On April 18, 2018 Checkpoint Therapeutics, Inc. ("Checkpoint") (NASDAQ: CKPT), a clinicalstage, immuno-oncology biopharmaceutical company focused on the acquisition, development and commercialization of novel treatments for patients with solid tumor cancers, reported that preclinical data supporting the clinical development of its BET inhibitor CK-103 (also known as TG-1601) will be presented today in a poster session at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting in Chicago, Illinois, at McCormick Place North/South (Press release, Checkpoint Therapeutics, APR 18, 2018, View Source [SID1234525506]). The Company’s poster is available for viewing today from 8:00 a.m. to 12:00 p.m. CT, during the Experimental and Molecular Therapeutics/Canonical Targets 2 Session in Exhibit Hall A.

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Key conclusions from the poster are as follows:
TG-1601 is a novel BET inhibitor with strong binding affinity and long-lasting effect in preclinical models
• CK-103 is a novel and potent BET inhibitor that specifically inhibits the binding of the BET subfamily of bromodomain-containing protein family;
• CK-103 potently inhibits cell growth of various multiple myeloma and lymphoma cell lines in vitro, but does not affect the growth of normal cell lines;
• CK-103 inhibits MYC and Bcl-2 expression in preclinical models; and
• CK-103 showed combinatorial effects in an in vivo model with anti-PD-1 antibodies.

James F. Oliviero, President and Chief Executive Officer of Checkpoint, said, "These data demonstrate CK103’s
potential to be a novel BET inhibitor that potently inhibits MYC expression. Elevated levels of MYC proteins are found in 60-70% of all cancers, making this family of oncogenes a promising therapeutic target. We believe the preclinical data presented today provides encouraging evidence to support the development of CK-103 as an anti-cancer agent, alone and in combination with our anti-PD-L1 antibody, and look forward to the advancement of CK-103 into a first-in-human Phase 1 trial expected to commence later this year."

The poster is available on the Publications page in the Pipeline section of Checkpoint’s website,
www.checkpointtx.com.

On April 18, 2018 Transgene (Paris:TNG), a biotech company that designs and develops virus-based immunotherapies, presents a poster with promising preclinical data on a novel viral vector (pseudocowpox, PCPV) at the AACR (Free AACR Whitepaper) (American Association for Cancer Research) Annual Meeting 2018, Chicago, IL, USA, April 14 – 18 (Press release, Transgene, APR 18, 2018, View Source [SID1234525490]).

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PCPV was found to be the most promising therapeutic candidate amongst the poxviridae evaluated by Transgene:

It displayed the strongest immunogenicity, and the best ability to reduce tumor size and increase survival in immunocompetent mice carrying fast-growing tumors.
It induced a very strong cellular response and showed an attractive cytokine/chemokine profile.
It also induced a strong local secretion of IFN-α and impressive changes in the tumor micro-environment, including decreased frequency of immunosuppressive cells in the tumor.
The abstract is available on the AACR (Free AACR Whitepaper) 2018 website (#LB-287) and will be published in Cancer Research in June 2018.

Poster title: Pseudocowpox: A next generation viral vector for cancer immunotherapy. A poxviral vector selected for its remarkable ability to induce IFN-alpha.

On April 18, 2018 Grid Therapeutics, LLC, a biotechnology company developing a first-in-class, novel human-derived targeted immunotherapy for cancer, reported the closing of its Series B financing (Press release, Grid Therapeutics, APR 18, 2018, View Source [SID1234526796]). Grid will use the proceeds from the financing to accelerate and expand the development of Grid’s lead therapeutic candidate, GT103, for the treatment of solid tumors, and to prepare for clinical trials in cancer patients scheduled to commence in early 2019. Grid’s foundation is the innovative science developed by Edward F. Patz, Jr., MD, and his team of scientists at Duke University Medical Center.

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Grid’s Series B financing was led by Milestone Holdings, a California-based venture company boasting a strong history of identifying and funding companies developing disruptive technologies with revolutionary intellectual property, Paul Funk, a veteran software entrepreneur and founder of Funk Software, and Jeffery "TJ" Heyman, Founder and Chief Investment Officer of Woodbourne Capital Management International.

Grid’s unique platform is based upon a groundbreaking approach of identifying specific tumor immunoglobulin G (IgG) antibodies from cancer patients with exceptional outcomes. Grid’s unique strategy obtained the sequence and isolated its lead IgG3 antibody directly from cancer patients’ single B cells, which will modulate the immune system to kill tumors without known side effects.

"Grid Therapeutics is very excited to welcome our new investors, all of whom bring a rich history of innovation and thought leadership. With this new round of capital, we are well positioned to accelerate the development and advancement of our novel antibody into the clinic," commented Dr. Patz, CEO of Grid.

On April 18, 2018 Tusk Therapeutics, an immuno-oncology company focused on developing immune-modulating therapeutics by targeting immune cells in cancer, presented pre-clinical proof-of-concept data generated in collaboration with Cancer Research UK and University College London (UCL), relating to its anti-CD25 programme at the 2018 American Association for Cancer Research (AACR) (Free AACR Whitepaper).

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Tusk Therapeutics presented data on its first-in-class anti-CD25 programme that has entered pre-clinical development. The antibody depletes regulatory T cells (Tregs) while preserving IL-2 binding and signalling on effector T cells (Teffs). Tusk, together with the University College London research group led by Dr. Sergio Quezada, has shown that targeting Tregs with non-IL-2 blocking anti-CD25 antibodies creates highly potent anti-tumour responses in monotherapy and combination therapy. Proof-of-concept has been established in multiple pre-clinical models.

Tregs, a subpopulation of T cells, are key players in the suppressive tumour microenvironment (TME). Tregs in the TME hinder the body’s ability to control the growth of cancerous cells and their presence is correlated with a worse prognosis in multiple cancers. Effective Treg targeting has been a topic in the cancer field for several years and Tusk’s approach demonstrates it is possible to deplete Tregs in solid tumour which leads to tumour control. Tusk’s antibody is specifically selected to preserve signalling of the IL-2 cytokine on effector cells which is a key regulator of immune-activation.

Commenting on the data, Luc Dochez, Chief Executive Officer of Tusk Therapeutics, said: "The data presented at AACR (Free AACR Whitepaper) demonstrate the unique mechanism of action of our anti-CD25 antibody. Unlike existing aCD25 antibodies our antibody has the ability to deplete Tregs without inhibiting effector cell responses. Based on the promising pre-clinical data, we believe that our anti-CD25 candidates will be an ideal combination partner for existing standard of care and immuno-oncology treatments."

​The data was presented as an oral presentation by Dr. Sergio Quezada, Group Leader and Cancer Research UK Senior Research Fellow at The UCL Cancer Institute, and Chairman of Tusk Therapeutics’ Scientific Advisory Board and in two posters, presented by the Tusk and UCL teams. Tusk Therapeutics’ first-in-class anti-CD25 antibody programme was built on novel biology discovered by Tusk Therapeutics in collaboration with Dr. Quezada and his team at UCL. Tusk Therapeutics, Cancer Research UK (via its Commercial Partnerships Team) and UCL announced in 2017, an exclusive licensing and collaboration deal to develop and commercialise antibody-based therapeutics against CD25.

On April 18, 2018 Genocea Biosciences, Inc. (NASDAQ:GNCA), a biopharmaceutical company developing neoantigen cancer vaccines, reported highlights from its scientific presentations at the 2018 Annual Meeting of the American Association for Cancer Research (AACR) (Free AACR Whitepaper) (AACR 2018), taking place April 14-18, 2018 in Chicago, IL (Press release, Genocea Biosciences, APR 18, 2018, View Source [SID1234525509]).

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Jessica Flechtner, Ph.D., Genocea’s chief scientific officer commented on the AACR (Free AACR Whitepaper) presentations: "We continue to generate data that demonstrate the versatility of our ATLAS platform. As the studies presented at AACR (Free AACR Whitepaper) indicate, ATLAS is a differentiator for Genocea – allowing us to do what in silico approaches cannot – to both identify and characterize neoantigens for use in personalized cancer vaccines. We believe that our ability to find stimulatory and inhibitory antigens during the neoantigen selection process combined with our capacity to explore mechanisms of inhibitory antigens in a murine model, may enable us to help cure cancer by pioneering next-generation cancer vaccines."

Summary of AACR (Free AACR Whitepaper) Poster #730, "Empirical neoantigen identification using the ATLAS platform across thousands of mutations and multiple tumor types highlights advantages over algorithmic prediction methods":

ATLAS enables identification of biologically relevant CD4+ and CD8+ T cell neoantigens in subjects in an unbiased manner, by using subjects’ own antigen-presenting cells (APCs) and T cells rather than predictive algorithms to identify and characterize T cell responses to all candidate neoantigens.
Neoantigen screening was performed on 23 individuals across eight tumor types with mutational burden ranging from 9 to 319 unique mutations.
Empiric identification of neoantigens derived from somatic mutations from each patient’s tumor independently of HLA type and without predictions resulted in the following observations:
ATLAS identified stimulatory neoantigens of both CD4+ and CD8+ T cells, which Genocea believes confirms the importance of including antigens of relevance for both T cell subsets in neoantigen vaccines;
There is little overlap between CD4+ and CD8+ T cell neoantigens; fewer than 2% of empirically confirmed neoantigens were shared between T cell subsets;
Prediction algorithms missed up to 69% of ATLAS-identified neoantigens, with only 2% of CD8+ neoantigens and 24% of CD4+ neoantigens accurately predicted;
The major histocompatibility complex (MHC) class I algorithm appeared to better predict CD4+, not CD8+, neoantigens;
ATLAS also identified inhibitory neoantigens of both CD4+ and CD8+ T cells
Inhibitory neoantigens outnumbered stimulatory neoantigens more than three-fold in aggregate in the screened patients;
Inhibitory antigens currently cannot be identified using in silico approaches.
Summary of Poster #5718, "ex vivo ATLASTM identification of neoantigens for personalized cancer immunotherapy in mouse melanoma":

The B16F10 mouse melanoma model was utilized to characterize neoantigens. More than 1,600 tumor-specific mutations (possible neoantigens) were interrogated using the ATLAS technology and CD8+ T cells from tumor-bearing C57BL/6 mice.
Similar to human neoantigen screens, mouse ATLAS (mATLAS) identified both stimulatory and inhibitory neoantigens:
99% of mutations identified using whole exome sequencing were screened;
68 stimulatory (4% of total mutations) and 57 inhibitory (3% of total mutations) neoantigens were identified.
NetMHCPan, a MHC-binding prediction algorithm, failed to identify the majority of mATLAS-identified neoantigens:
Only 2% of B16F10 neoantigens predicted by algorithms were empirically confirmed to be stimulatory antigens;
91% of stimulatory neoantigens empirically identified with mATLAS were not predicted;
6% of algorithm-predicted neoantigens were inhibitory.
These data demonstrate that inhibitory antigens can be identified in mouse models, allowing for future research into the mechanism of ATLAS-identified inhibitory responses and their relationship to stimulatory neoantigens in mediating tumor control.