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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

5017 - Combination of Pegilodecakin and Docetaxel Shows Synergy in Tumor Rejection in Immune Resistant TNBC model

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

Cancer Biology

Tumour Site

Presenters

Navneet Ratti

Citation

Annals of Oncology (2018) 29 (suppl_8): viii400-viii441. 10.1093/annonc/mdy288

Authors

N. Ratti1, N. Shifrin2, S. McCauley2, R. Verma2, P. Van Vlasselaer3, M. Oft2, J. Leveque4

Author affiliations

  • 1 Pre-clinical And Clinical Development, ARMO BioSciences, 940 - Redwood City/US
  • 2 Pre-clinical And Clinical Development, ARMO BioSciences, Redwood City/US
  • 3 Pre-clinical And Clinical Development, ARMO BioSciences, 94063 - Redwood City/US
  • 4 Scientific Affiars, ARMO BioSciences, 94063 - Redwood City/US
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Abstract 5017

Background

Immune checkpoint inhibitors (ICI) induce durable tumor responses and increased overall survival (OS) of cancer patients. Patients with low PD-L1, low tumor mutational burden (TMB) or without intra-tumoral CD8+ T cells, have a poor response rate to ICIs. Pegilodecakin (AM0010) is a pegylated recombinant human interleukin-10, which overcomes tumor immune escape by stimulating the activation, survival and clonal expansion of intra-tumoral, tumor antigen specific CD8+ T cells. Pegilodecakin up-regulates IFNγ in CD8+ T cells and MHC expression, which facilitates antigen presentation even in tumors with low CD8+ T cells and low TMB. Here we explore the combination of Pegilodecakin with SOC docetaxel in an ICI resistant mouse triple negative breast cancer model.

Methods

4T1 cells were established SC for two weeks prior to treatment. Pegilodecakin was administered at suboptimal doses, docetaxel was dosed at the MTD. Quantitation of T cell infiltration and tumor cell death was quantified by IHC. Intra-tumoral and systemic cytokine and T cell activity were evaluated.

Results

Docetaxel did not induce regressions but inhibited tumor growth by 65%. Pegilodecakin alone induced tumor growth inhibition and delayed tumor regression in 75% of mice with an 80% reduction of tumor size after 4 weeks of treatment. Pegilodecakin + docetaxel lead to a synergistic tumor control and complete responses in 75% of mice. While pegilodecakin induced T cell infiltration and tumor cell apoptosis with 95% of the measurable tumor being reduced to scar tissue, the tumor size initially continued to increase, indicative of pseudo-progression. In contrast, Pegilodecakin / docetaxel therapy led to a complete eradication of the tumor without pseudoprogression.

Conclusions

The determination of clinical efficacy of immune therapy can be difficult due to delayed immune responses and pseudoprogression related to immune effector cell infiltration. Here we show that largely necrotic tumors on pegilodecakin may have a delayed clearance despite overwhelming anti-tumor efficacy. The combination of immunotherapy with chemotherapy may facilitate clearance of the necrotic tumor mass leading to complete responses of measurable tumor burden.

Clinical trial identification

Legal entity responsible for the study

ARMO BioSciences.

Funding

ARMO BioSciences.

Disclosure

N. Ratti, N. Shifrin, S. McCauley, R. Verma, P. Van Vlasselaer, M. Oft, J. Leveque: Employee: ARMO BioSciences.

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