC patients were presented and 19/59 achieved PR (32.2% ORR) and 33/59 achieved SD (88.1% DCR).”
From Selective KRAS G12C inhibitors in non-small cell lung cancer: chemistry, concurrent pathway alterations, and clinical outcomes (2021) · cites this paper as [28]
In the citing paper
“Of the 59 patients, 34 were treated at 960 mg with an ORR of 35.3% and DCR of 91.2%.”
From Selective KRAS G12C inhibitors in non-small cell lung cancer: chemistry, concurrent pathway alterations, and clinical outcomes (2021) · cites this paper as [28]
In the citing paper
“Within the NSCLC cohort, the median progression-free survival (PFS) was 6.3 months, and within the colorectal cancer cohort the PFS was 4.0 months28.”
From Selective KRAS G12C inhibitors in non-small cell lung cancer: chemistry, concurrent pathway alterations, and clinical outcomes (2021) · cites this paper as [28]
In the citing paper
“In colorectal cancer, 3 of 42 patients achieved PR (ORR 7.1%) and another 28/42 achieved SD (DCR 73.8%).”
From Selective KRAS G12C inhibitors in non-small cell lung cancer: chemistry, concurrent pathway alterations, and clinical outcomes (2021) · cites this paper as [28]
In the citing paper
“In August 2018, sotorasib (AMG510) became the first KRASG12C inhibitor to enter human clinical trials and demonstrated its safety and clinical efficacy.”
From KRAS, a New Target for Precision Medicine in Colorectal Cancer? (2024) · cites this paper as [10]
In the citing paper
“Overall, 73 patients (56.6%) experienced treatment-related adverse events, and 15 patients (11.6%) experienced grade 3 or 4 adverse events.”
From KRAS, a New Target for Precision Medicine in Colorectal Cancer? (2024) · cites this paper as [10]
In the citing paper
“Adagrasib and sotorasib are both selective covalent inhibitors of KRASG12C, but pharmacological differences between the two drugs have been reported, including half-life (5 h for sotorasib and 23 h for adagrasib), dose-dependent exposure with adagrasib, and potential penetration into the central nervous system with adagrasib [10,11]”
From KRAS, a New Target for Precision Medicine in Colorectal Cancer? (2024) · cites this paper as [10]
In the citing paper
“An overall response rate (ORR) of only 7.1% and median progression-free survival (mPFS) of 4.0 months were observed in the group of patients with mCRC.29 30”
From Current and emerging concepts for systemic treatment of metastatic colorectal cancer (2025) · cites this paper as [30]
In the citing paper
“A phase I trial of AMG 510, which is the first-in-class KRAS G12C inhibitor, achieved a partial response in 30% of patients with non-small cell lung cancer and in 7.1% of patients with CRC [8].”
From The Prognostic Impact of KRAS G12C Mutation in Patients with Metastatic Colorectal Cancer: A Multicenter Retrospective Observational Study (2021) · cites this paper as [8]
In the citing paper
“Both sotorasib and adagrasib are orally bioavailable small molecules that selectively and irreversibly bind KRAS G12C in its GDP-bound state, locking it in its inactive conformation (Fig. 5).”
From Drugging KRAS: Current perspectives and state-of-art review (2022) · cites this paper as [93]
In the citing paper
“In the phase I dose escalation portion, no dose-limiting toxicities were encountered at the planned dose levels of 180 mg, 360 mg, 720 mg, and 960 mg, with 960 mg established as the recommended phase II dose.”
From Drugging KRAS: Current perspectives and state-of-art review (2022) · cites this paper as [93]
In the citing paper
“In the 129 patients treated across dose levels, treatment-related adverse events (TRAE) were observed in 56.6% of patients but only 11.6% of patients experienced grade 3 or 4 TRAE.”
From Drugging KRAS: Current perspectives and state-of-art review (2022) · cites this paper as [93]
In the citing paper
“With a median follow-up of 11.7 months, the response rate among patients with KRAS G12C NSCLC (n = 59) was 32.2% with a disease control rate of 88.1%.”
From Drugging KRAS: Current perspectives and state-of-art review (2022) · cites this paper as [93]
In the citing paper
“In early clinical studies, they have demonstrated promising activity in patients whose tumors harbor KRASG12C mutation (23, 24).”
From KRAS mutation in pancreatic cancer (2021) · cites this paper as [24]
In the citing paper
“In a phase II trial with sotorasib, 12 patients with KRASG12C pancreatic cancer were enrolled.”
From KRAS mutation in pancreatic cancer (2021) · cites this paper as [24]
In the citing paper
“Among these 12, 1 patient had a partial response, 8 patients had stable disease and 2 patients had progressive disease (24).”
From KRAS mutation in pancreatic cancer (2021) · cites this paper as [24]
In the citing paper
“Two KRASG12C inhibitors, sotorasib (AMG510) and adagrasib (MRTX849) have entered clinical development and they have demonstrated promising activities in solid tumors with KRASG12C mutation, particularly among patients with KRASG12C non-small cell lung cancer (23, 24).”
From KRAS mutation in pancreatic cancer (2021) · cites this paper as [24]
In the citing paper
“Currently, Food and Drug Administration (FDA) has approved an allele-specific covalent inhibitor of KRAS (G12C), AMG510 (sotorasib) having marked clinical responses across multiple tumor types [21–24].”
From Targeting KRAS mutant cancers: from druggable therapy to drug resistance (2022) · cites this paper as [23]
In the citing paper
“According to the results of AMG510 in the phase I trial, this KRAS (G12C) inhibitor is effective in NSCLC (NCT03600883). 7 out of the 13 patients had a partial response (PR) and 6 had stable disease (SD).”
From Targeting KRAS mutant cancers: from druggable therapy to drug resistance (2022) · cites this paper as [23]
In the citing paper
“However, only 1 of 12 patients had a PR and 10 patients had SD in CRC [23].”
From Targeting KRAS mutant cancers: from druggable therapy to drug resistance (2022) · cites this paper as [23]
In the citing paper
“Therefore, CRC is more difficult to treat than NSCLC, suggesting that CRC will require combination therapy.”
From Targeting KRAS mutant cancers: from druggable therapy to drug resistance (2022) · cites this paper as [23]
In the citing paper
“First, tumor type can significantly affect response rates.”
From Targeting KRAS mutant cancers: from druggable therapy to drug resistance (2022) · cites this paper as [23]
In the citing paper
“Preclinical and clinical data have revealed that drug resistance to KRAS G12C inhibitors eventually develops with long‐term treatment.[ 6, 33, 41 ]”
From Focal Adhesion Kinase (FAK) Inhibition Synergizes with KRAS G12C Inhibitors in Treating Cancer through the Regulation of the FAK–YAP Signaling (2021) · cites this paper as [33]
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Citations
Cites
PD-1 and PD-L1 Immune Checkpoint Blockade to Treat Breast Cancer
Hartkopf, A. D., Taran, F., Wallwiener, M., Walter, C. B., Krämer, B., Grischke, E., & Brucker, S. Y. (2016) · Breast Care · doi:10.1159/000453569 · Cited by 30,989
Adverse Renal Effects of Immune Checkpoint Inhibitors: A Narrative Review
Wanchoo, R., Karam, S., Uppal, N. N., Barta, V. S., Deray, G., Devoe, C., Launay‐Vacher, V., Jhaveri, K. D., & on behalf of Cancer and Kidney International Network Workgroup on Immune Checkpoint Inhibitors (2017) · American Journal of Nephrology · doi:10.1159/000455014 · Cited by 15,320
Herbst, R. S., Baas, P., Kim, D.-W., Felip, E., Pérez-Gracia, J. L., Han, J.-Y., Molina, J., Kim, J.-H., Arvis, C. D., Ahn, M.-J., et al. (2016) · The Lancet · doi:10.1016/s0140-6736(15)01281-7 · Cited by 6,449
Self-citationTHE USE OF CONFIDENCE OR FIDUCIAL LIMITS ILLUSTRATED IN THE CASE OF THE BINOMIAL
Clopper, C. J., & Pearson, E. S. (1934) · Biometrika · doi:10.1093/biomet/26.4.404 · Cited by 5,327
Wild-Type KRAS Is Required for Panitumumab Efficacy in Patients With Metastatic Colorectal Cancer
Amado, R. G., Wolf, M., Peeters, M., Van Cutsem, E., Siena, S., Freeman, D. J., Juan, T., Sikorski, R., Suggs, S., Radinsky, R., et al. (2008) · Journal of Clinical Oncology · doi:10.1200/jco.2007.14.7116 · Cited by 3,207
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K-Ras(G12C) inhibitors allosterically control GTP affinity and effector interactions
Ostrem, J. M., Peters, U., Sos, M. L., Wells, J. A., & Shokat, K. M. (2013) · Nature · doi:10.1038/nature12796 · Cited by 2,557
COSMIC: mining complete cancer genomes in the Catalogue of Somatic Mutations in Cancer
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The Clinical KRAS(G12C) Inhibitor AMG 510 Drives Anti-Tumour Immunity
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Self-citationKRAS Mutation Status Is Predictive of Response to Cetuximab Therapy in Colorectal Cancer
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Kano, Y. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27135796
Metadata
- Authors
- Hong, D. S., Fakih, M. G., Strickler, J. H., Desai, J., Durm, G. A., Shapiro, G. I., Falchook, G. S., Price, T. J., Sacher, A., Denlinger, C. S., Bang, Y.-J., Dy, G. K., Krauss, J. C., Kuboki, Y., Kuo, J. C., Coveler, A. L., Park, K., Kim, T. W., Barlesi, F., Munster, P. N., Ramalingam, S. S., Burns, T. F., Meric-Bernstam, F., Henary, H., Ngang, J., Ngarmchamnanrith, G., Kim, J., Houk, B. E., Canon, J., Lipford, J. R., Friberg, G., Lito, P., Govindan, R., & Li, B. T.
- Affiliations
- City Of Hope National Medical Center (US)
- From the Department of Investigational Cancer Therapeutics, Phase I Clinical Trials Program, University of Texas M.D. Anderson Cancer Center, Houston (D.S.H., F.M.-B.); the Department of Medical Oncology and Experimental Therapeutics, City of Hope Comprehensive Cancer Center, Duarte (M.G.F.), the University of California, San Francisco, San Francisco (P.N.M.), and Amgen, Thousand Oaks (H.H., J.N., G.N., J.K., B.E.H., J.C., J.R.L., G.F.) — all in California; Duke University Medical Center, Durham, NC...
- Fox Chase Cancer Center (US)
- Roswell Park Comprehensive Cancer Center (US)
- ORCID
- Hong, David S.
- Fakih, Marwan G.
- Strickler, John H.
- Desai, Jayesh
- Shapiro, Geoffrey I.
- Falchook, Gerald S.
- Price, Timothy J.
- Sacher, Adrian
- Denlinger, Crystal S.
- Bang, Yung-Jue
- Dy, Grace K.
- Krauss, John C.
- Kuboki, Yasutoshi
- Kuo, James C.
- Coveler, Andrew L.
- Park, Keunchil
- Kim, Tae Won
- Ramalingam, Suresh S.
- Burns, Timothy F.
- Kim, June
- Houk, Brett E.
- Canon, Jude
- Lito, Piro
- Govindan, Ramaswamy
- Li, Bob T.
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 2020-09-24
- Volume
- 383
- Issue
- 13
- Pages
- 1207-1217
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- PMC
- PMC7571518
- OpenAlex
- W3087229737
- Cited by
- 1,733
- References
- 40
- Citations by year
- 2026: 175 · 2025: 265 · 2024: 270 · 2023: 255 · 2022: 391 · 2021: 351 · 2020: 26
- FWCI
- 144.80
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Digital Commons@Becker (Washington University School of Medicine) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Minerva Access (University of Melbourne) (submittedVersion)
- Seoul National University Open Repository (Seoul National University) (submittedVersion)
- IUScholarWorks (Indiana University) (submittedVersion)
- Purdue University Indianapolis (Indiana University) (submittedVersion)
- Funders
- Amgen
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Keywords
- KRAS G12C mutation, sotorasib, KRAS inhibitors, advanced solid tumors, non-small cell lung cancer, colorectal cancer, treatment-related adverse events, objective response, progression-free survival, metastatic disease
- MeSH terms
- Aged, Antineoplastic Agents, Carcinoma, Non-Small-Cell Lung, Dose-Response Relationship, Drug, Female, Humans, Lung Neoplasms, Male, Middle Aged, Mutation, Neoplasms, Piperazines, Pyridines, Pyrimidines, Colorectal Neoplasms, Proto-Oncogene Proteins p21(ras)
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