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Sotorasib for Lung Cancers with KRAS p.G12C Mutation
Open accessAbstract
BACKGROUND: p.G12C-mutated advanced solid tumors in a phase 1 study, and particularly promising anticancer activity was observed in a subgroup of patients with non-small-cell lung cancer (NSCLC). METHODS: p.G12C-mutated advanced NSCLC previously treated with standard therapies. The primary end point was objective response (complete or partial response) according to independent central review. Key secondary end points included duration of response, disease control (defined as complete response, partial response, or stable disease), progression-free survival, overall survival, and safety. Exploratory biomarkers were evaluated for their association with response to sotorasib therapy. RESULTS: . CONCLUSIONS: p.G12C-mutated NSCLC. (Funded by Amgen and the National Institutes of Health; CodeBreaK100 ClinicalTrials.gov number, NCT03600883.).
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“The sotorasib response rate in colorectal cancer is lower than that in NSCLC (7).”
From Cetuximab Enhances the Efficacy of MRTX1133, a Novel KRASG12DInhibitor, in Colorectal Cancer Treatment (2023) · cites this paper as [7]
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
“Of note, in a preliminary analysis, the response rate of MRTX849 in NSCLC patients harboring mutations in both KRAS G12C and KEAP1 was reduced compared to the response rate in KRAS G12C , KEAP1 WT patients [13, 14].”
From Anti-tumor efficacy of a potent and selective non-covalent KRASG12D inhibitor (2022) · cites this paper as [14]
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
“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 [26]
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 example, KRAS G12C inhibition produces substantially different outcomes in NSCLC and CRC, largely due to lineage-specific feedback regulation [23,26,27,28,32].”
From Precision Targeting of KRAS-Mutant Cancers: Beyond G12C Toward G12D and Pan-RAS Therapeutic Strategies (2026) · cites this paper as [23]
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 [49]
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
“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 [7]
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
“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 [4]
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
“but all patients eventually developed therapeutic resistance, limiting long-term survival.19”
From Therapeutic targeting of syndecan-1 axis overcomes acquired resistance to KRAS-targeted therapy in gastrointestinal cancers (2025) · cites this paper as [19]
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 [26]
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 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 [26]
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
“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 [26]
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
“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 [26]
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 revealed that sotorasib demonstrates satisfactory efficacy in patients with non–small cell lung cancer, with a satisfactory response rate [12, 13].”
From Feedback activation of EGFR/wild-type RAS signaling axis limits KRASG12D inhibitor efficacy in KRASG12D-mutated colorectal cancer (2023) · cites this paper as [12]
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 example, patients with KRASG12C-mutated non–small cell lung cancer achieved a durable clinical benefit from sotorasib, the first approved KRASG12C mutant-selective inhibitor, whereas patients with CRC bearing the same mutation responded less to the same treatment [12].”
From Feedback activation of EGFR/wild-type RAS signaling axis limits KRASG12D inhibitor efficacy in KRASG12D-mutated colorectal cancer (2023) · cites this paper as [12]
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 [14]
The cited source says what the claim attributes to it.
In the citing paper
“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 [7]
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 [19]
The cited source says what the claim attributes to it.
In the citing paper
“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 [25]
The cited source says what the claim attributes to it.
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 [26]
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 [13]
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“In addition, some patients selected for these trials may have preexisting multidrug resistance (9, 37, 74), which could contribute to treatment failure.”
From SRC kinase drives multidrug resistance induced by KRAS-G12C inhibition (2024) · cites this paper as [9]
Experimental — accuracy not yet measuredIn the citing paper
“In addition, sotorasib has been shown to strongly inhibit phosphorylation of ERK protein in KRASG12C cells, thereby suppressing cell proliferation.”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [53]
In the citing paper
“Sotorasib specifically and irreversibly inhibits KRASG12C by binding to GDP and locking KRAS in an inactive state.”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [53]
In the citing paper
“The approval of Lumakras, an Amgen-developed drug, in May 2021 for treating NSCLC patients with KRASG12C mutations marks a significant milestone in KRAS-targeting drug discovery.53”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [53]
In the citing paper
“Some preclinical and clinical studies have reported that some drugs could reverse resistance induced by RAS, such as sotorasib, dasatinib and metformin [155,156,157].”
From Drug Resistance in Colorectal Cancer: From Mechanism to Clinic (2022) · cites this paper as [157]
In the citing paper
“In terms of gastrointestinal adverse effects frequently observed in other KRAS G12C inhibitors, 11,12,28 the incidence was generally lower in garsorasib (diarrhea at 11.5%, nausea at 7.7%, and no vomiting reported), compared to those reported of other KRAS G12C inhibitors (diarrhea at 31.7-69%, nausea at 19-78%, and vomiting at 7.9-58%).”
In the citing paper
“Both also showed antitumor activity against KRASG12C-mutated tumors in early-phase clinical trials (20), leading to the accelerated approval of sotorasib by the FDA in May 2021 and conditional marketing authorization by the European Commission in January 2022.”
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
“Some of these inhibitors have proven efficacy in patients with KRASG12C-mutant cancers and have become practice changing.”
From The current state of the art and future trends in RAS-targeted cancer therapies (2022) · cites this paper as [67]
In the citing paper
“improvements in drug design have culminated in the development of inhibitors that are selective for mutant KRAS in its active or inactive state.”
From The current state of the art and future trends in RAS-targeted cancer therapies (2022) · cites this paper as [67]
In the citing paper
“The phase II portion of CodeBreaK 100, which involved 124 evaluable patients with previously treated advanced-stage KRASG12C-mutant NSCLC, demonstrated an ORR of 37.1%, a median duration of response (DoR) of 11.1 months, median PFS of 6.8 months and median OS of 12.5 months67. These impressive results led to the 2021 FDA accelerated approval of sotorasib for this indication.”
From The current state of the art and future trends in RAS-targeted cancer therapies (2022) · cites this paper as [67]
In the citing paper
“However, the data on KRASG12C inhibitors, which have advanced the furthest in development and are entering clinical practice, emphasize that these agents are far from curative67.”
From The current state of the art and future trends in RAS-targeted cancer therapies (2022) · cites this paper as [67]
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 [7]
In the citing paper
“Preclinical and clinical studies, however, have demonstrated that cancers lose sensitivity to KRASG12Ci and re-establish RAS-MAPK signaling through multiple mechanisms, including increased activation of mutant or wild-type (WT) RAS and/or gain of upstream/downstream bypass events1,7,9,10,13,14.”
From Co-targeting SOS1 enhances the antitumor effects of KRASG12C inhibitors by addressing intrinsic and acquired resistance (2024) · cites this paper as [7]
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 [24]
In the citing paper
“Exploratory correlative analyses from the KRYSTAL-1 and CodeBreaK 100 trials in this context suggest higher response rates for single agent adagrasib (64% vs 45%) and sotorasib (50% vs 39%) among patients whose tumors harbored an STK11 co-mutation, versus the entire treatment cohort (24, 25).”
From Expanding the Reach of Precision Oncology by Drugging All KRAS Mutants (2022) · cites this paper as [24]
In the citing paper
“While KRASG12C inhibitors deliver clinical benefit, all patients who achieved an objective response ultimately progressed on treatment with sotorasib in a Phase II study (24).”
From Expanding the Reach of Precision Oncology by Drugging All KRAS Mutants (2022) · cites this paper as [24]
In the citing paper
“The median overall survival was estimated at 12.5 months, which compares favorably to historical benchmarks in this disease setting (i.e. docetaxel combined with ramucirumab had 10.5 months overall survival in the REVEL study)32.”
From Selective KRAS G12C inhibitors in non-small cell lung cancer: chemistry, concurrent pathway alterations, and clinical outcomes (2021) · cites this paper as [31]
In the citing paper
“In the updated analysis, the overall response rate remained at 37.1% although one of the partial responses converted to a complete response.”
From Selective KRAS G12C inhibitors in non-small cell lung cancer: chemistry, concurrent pathway alterations, and clinical outcomes (2021) · cites this paper as [31]
In the citing paper
“The updated analysis provided the first report of overall survival for NSCLC patients treated with a selective KRAS G12C inhibitor.”
From Selective KRAS G12C inhibitors in non-small cell lung cancer: chemistry, concurrent pathway alterations, and clinical outcomes (2021) · cites this paper as [31]
In the citing paper
“The median overall survival was estimated at 12.5 months, which compares favorably to historical benchmarks in this disease setting (i.e. docetaxel combined with ramucirumab had 10.5 months overall survival in the REVEL study)32.”
From Selective KRAS G12C inhibitors in non-small cell lung cancer: chemistry, concurrent pathway alterations, and clinical outcomes (2021) · cites this paper as [31]
In the citing paper
“Per recent subgroup analyses of the Phase II NSCLC cohort from CodeBreaK 100, patients appear to derive benefit after PD1/PD-L1 checkpoint inhibition, including the application of the checkpoint inhibitor within 3 months of sotorasib initiation31.”
From Selective KRAS G12C inhibitors in non-small cell lung cancer: chemistry, concurrent pathway alterations, and clinical outcomes (2021) · cites this paper as [31]
In the citing paper
“The vast majority of patients (115 of 126) received prior PD-1/PD-L1 checkpoint inhibition and the response rate was 36.3% (vs. 37.1% in the overall population) and median overall survival was 12.0 months (versus 12.5 months in the overall population).”
From Selective KRAS G12C inhibitors in non-small cell lung cancer: chemistry, concurrent pathway alterations, and clinical outcomes (2021) · cites this paper as [31]
In the citing paper
“Patients whom have had checkpoint therapy within 3 months had overall response of 34.4% and median overall survival of 11.7 months, compared to 39.7% and not evaluable in patients that had more than 3 months between checkpoint inhibition and sotorasib.”
From Selective KRAS G12C inhibitors in non-small cell lung cancer: chemistry, concurrent pathway alterations, and clinical outcomes (2021) · cites this paper as [31]
In the citing paper
“The vast majority of patients (115 of 126) received prior PD-1/PD-L1 checkpoint inhibition and the response rate was 36.3% (vs. 37.1% in the overall population) and median overall survival was 12.0 months (versus 12.5 months in the overall population).”
From Selective KRAS G12C inhibitors in non-small cell lung cancer: chemistry, concurrent pathway alterations, and clinical outcomes (2021) · cites this paper as [31]
In the citing paper
“These data may indicate that prior immune therapy does not meaningfully negatively impact the activity of sotorasib, suggesting a possible combination approach may be further explored given non-overlapping mechanisms of action.”
From Selective KRAS G12C inhibitors in non-small cell lung cancer: chemistry, concurrent pathway alterations, and clinical outcomes (2021) · cites this paper as [31]
In the citing paper
“The vast majority of patients (115 of 126) received prior PD-1/PD-L1 checkpoint inhibition and the response rate was 36.3% (vs. 37.1% in the overall population) and median overall survival was 12.0 months (versus 12.5 months in the overall population).”
From Selective KRAS G12C inhibitors in non-small cell lung cancer: chemistry, concurrent pathway alterations, and clinical outcomes (2021) · cites this paper as [31]
In the citing paper
“Recent overall survival data has been favorable with an overall survival of 12.5 months including second and third line and beyond patients receiving benefit.”
From Selective KRAS G12C inhibitors in non-small cell lung cancer: chemistry, concurrent pathway alterations, and clinical outcomes (2021) · cites this paper as [31]
In the citing paper
“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 [12]
In the citing paper
“Median PFS was 6.8 months and median survival was 12.5 months (Table 2).”
From Drugging KRAS: Current perspectives and state-of-art review (2022) · cites this paper as [94]
In the citing paper
“The NSCLC cohort included 126 patients, 81% of whom had received prior platinum-based chemotherapy and PD(L)1 inhibitor therapy. With a median follow-up of 15.3 months, the response rate was 37.1%; 80.6% of patients achieved disease control.”
From Drugging KRAS: Current perspectives and state-of-art review (2022) · cites this paper as [94]
In the citing paper
“While ORR was 50% in those with mutated STK11 and wild-type KEAP1, it was only 23% when both KEAP1 and STK11 were mutated and 14% when KEAP1 was mutated with wild-type STK11 (Table 3).”
From Drugging KRAS: Current perspectives and state-of-art review (2022) · cites this paper as [94]
In the citing paper
“Nevertheless, drugs again other KRAS mutations in codons 12, 13 and 61 still remain to be developed [87].”
From Resistance to anti-EGFR therapies in metastatic colorectal cancer: underlying mechanisms and reversal strategies (2021) · cites this paper as [87]
In the citing paper
“Sotorasib (AMG-510) (Table 1) was the first selective KRAS(G12C) inhibitor to enter clinical trials in 2018 and was developed by Amgen, building on discoveries from a partnership with Carmot Therapeutics in which a custom library of small molecules that covalently bind cysteine were screened against KRAS(G12C)93.”
From Advances in covalent drug discovery (2022) · cites this paper as [95]
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Gray, S., Lamarca, Á., Edeline, J., Klümpen, H., Hubner, R. A., McNamara, M. G., & Valle, J. W. (2022) · Cancers · doi:10.3390/cancers14071789 · Cited by 11
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High Expression of NT5DC2 Is a Negative Prognostic Marker in Pulmonary Adenocarcinoma
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AZD4625 is a Potent and Selective Inhibitor of KRASG12C
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The end of the beginning: progress and next steps in KRAS-mutant non-small-cell lung cancer
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Metadata
- Authors
- Skoulidis, F., Li, B. T., Dy, G. K., Price, T. J., Falchook, G. S., Wolf, J., Italiano, A., Schuler, M., Borghaei, H., Barlesi, F., Kato, T., Curioni-Fontecedro, A., Sacher, A., Spira, A., Ramalingam, S. S., Takahashi, T., Besse, B., Anderson, A., Ang, A., Tran, Q., Mather, O., Henary, H., Ngarmchamnanrith, G., Friberg, G., Velcheti, V., & Govindan, R.
- Affiliations
- Roswell Park Comprehensive Cancer Center (US)
- From the University of Texas M.D. Anderson Cancer Center, Houston (F.S.), and U.S. Oncology Research, the Woodlands (A. Spira) — both in Texas; Memorial Sloan Kettering Cancer Center and Weill Cornell Medicine (B.T.L.) and Thoracic Medical Oncology, Perlmutter Cancer Center, New York University (V.V.), New York, and Roswell Park Cancer Institute, Buffalo (G.K.D.) — all in New York; the Queen Elizabeth Hospital and University of Adelaide, Woodville, SA, Australia (T.J.P.); Sarah Cannon Research Institute at HealthONE, Denver (G.S.F.); Department I of Internal Medicine, Center for Integrated Oncology, University Hospital Cologne, Cologne (J.W.), the West German Cancer Center, University Hospital Essen, University Duisburg–Essen, Essen (M.S.), and the German Cancer Consortium, Heidelberg (M.S.) — all in Germany; the Early Phase Trials and Sarcoma Units, Bergonie Cancer Institute, Bordeaux (A.I.), and Gustave Roussy Institute, Villejuif (F.B., B.B.) — both in France; Fox Chase Cancer Center, Philadelphia (H.B....
- Fox Chase Cancer Center (US)
- ORCID
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 2021-06-24
- Volume
- 384
- Issue
- 25
- Pages
- 2371-2381
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- PMC
- PMC9116274
- OpenAlex
- W3172081492
- Semantic Scholar
- 3c89f24ad219bec52684f03b8df3c5d8feb81a72
- Cited by
- 1,849
- References
- 39
- Citations by year
- 2026: 317 · 2025: 348 · 2024: 398 · 2023: 382 · 2022: 319 · 2021: 84
- FWCI
- 192.15
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Kölner Universitäts PublikationsServer (Universität zu Köln) (publishedVersion)
- PubMed Central (acceptedVersion)
- Digital Commons@Becker (Washington University School of Medicine) (submittedVersion)
- Universitätsbibliographie, Universität Duisburg-Essen (submittedVersion)
- Funders
- Amgen
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Health Sciences › Medicine › Oncology › Lung Cancer Research Studies
- Keywords
- sotorasib, non-small cell lung cancer, KRAS inhibitors, advanced solid tumors, objective response, progression-free survival, biomarkers, drug safety
- MeSH terms
- Progression-Free Survival, Adult, Aged, Aged, 80 and over, Antineoplastic Agents, Carcinoma, Non-Small-Cell Lung, Female, Humans, Lung Neoplasms, Male, Middle Aged, Mutation, Piperazines, Pyridines, Pyrimidines, Biomarkers, Proto-Oncogene Proteins p21(ras), B7-H1 Antigen
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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