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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Adagrasib and sotorasib are both selective covalent KRAS G12C inhibitors, but they differ pharmacologically, including half-life, dose-dependent exposure, and potential CNS penetration.
“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 <i>KRAS</i> G12C (2023) · cites this paper as [29]
The Abstract (Background) and Discussion identify sotorasib as a selective, covalent KRAS G12C inhibitor. Results (Pharmacokinetics; page unavailable) report its mean elimination half-life as 5.5 hours, consistent with the cited 5-hour figure. Our copy does not address adagrasib’s selectivity, half-life, dose-dependent exposure, or potential CNS penetration, so it does not establish the comparison between the drugs. (LLM, conf=0.91)
Experimental — accuracy not yet measuredSotorasib and adagrasib were effective at halting the growth of G12C-mutant cancer cells in 2-dimensional, 3-dimensional, and xenograft models.
“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]
The introductory passage following the Abstract Conclusions reports that preclinical sotorasib treatment led to durable tumor regression in mice bearing KRAS p.G12C tumors, supporting part of the claim. Our copy does not report results for adagrasib or specify 2-dimensional, 3-dimensional, or xenograft models. Page numbers are not available in the supplied copy. (LLM, conf=0.85)
Experimental — accuracy not yet measuredIn 2021, the FDA approved sotorasib for the treatment of adult patients with KRAS G12C-mutated NSCLC, while adagrasib received similar approval the following year.
“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]
The Methods and Results describe sotorasib treatment in adults with KRAS G12C-mutated NSCLC. The paper does not report FDA approval of sotorasib in 2021 or adagrasib in 2022; its Background says no KRAS-targeting therapies had been approved at the time of publication in 2020. (LLM, conf=0.84)
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 [51]
The Results > Efficacy section reports responses to sotorasib in patients with KRAS G12C-mutant NSCLC, supporting the sotorasib-trial portion of the claim. This paper does not report KRYSTAL-1 data for adagrasib or establish that either trial’s data led to regulatory approval. Page numbers are not available in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredEven in NSCLC, median response rates to single-agent KRAS G12C inhibitors were in the 6-7 month range before relapse occurred.
“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]
The Results (Efficacy, NSCLC) report median progression-free survival of 6.3 months, which matches the cited 6–7-month range. But median duration of response was 10.9 months, not 6–7 months. The Discussion notes that some patients progressed soon after an initial response; it does not establish that the vast majority of tumors developed resistance. (LLM, conf=0.88)
Experimental — accuracy not yet measured
Neither sotorasib nor adagrasib was approved as single agents against colorectal cancer or other types of cancer with KRAS G12C due to subpar objective response rates.
“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]
The Abstract (Background; page not provided) says no KRAS-targeted therapies had been approved at the time, and Results > Efficacy reports a 7.1% objective response rate for sotorasib in colorectal cancer. The paper does not address adagrasib or say that low response rates caused either drug to be denied approval as a single agent. (LLM, conf=0.86)
Experimental — accuracy not yet measuredClinical trials of multiple KRASG12C inhibitors have shown promising efficacy in advanced, previously treated NSCLC, leading to FDA accelerated approval of adagrasib and sotorasib.
“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]
The Results (Efficacy; page unavailable) report a 32.2% confirmed response rate in patients with NSCLC, and the Trial Population section says most had received prior treatment. This supports promising efficacy for sotorasib, but the paper does not report clinical efficacy for multiple inhibitors or FDA accelerated approval of adagrasib or sotorasib; its Background says no KRAS-targeting therapies had been approved at the time. (LLM, conf=0.90)
Experimental — accuracy not yet measuredIn clinical studies of other KRAS G12C inhibitors, higher response rates were observed when used in combination with an EGFR inhibitor compared to single-agent treatment in patients with colorectal cancer.
“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]
The Results > Efficacy section reports a 7.1% response rate with sotorasib monotherapy in patients with colorectal cancer. The Discussion suggests that combining sotorasib with therapies targeting other pathways may be viable, but this paper does not report clinical response rates for a KRAS G12C inhibitor combined with an EGFR inhibitor or establish that they were higher than with monotherapy. The supplied copy has no page numbers. (LLM, conf=0.87)
Experimental — accuracy not yet measuredFor sotorasib, an overall response rate of 7.1-9.7% was observed in patients with advanced CRC, compared to 32.2-37.1% in those with advanced NSCLC.
“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]
The Results > Efficacy passages report confirmed response rates of 7.1% for colorectal cancer and 32.2% for NSCLC, supporting the lower endpoint of each range. This paper does not report the claimed 9.7% or 37.1% rates; the sentence cites multiple sources but does not assign those endpoints to a particular source. (LLM, conf=0.88)
Experimental — accuracy not yet measuredMany 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 [46]
The Abstract Results (page not provided) report confirmed objective responses to sotorasib in 32.2% of patients with NSCLC and 7.1% of patients with colorectal cancer, supporting that many patients did not have an objective response. The paper reports a sotorasib trial, not clinical outcomes for adagrasib, so it does not support that part of the claim. (LLM, conf=0.90)
Experimental — accuracy not yet measuredThe KRASG12C inhibitor AMG510 (sotorasib) has shown remarkable single-agent activity in KRASG12C-mutant lung cancer, but efficacy was not encouraging in KRASG12C-mutant colorectal cancer.
“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 <i>KRASG12C</i> -mutant Colorectal Cancer (2023) · cites this paper as [10]
The Results > Efficacy report a 32.2% confirmed response rate in NSCLC versus 7.1% in colorectal cancer, supporting substantially stronger single-agent activity in lung cancer. However, the Discussion calls the responses and disease stability in both groups “encouraging,” so the paper does not support describing colorectal-cancer efficacy as unencouraging without qualification. Page numbers are unavailable in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredIn early-phase trials, adagrasib and sotorasib showed promising results in NSCLC and more modest efficacy in colorectal cancer.
“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 <sup>G12C</sup> Inhibition in Cancer (2021) · cites this paper as [10]
Experimental — accuracy not yet measuredSotorasib produced an objective response rate of 37.1% and median progression-free survival of 6.8 months in NSCLC and a response rate of 7.1% in colorectal cancer.
“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 <sup>G12C</sup> Inhibition in Cancer (2021) · cites this paper as [10]
AMG510 treatment in patients with KRASG12C-driven NSCLC achieved a response rate of over 30%.
“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]
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 [46]
KRASG12C inhibitors have shown limited response rates in patients with KRASG12C-mutant colorectal cancer.
“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 <i>KRASG12C</i> -mutant Colorectal Cancer (2023) · cites this paper as [10]
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.
“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]
Downstream effectors of KRAS signaling mutated post-KRAS inhibition included activating lesions in PIK3CA, MEK1, BRAF, and RAF1.
“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]
The Introduction describes KRAS signaling, and the Discussion discusses possible alternative pathways in colorectal cancer, but neither reports mutations emerging after KRAS inhibition. Searches for the four named genes and acquired resistance found no passage documenting post-treatment activating lesions in PIK3CA, MEK1, BRAF, or RAF1. (LLM, conf=0.74)
Experimental — accuracy not yet measuredThe KRAS G12C mutation accounts for only one to three percent of all CRC patients.
“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]
Single-agent JDQ443 demonstrated antitumor activity in both NSCLC and colorectal cancer PDX panels, with deeper responses in NSCLC than colorectal cancer.
“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).”
Disease progression occurs in many patients treated with KRASG12Ci, and resistance is recapitulated in preclinical studies.
“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]
Initial monotherapy response rates for sotorasib and adagrasib in colorectal cancer are lower than in NSCLC.
“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 <i>KRAS</i> Mutants (2022) · cites this paper as [23]
In advanced KRASG12C-mutant NSCLC, sotorasib and adagrasib have objective response rates of 37% and 45%, and disease control rates of 81% and 96%, respectively.
“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 <i>KRAS</i> Mutants (2022) · cites this paper as [23]
RTK dependency and signaling rebound kinetics are potential mechanisms of resistance to KRASG12C inhibition in colorectal cancer.
“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 <i>KRAS</i> Mutants (2022) · cites this paper as [23]
In pancreatic ductal adenocarcinoma, KRAS G12D and G12V mutations account for about 65% of cases, while KRAS G12C mutations are rare, occurring in 1.1%.
“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 <i>KRAS</i> Mutants (2022) · cites this paper as [23]
In KRASG12C-mutated colorectal cancer, sotorasib had an initial objective response rate of 7% (3/42) and adagrasib had a preliminary response rate of 17% (3/18).
“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 <i>KRAS</i> Mutants (2022) · cites this paper as [23]
28 patients with diagnosed cancers other than NSCLC or colorectal cancer were evaluated, with four reaching partial response and 17/28 achieving stable disease.
“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 2020, updated results of 59 evaluable NSCLC patients showed 19/59 achieved partial response (32.2% ORR) and 33/59 achieved stable disease (88.1% DCR).
“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]
Of the 59 patients, 34 were treated at 960 mg with an ORR of 35.3% and DCR of 91.2%.
“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]
Within the NSCLC cohort, median progression-free survival was 6.3 months, and within the colorectal cancer cohort progression-free survival was 4.0 months.
“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 colorectal cancer, 3 of 42 patients achieved partial response (ORR 7.1%) and another 28/42 achieved stable disease (DCR 73.8%).
“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]
Sotorasib was the first KRASG12C inhibitor to enter human clinical trials and demonstrated safety and clinical efficacy.
“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 a phase I trial of sotorasib in advanced solid tumors with KRASG12C, 73 of 129 patients (56.6%) experienced treatment-related adverse events and 15 (11.6%) experienced grade 3 or 4 adverse events.
“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]
Adagrasib and sotorasib are both selective covalent inhibitors of KRASG12C, but differ in half-life (5 h for sotorasib and 23 h for adagrasib), dose-dependent exposure, and central nervous system penetration.
“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 phase I CodeBreak100 trial, an overall response rate of only 7.1% and median progression-free survival of 4.0 months were observed in the group of patients with mCRC.
“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]
A phase I trial of AMG 510 achieved a partial response in 30% of patients with non-small cell lung cancer and in 7.1% of patients with colorectal cancer.
“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 <i>KRAS</i> G12C Mutation in Patients with Metastatic Colorectal Cancer: A Multicenter Retrospective Observational Study (2021) · cites this paper as [8]
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.
“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 CodeBreaK100 phase I/II, no dose-limiting toxicities were encountered at planned dose levels of 180 mg, 360 mg, 720 mg, and 960 mg, with 960 mg established as recommended phase II dose.
“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 129 patients treated across dose levels in CodeBreaK100, treatment-related adverse events were observed in 56.6% and grade 3 or 4 TRAE in 11.6%.
“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]
With median follow-up of 11.7 months, response rate among patients with KRAS G12C NSCLC (n = 59) was 32.2% with disease control rate 88.1%.
“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 early clinical studies, KRASG12C inhibitors show promising activity in patients whose tumors harbor KRASG12C mutation.
“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]
A phase II trial of sotorasib included 12 patients with KRASG12C pancreatic cancer.
“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 that sotorasib trial, of the 12 patients with KRASG12C pancreatic cancer, one achieved partial response, eight had stable disease, and two had progressive disease.
“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]
Sotorasib and adagrasib, both KRASG12C inhibitors, have shown encouraging activity in KRASG12C-mutant solid tumors, especially non-small cell lung cancer with KRASG12C.
“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]
The FDA has approved an allele-specific covalent inhibitor of KRAS G12C, AMG510 (sotorasib), which has marked clinical responses across multiple tumor types.
“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]
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).
“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 CRC, only 1 of 12 patients had a partial response and 10 patients had stable disease with AMG510.
“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]
CRC is more difficult to treat than NSCLC, suggesting that CRC will require combination therapy.
“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]
Tumor type can significantly affect response rates.
“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]
Drug resistance to KRAS G12C inhibitors eventually develops with long-term treatment.
“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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KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance
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Silent mutations reveal therapeutic vulnerability in RAS Q61 cancers
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PAK and PI3K pathway activation confers resistance to KRASG12C inhibitor sotorasib
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Kras oncogene ablation prevents resistance in advanced lung adenocarcinomas
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Targeting the DNA Damage Response Pathway as a Novel Therapeutic Strategy in Colorectal Cancer
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Cancer Therapy Guided by Mutation Tests: Current Status and Perspectives
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Current and emerging concepts for systemic treatment of metastatic colorectal cancer
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The Therapeutic Landscape for KRAS-Mutated Colorectal Cancers
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Self-citationKSR induces RAS‐independent MAPK pathway activation and modulates the efficacy of KRAS inhibitors
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Non-genetic adaptive resistance to KRASG12C inhibition: EMT is not the only culprit
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Targeting autophagy as a therapeutic strategy against pancreatic cancer
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Therapeutic Targets of KRAS in Colorectal Cancer
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Oncogenic KRAS creates an aspartate metabolism signature in colorectal cancer cells
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Suppressing nucleotide exchange to inhibit KRAS-mutant tumors
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Self-citationOne Step at a Time — Clinical Evidence That KRAS Is Indeed Druggable
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The Next Generation of KRAS Targeting: Reasons for Excitement and Concern
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Therapeutic Targeting the Allosteric Cysteinome of RAS and Kinase Families
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KRAS, a New Target for Precision Medicine in Colorectal Cancer?
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Hedgehog signalling is involved in acquired resistance to KRASG12C inhibitors in lung cancer cells
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Differential Response and Resistance to KRAS-Targeted Therapy
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“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, 28, 29].”
InfluentialSRC at the Crossroads of KRAS Inhibitor Resistance: Mechanisms and Therapeutic Opportunities
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- 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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