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Poster display session: Biomarkers, Gynaecological cancers, Haematological malignancies, Immunotherapy of cancer, New diagnostic tools, NSCLC - early stage, locally advanced & metastatic, SCLC, Thoracic malignancies, Translational research

4523 - Trilaciclib (trila) preserves and enhances immune system function in extensive-stage small cell lung cancer (ES-SCLC) patients receiving first-line chemotherapy

Date

20 Oct 2018

Session

Poster display session: Biomarkers, Gynaecological cancers, Haematological malignancies, Immunotherapy of cancer, New diagnostic tools, NSCLC - early stage, locally advanced & metastatic, SCLC, Thoracic malignancies, Translational research

Topics

Cytotoxic Therapy;  Tumour Immunology

Tumour Site

Presenters

Jessica Sorrentino

Citation

Annals of Oncology (2018) 29 (suppl_8): viii596-viii602. 10.1093/annonc/mdy298

Authors

J.A. Sorrentino1, A. Lai1, J.M. Weiss2, K.H. Dragnev3, T.K. Owonikoko4, S. Adler5, J.M. Antal5, R.K. Malik5, P.J. Roberts1

Author affiliations

  • 1 Translational Medicine, G1 Therapeutics, Inc, NC 27709 - Research Triangle Park/US
  • 2 Hematology/oncology, University of North Carolina at Chapel Hill, Chapel Hill/US
  • 3 Hematology/oncology, Norris Cotton Cancer Center Dartmouth-Hitchcock Medical Center, 3756 - Lebanon/US
  • 4 Medical Oncology, Emory University Winship Cancer Institute, 30322 - Atlanta/US
  • 5 Clinical Development, G1 Therapeutics, Inc, NC 27709 - Research Triangle Park/US

Resources

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Abstract 4523

Background

Chemotherapy (chemo) efficacy may be limited due to damage to hematopoietic stem and progenitor cells (HSPCs) leading to multi-lineage myelosuppression. Trila is an iv CDK4/6 inhibitor in development to preserve HSPC and immune system function during chemo (myelopreservation). Preclinically, transient trila-induced G1 arrest renders HSPCs resistant to chemo cytotoxicity, leading to faster hematopoietic recovery and enhanced anti-tumor immunity. In a randomized, placebo-controlled, double-blind Phase 2 trial (NCT02499770), the addition of trila to etoposide/carboplatin (EP) in ES-SCLC patients showed multi-lineage myelopreservation, fewer supportive care interventions and dose reductions, and encouraging duration of response and progression free survival. Peripheral blood immunophenotyping was performed to characterize the effects of trila on the immune system.

Methods

Whole blood from patients in the EP + trila or EP + placebo arms was collected at baseline, during, and after treatment for flow cytometry analyses of monocytes, T, B, NK, dendritic, and myeloid-derived suppressor cells. T cells were also stimulated ex vivo to evaluate their ability to produce cytokines upon activation.

Results

Preliminary analyses indicate that B cells were significantly depleted during treatment with EP + placebo, but not with EP + trila. In addition to an increase in total CD8+ cells during treatment, EP + trila resulted in a larger population of activated CD8+ T cells, and fewer regulatory T cells which is consistent with a more robust immune response. Further analyses of trila’s effect on other immune cell types is ongoing.

Conclusions

These clinical trial findings demonstrate that in addition to preserving neutrophil and red blood cell lineages, adding trila to EP treatment can preserve B cells and enhance T lymphocyte function. In preclinical models, trila similarly enhanced activity of intra-tumor T cells, leading to superior anti-tumor efficacy when combined with chemo + anti-PDL1. A Phase 2 study to assess safety and efficacy of trila or placebo with EP and atezolizumab in first-line ES-SCLC has completed enrollment (NCT03041311).

Clinical trial identification

NCT02499770.

Legal entity responsible for the study

Delaware.

Funding

G1 Therapeutics.

Editorial Acknowledgement

Disclosure

J.A. Sorrentino, A. Lai, R.K. Malik, P.J. Roberts, S. Adler, J.M. Antal: Employee: G1 Therapeutics. J.M. Weiss: Financial support to institution: AstraZeneca, Celgene, Merck; Advisory board: AstraZeneca, Celgene, Boston Biomedical. All other authors have declared no conflicts of interest.

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