Prevalence of oncogenic drivers in non-squamous NSCLC
With the addition of KRAS G12C, nearly 40% of patients with NSCLC now have an actionable biomarker1,2
Based on an analysis of NSCLC participants in the AACR genie version 8.0 dataset (n=14,485). This graph only includes alterations predictive of response to an FDA-approved drug in locally advanced or metastatic NSCLC.2
AACR, American Association for Cancer
Research; ALK, anaplastic
kinase; BRAF, v-Raf murine sarcoma viral oncogene homolog B;
EGFR, epidermal growth factor receptor; KRAS, Kirsten rat sarcoma viral oncogene homolog; MET, mesenchymal epithelial transition; NSCLC, non-small cell lung cancer; NTRK, neurotrophic-tropomyosin receptor kinase; RET, rearranged during transfection; ROS1, rearrangement of the receptor tyrosine kinase 1.
LUMAKRAS™ is not a chemotherapy, immunotherapy, or TKI. It’s a highly selective* oral inhibitor designed specifically for patients with a KRAS G12C mutation1,4
*Cysteine proteome analysis of 6,451 peptides showed sotorasib only covalently engages with Cys12 of KRASG12C. Preclinical studies in 22 cell lines and xenograft models demonstrated that sotorasib does not inhibit KRAS wild-type or non-KRAS G12C lines/tumors.4
GDP, guanosine diphosphate; TKI, tyrosine kinase inhibitor.
Interstitial Lung Disease (ILD)/Pneumonitis
Most common adverse reactions
LUMAKRAS™ is indicated for the treatment of adult patients with KRAS G12C‑mutated locally advanced or metastatic non‑small cell lung cancer (NSCLC), as determined by an FDA‑approved test, who have received at least one prior systemic therapy.
This indication is approved under accelerated approval based on overall response rate (ORR) and duration of response (DOR). Continued approval for this indication may be contingent upon verification and description of clinical benefit in a confirmatory trial(s).
Please see full Prescribing Information.