Abstract 1387P
Background
KRAS G12C mutation is the second most prevalent oncogenic driver in non-squamous NSCLC. Sotorasib is a potent selective oral inhibitor for treating KRAS G12C mutation-in positive locally advanced or metastatic NSCLC patients whose disease has progressed on, or who cannot tolerate platinum-based chemotherapy or anti PD-1/PD-L1 immunotherapy. It has been approved to use in the second line by NHS England since late 2021. We aim to present real world data collected from 12 cancer centres across the UK exploring the clinical outcomes and tolerability of Sotorasib.
Methods
Retrospective data was collected from 12 hospitals across the UK for patients who received Sotorasib (n=125). We reviewed data including demographics, stage histopathology, PD-L1 status, metastatic disease including CNS, ECOG performance status and toxicity markers. Outcomes including PFS, OS and response rates were also calculated. Here, we report real-world data against the registry trial CodeBreak 100.
Results
Table: 1387P
Real-world CodeBreak 100 |
n=patients 125 126 |
Median age -Yr 68 (41-93) 63.5 (37-80) |
Female-no (%) 78 (62.4) 63 (50.0) |
ECOG performance status no. (%) 0 15 (12) 0-1 PS =100 |
1 80 (64) |
Brain mets no. (%) |
Yes 29 (23) 26 (20.6) |
No 96 (77) 100(79.4) |
Objective response rate % 36.8 37.1 |
Response -no.(%) out of 124 patients |
Complete response 3 (2.4) 4 (3.2) |
Partial response 43 (34.4) 42 (33.9) |
Progression free survival -months 6.5 6.8 |
Median Overall survival-months 10 12.5 |
Treatment related adverse events leading to discontinuation of therapy– any grade -no-(%) 19 (15.2) 9 (7.1) |
Treatment related adverse event leading to dose modification- any grade -no.(%)26 (20.8) 28 (22.2) |
Conclusions
Our outcome data closely aligns with those from Codebreak100. As expected mOS is lower, reflective of the overall frailer real world patient cohort in comparison to the trial group. Diarrhoea and elevated liver enzymes are the primary causes for stopping medication in real-world observations. Further real-world data is necessary to explore how efficacy varies based on PDL-1 status and other co-existing mutations.
Clinical trial identification
Editorial acknowledgement
Legal entity responsible for the study
The authors.
Funding
Has not received any funding.
Disclosure
All authors have declared no conflicts of interest.
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