:). The next deal is coming soon. They do have finances to get into the third quarter.
I believe we will see Merck partner with them on the TIM-3, at minimum. That paper you had me read was the same one that came out in February. Merck was one of the big Pharma who paid for the analysis of the paper below. Interestingly enough, after it came out, Merck extending ther collaboration deal they have with Enumeral to also include interrogation of Patient Lung samples and we only learned of it within the 10K:
"Collaborations
Merck
In December 2014, we entered into a collaboration with Merck Sharp & Dohme Corp., or Merck. Pursuant to our study agreement with Merck, we are conducting a specified research program using our platform technology to identify functional response of single cell types in colorectal cancer in the presence or absence of Merck’s proprietary immunomodulatory receptor (IMR) modulators. In FEBRUARY 2016, we and Merck subsequently amended the work plan under the study agreement to include non-small cell lung cancer tissue sample". -- ENUM 10K
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The article:
"Adaptive resistance to therapeutic PD-1 blockade is associated with upregulation of alternative immune checkpoints
Shohei Koyama, Esra A. Akbay, Yvonne Y. Li, Grit S. Herter-Sprie, Kevin A. Buczkowski, William G. Richards, Leena Gandhi, Amanda J. Redig, Scott J. Rodig, Hajime Asahina, Robert E. Jones,Meghana M. Kulkarni, Mari Kuraguchi, Sangeetha Palakurthi, Peter E. Fecci, Bruce E. Johnson,Pasi A. Janne, Jeffrey A. Engelman, Sidharta P. Gangadharan, Daniel B. Costa et al.
ABSTRACT
Despite compelling antitumour activity of antibodies targeting the programmed death 1 (PD-1): programmed death ligand 1 (PD-L1) immune checkpoint in lung cancer, resistance to these therapies has increasingly been observed. In this study, to elucidate mechanisms of adaptive resistance, we analyse the tumour immune microenvironment in the context of anti-PD-1 therapy in two fully immunocompetent mouse models of lung adenocarcinoma. In tumours progressing following response to anti-PD-1 therapy, we observe upregulation of alternative immune checkpoints, notably T-cell immunoglobulin mucin-3 (TIM-3), in PD-1 antibody bound T cells and demonstrate a survival advantage with addition of a TIM-3 blocking antibody following failure of PD-1 blockade. Two patients who developed adaptive resistance to anti-PD-1 treatment also show a similar TIM-3 upregulation in blocking antibody-bound T cells at treatment failure. These data suggest that upregulation of TIM-3 and other immune checkpoints may be targetable biomarkers associated with adaptive resistance to PD-1 blockade."
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A couple of notable sections:
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"Our data suggest that targeting specific immune checkpoints engaged by lung tumours, as identified by flow cytometry and/or gene expression analysis, may represent a rational approach to the selection of specific immunotherapy regimens. Given the current clinical interest in building upon the success of anti-PD-1 therapy in lung cancer, we feel that direct measurement of multiple checkpoints could allow for the development of targeted immunotherapy approaches in selected patients based on direct analysis of immune checkpoint biomarkers. We also feel that the specific immune checkpoints engaged will likely be impacted by cancer therapies, as we observe with TIM-3 and LAG-3 upregulation following PD-1 blockade, and that serial measurements will be necessary to best understand the status of the tumour immune microenvironment and to aid the selection of appropriate immunotherapies."
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"As we reported previously, checkpoint blockade also affected immune suppressive cytokine production in the tumour microenvironment17. We found that IL-6 and progranulin (PGRN) were significantly reduced with combined anti-PD-1 and anti-TIM-3 treatment following anti-PD-1 antibody failure as compared with the levels at the time of anti-PD-1 resistance (Fig. 3e). This result suggests that TIM-3 blockade may not only enhance T-cell function following anti-PD-1 antibody failure, but also decrease the levels of tumour-promoting cytokines, similar to our previous observation in naive mice treated with anti-PD-1 alone17. "
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Net net, big Pharma is interested in what these authors have to say:
"Competing financial interests
G.D. received sponsored research support from Bristol-Myers Squibb and Novartis. He is currently an employee of Novartis. F.S.H. is a Bristol-Myers Squibb nonpaid consultant, Novartis, Merck and Genentech consultant and receives clinical trial support to the institution from these companies. G.J.F. receives patent royalties on the PD-1 pathway from Bristol-Myers-Squibb, Roche, Merck, EMD-Serrono, Boehringer-Ingelheim, Amplimmune/AstraZeneca and Novartis and patent royalties on the TIM-3 pathway from Novartis. D.B.C. is a consultant for Pfizer. S.J.R. receives research support from Bristol-Myers Squibb and the Center for Immune Oncology, DFCI. The remaining authors declare no competing financial interests."
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