Background

Chemotherapy-induced myelosuppression, which leads to reduced production of multiple cell lineages (white blood cells, red blood cells [RBCs], and/or platelets), is a major dose-limiting toxicity of chemotherapy. A previous study reported 56.6% of chemotherapy-treated patients with extensive-stage small cell lung cancer (ES-SCLC) in The US Oncology Network (‘Network’) had grade ≥3 myelosuppression events in ≥1 lineage and 33.0% in ≥2 lineages after chemotherapy initiation.¹ This study evaluated real-world outcomes in patients with ES-SCLC treated with trilaciclib in the community oncology setting.

Methods

This retrospective study included adult patients with ES-SCLC who initiated trilaciclib during chemotherapy in Network clinics between February 1, 2021–April 30, 2022. Patients without evidence of chemotherapy treatment or in clinical trials were excluded. Outcomes included myelosuppression events (anemia, neutropenia, thrombocytopenia) and supportive care utilization (eligibility for RBC or platelet transfusion, granulocyte colony-stimulating factor [G-CSF] use) occurring between the first trilaciclib administration and 14 days after the last trilaciclib administrations during index chemotherapy.

Results

Patients with ES-SCLC (N=31) received, on average, 3.5 cycles (median=4) of index chemotherapy during use of trilaciclib and, on average, 8.6 administrations (median=9) of trilaciclib during index chemotherapy. Grade ≥3 myelosuppression events in ≥1 lineage occurred in 35.7% of patients (anemia=7.1%; neutropenia=28.6%; thrombocytopenia=7.1%), and 7.1% of patients had grade ≥3 myelosuppression events in ≥2 lineages. During the index chemotherapy when trilaciclib was used, 9.7% of patients received G-CSF, 3.2% were eligible for RBC transfusions, and none were eligible for platelet transfusions.

Conclusions

Early real-world data in this study suggest that trilaciclib may reduce myelosuppression in patients with ES-SCLC treated in the community oncology setting. More research is recommended to validate the findings.

Disclosures

This study was funded by G1 Therapeutics, Inc. L. Lopez-Gonzalez and H. Huang are employees of G1 Therapeutics, Inc. J. Goldschmidt is an employee of Blue Ridge Cancer Care & The US Oncology Network, which received funding from G1 Therapeutics, Inc., for this work. A. Monnette, P. Shi, and D. Venkatasetty are employees of Ontada, which received funding from G1 Therapeutics, Inc., for this work. P.R. Conkling has received research funding from Ignyta, Roche, BMS, Arcus Bioscience, Janssen, Aptose, and US Oncology Research.