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TG Therapeutics, Inc. Announces Preclinical Data Presentation on the Company’s BET Inhibitor, TG-1601, at the 2018 American Association for Cancer Research (AACR) Annual Meeting

On April 18, 2018 TG Therapeutics, Inc. (NASDAQ:TGTX), reported preclinical data for TG-1601, the Company’s novel BET inhibitor at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) annual meeting, taking place this week in Chicago, Illinois, at McCormick Place North/South (Press release, TG Therapeutics, APR 18, 2018, View Source [SID1234525512]). The Company’s poster is available for viewing today from 8:00am to 12:00pm CT, during the Experimental and Molecular Therapeutics/ Canonical Targets 2 Session in Exhibit Hall A.

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Highlights from this poster include:

Title: TG-1601 is a novel BET inhibitor with strong binding affinity and long-lasting effect in pre-clinical models (Abstract Number 5790)
— TG-1601 is a novel and potent BET inhibitor that specifically inhibits the binding of the BET sub-family of bromodomain-containing protein family;
— TG-1601 potently inhibits cell growth of various multiple myeloma and lymphoma cell lines in vitro, but does not affect the growth of normal cell lines;
— TG-1601 inhibits MYC and Bcl-2 expression in preclinical models;
— TG-1601 showed combinatorial effects in an in vivo model with anti-PD-1 antibodies. Clinical trials will be focused on a potential synergism between TG-1601 and other drugs in the TG pipeline.
Michael S. Weiss, the Company’s Executive Chairman and Chief Executive Officer stated, "We are encouraged by the preclinical data presented today for TG-1601 which we believe to be a potent BET inhibitor that could have activity in a number of hematological malignancies. Importantly, by inhibiting c-Myc and Bcl-2 protein expression, TG-1601 may provide complimentary and/or synergistic effects when combined with our other products under development to potentially create best-in-class combinations. We look forward to continuing our research and advancing this compound into the clinic later this year."

PRESENTATION DETAILS

A copy of the above referenced poster is available on the Company’s website at www.tgtherapeutics.com, located on the Publications Page

Shire to announce first quarter 2018 results

On April 18, 2018 Shire plc (LSE: SHP, NASDAQ: SHPG), reported that it will announce first quarter 2018 earnings on Thursday April 26, 2018 (Press release, Shire, APR 18, 2018, View Source [SID1234525511]).

Results press release will be issued at:

12:00 BST / 07:00 EDT

Investor conference call time:

14:00 BST / 09:00 EDT

Live conference call for investors:
Flemming Ornskov, MD, M.P.H., Chief Executive Officer and Thomas Dittrich, Chief Financial Officer will host the investor and analyst conference call at 9:00 am EDT / 14:00 BST.

The details of the conference call are as follows:

UK dial in:

0800 358 9473 or +44 333 300 0804

US dial in:

1 855 857 0686 or 1 631 913 1422

International Access Numbers:

Click here

Password/Conf ID:

83293759 #

Live Webcast:

Click here

Replay:
A replay of the presentation will be available for two weeks by phone and by webcast for three months. Replay information can be found on the Investor Relations section of Shire’s website at View Source

For further information please contact:
Investor Relations

Christoph Brackmann [email protected] +41 795 432 359
Sun Kim [email protected] +1 617 588 8175
Robert Coates [email protected] +44 203 549 0874
Media
Katie Joyce [email protected] +1 781 482 2779

Numerate to join ATOM Consortium to Rapidly Accelerate Preclinical Drug Development

On April 18, 2018 Computational drug design company Numerate reported that it has signed a letter of intent to join an open consortium of scientists staffed from two U.S. national laboratories, industry, and academia working to transform drug discovery and development into an approach that is rapid, integrated and with better patient outcomes (Press release, Numerate, APR 18, 2018, View Source [SID1234525510]).

Accelerating Therapeutics for Opportunities in Medicine (ATOM) formed in October 2017 with the goal of reducing preclinical drug discovery from six years to just one, using cancer as the exemplar disease.

ATOM is integrating high-performance computing and biological, chemical, preclinical, and clinical data from public and industry sources to create an active learning platform that considers all aspects of drug discovery and pharmacology. ATOM will integrate emerging high-fidelity, data-rich experimental technologies, and cutting-edge software into the approach.

"This will create an ecosystem which will foster the rapid and dynamic collaboration needed to advance precision medicine and tremendously benefit patients," wrote Guido Lanza, president and CEO of Numerate, and Brandon Allgood, CTO, in the letter signed April 3, 2018.

"Our organization’s business priorities and directions are strongly aligned with the fundamental elements of ATOM … and we look forward to outlining the specific contributions we can make to the ATOM consortium as collaborators," they wrote.

John Baldoni, ATOM founder and governing board co-chair, and senior vice president for R&D at GSK, said Numerate is well-known for its innovative software approach to drug discovery.

"This collaboration provides Numerate with extensive and unique data sources and computer power with which they can optimize their drug discovery algorithms," Baldoni said. "This letter of intent signals how cutting-edge private-sector organizations can benefit in this public/private consortium."

Numerate joins the founding members of ATOM: GSK, the National Cancer Institute’s Frederick National Laboratory for Cancer Research (FNLCR), the University of California, San Francisco (UCSF), and the Department of Energy/National Nuclear Security Administration (NNSA)’s Lawrence Livermore National Laboratory (LLNL), which is contributing supercomputer resources and cognitive simulation expertise to the ATOM consortium. ATOM headquarters is located in the Mission Bay neighborhood of San Francisco.

ATOM seeks other organizations to join the consortium to bring their expertise into this new environment.

"We are excited to see the addition of industry leaders to the consortium and to the effort to bring effective new drugs to cancer patients more rapidly," said Eric Stahlberg, director of high performance computing at the Frederick National Laboratory.

The partners agree to work together to develop, test, and validate a multidisciplinary approach to drug discovery where science, technology and engineering, supercomputing simulations, data science, and artificial intelligence are integrated into a drug-discovery platform, ultimately to be shared with the drug development community at large.

Genocea Presents Data at AACR Annual Meeting Further Highlighting Advantages of ATLAS Platform in Identification of Neoantigens over in silico Methods

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]).

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.

Checkpoint Therapeutics Reports Preclinical Data on BET Inhibitor CK-103 at the American Association for Cancer Research Annual Meeting

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.

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.