On April 18, 2018 Medigene AG (FSE: MDG1, Prime Standard, TecDAX) reported its participation at the following upcoming conferences (Press release, MediGene, APR 18, 2018, View Source [SID1234525515]):

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Kempen Life Sciences Conference
Date: 18 – 19 April 2018
Location: Amsterdam, Netherlands

16th CIMT (Free CIMT Whitepaper) Annual Meeting
Date: 15 – 17 May 2018
Location: Mainz, Germany

The American Society of Gene and Cell Therapy (ASGCT) (Free ASGCT Whitepaper) Annual Meeting
Date: 16 – 19 May 2018
Location: Chicago, USA

UBS Global Life Science Conference
Date: 21 – 23 May 2018
Location: New York, USA
Dr. Thomas Taapken, CFO of Medigene, will hold a company presentation on 22 May.

3rd Annual Advances in Immuno-Oncology Congress
Date: 24 – 25 May 2018
Locations: London, UK
Prof. Dolores Schendel, CEO and CSO of Medigene AG, will present on "T cell receptor discovery to match medical needs worldwide" on May 24.

Medigene AG (FSE: MDG1, ISIN DE000A1X3W00, Prime Standard, TecDAX) is a publicly listed biotechnology company headquartered in Martinsried near Munich, Germany. The company is developing highly innovative immunotherapies to target various forms and stages of cancer. Medigene concentrates on the development of personalized T cell-based therapies, with associated projects currently in pre-clinical and clinical development.

For more information, please visit www.medigene.com

On April 18, 2018 Xencor, Inc. (NASDAQ: XNCR), a clinical-stage biopharmaceutical company developing engineered monoclonal antibodies for the treatment of autoimmune diseases, asthma and allergic diseases and cancer, reported that preclinical data on XmAb24306, an IL15/IL15-receptor alpha complex fused to a bispecific XmAb Fc domain (IL15/IL15Rα-Fc) for the treatment of multiple oncology indications (Press release, Xencor, APR 18, 2018, View Source [SID1234525514]). Data show that the engineered complex enhanced the duration and magnitude of T and NK cell proliferation in vitro and in vivo. XmAb24306 is designed for reduced potency and extended half-life, and exhibited a steady, tolerable and sustained increase in T-cells in primates.

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Key findings from the study presented today at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) 2018 Annual Meeting include:

Fusing IL15/IL15Rα with Xencor’s highly stable heterodimer Fc platform and Xtend Fc domain creates a long-acting CD122 agonist, without targeting CD25
Potency reduction of the complex promotes improved exposure and sustained pharmacodynamics
Preserves native CD122/CD132 signaling despite potency reduction
Marked and sustained peripheral NK and T cell expansion at well-tolerated doses
"The plug and play nature of our XmAb technology provides tremendous opportunity to build a suite of tumor microenvironment activators with tunable potency and sustained activity, which have the potential for improved performance over current approaches," said Bassil Dahiyat, president and chief executive officer of Xencor. "With the IL15/IL15Rα-Fc platform, we have an engine to develop these candidates quickly, and are on track to file an IND for XmAb24306 in 2019."

XmAb24306 is the first of a suite of tumor microenvironment activators using the IL15 bispecific platform. Additional IL15 bispecific candidates, which target specific sub-populations of T cells, in preclinical development include:

A PD1 targeted IL15/IL15Rα (PD1 x IL15) candidate to promote selective expansion and activation of exhausted T cells
Additional targeted IL15/IL15Rα candidates
About XmAb IL15 Bispecific Platform

Xencor’s XmAb IL15 bispecific antibody platform provides a more druggable version of IL15 with reduced potency to improve tolerability, slow receptor-mediated clearance, and prolong half-life. IL15 is an extremely potent cytokine that stimulates the proliferation of lymphocytes, however its potential as a therapeutic has been limited by low tolerability and very fast clearance that limits therapeutic window. IL15 naturally targets CD122 without targeting CD25. Xencor has engineered the IL15/IL15Rα-Fc complex to create lead candidate XmAb24306 and to provide a basis for rapid generation of targeted T-cell activators. These Fc-fusions have been tuned for enhanced in vivo lymphocyte proliferation as a result of more sustained exposure.

On April 18, 2018 Verseon, a technology-based pharmaceutical company employing a computer-driven platform to develop a diverse drug pipeline, reported new preclinical data on its anticancer drug candidates at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) annual meeting yesterday (Press release, Verseon, APR 18, 2018, View Source [SID1234525513]). Dr. Mohan Sivaraja, Associate Director of Discovery Biology, presented studies showing that Verseon’s drug candidates are potent against a range of cancer cell lines, including those that exhibit multidrug resistance.

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While chemotherapy remains the first line of treatment against most cancers, many tumors develop resistance to chemotherapy agents over time, limiting their efficacy. A common way for cancer cells to render drugs ineffective is by triggering an overproduction of transport proteins (efflux pumps) that expel many chemicals, including chemotherapeutics. In addition, cells can become resistant to tubulin-targeting chemotherapy drugs by overexpression of β-III tubulin.

The preclinical studies presented at the AACR (Free AACR Whitepaper) conference demonstrate that Verseon’s drug candidates target cancer cells by inhibiting the protein tubulin, which leads to cell cycle arrest. While marketed chemotherapies such as doxorubicin, paclitaxel, and vincristine show up to 2,000-fold reduced potency in cell lines overexpressing the major MDR1, MRP1, and BCRP efflux pumps, Verseon’s drug candidates are only weakly affected by these transporters (typically less than 2-fold). The Company’s drug candidates also appear unaffected by the overexpression of β-III tubulin. Dr. Sivaraja also presented pharmacokinetic data for one of Verseon’s tubulin inhibitors, which shows good exposure suitable for infusion. The candidate was also well tolerated in a preclinical repeat-dosing study.

"We are very encouraged by these preclinical results," said Dr. Sivaraja. "Multidrug resistance is one of the main reasons why chemotherapies fail. The insensitivity of our compounds to the major transporters and to the overexpression of β-III tubulin may help us address the need for a more effective, precise therapy."

About Verseon’s oncology program
Verseon plans to use its promising class of tubulin inhibitors to target multidrug resistant cancers. Several drug candidates show potency in functional and cellular assays. Furthermore, Verseon’s inhibitors maintain their efficacy across multiple chemotherapy-resistant cancer cell lines and are either unaffected or only weakly affected by the overexpression of common transporters, a primary source of multidrug resistance.

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

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]).

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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