On December 5, 2016 TG Therapeutics, Inc. (NASDAQ:TGTX), reported the presentation of two preclinical data sets, one oral presentation and one poster presentation, for TGR-1202, the Company’s once-daily PI3K delta inhibitor, at the 58th American Society of Hematology (ASH) (Free ASH Whitepaper) annual meeting in San Diego, California (Press release, TG Therapeutics, DEC 5, 2016, View Source [SID1234516932]).

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Michael S. Weiss, the Company’s Executive Chairman and Interim Chief Executive Officer, stated, "We want to thank the teams at Columbia and Moffitt for their extensive laboratory work on TGR-1202 to better understand the mechanism of action and impact on the immune system. The preclinical data they have generated helps to better explain and perhaps offer a rationale for the differentiated safety profile seen with TGR-1202 as compared to earlier generation PI3K delta inhibitors. We believe these preclinical findings along with the robust safety and efficacy data we have observed in the clinic, support our belief that TGR-1202 is a differentiated best in class PI3K delta inhibitor. We look forward to continuing our research collaborations with Columbia and Moffitt and to presenting updated safety and efficacy data for TGR-1202 to further confirm its unique profile."

"Dr. Deng’s presentation today has really begun to shed some long-needed light on the important differences among the PI3K delta inhibitors. His work has identified that a novel kinase important in the PI3K pathway, CK-1epsilon, is uniquely inhibited by TGR-1202, which may explain the drug’s effects on c-Myc. These chemical differences may also help to explain the important immunologic differences in the safety profiles of these agents," stated Dr. Owen A. O’Connor, Professor of Medicine and Experimental Therapeutics, Director Lymphoid Malignancies at Columbia Presbyterian Medical Center.

The following summarizes the oral presentation and poster presentation which occurred yesterday:

Oral Presentation: Silencing c-Myc Translation as a Therapeutic Strategy through Targeting PI3K Delta and CK1 Epsilon in Hematological Malignancies (Abstract Number 291)

This oral presentation includes data from the manuscript titled, "Silencing c-Myc Translation as a Therapeutic Strategy through Targeting PI3K Delta and CK1 Epsilon in Hematological Malignancies," which was recently published in Blood, the Journal of the American Society of Hematology (ASH) (Free ASH Whitepaper). The presentation was delivered by Changchung Deng, MD, PhD of Columbia Presbyterian Medical Center and included the following highlights:

TGR-1202 and carfilzomib, but not combinations of other drugs in the same classes, synergistically inhibit c-Myc translation and c-Myc dependent gene transcription, by potently inhibiting phosphorylation of 4E-BP1;
TGR-1202 and carfilzomib synergistically induce apoptosis in lymphoma cells through targeting c-Myc, whereas the other combinations did not;
TGR-1202, but not idelalisib or duvelisib, was found to uniquely inhibit casein kinase-1 (CK1) epsilon; and
Based on this extensive preclinical work, the Company recently announced the launch of a Phase 1/2 study to evaluate the safety and efficacy of TGR-1202 in combination with carfilzomib, in patients with relapsed or refractory lymphoma.
Poster Presentation: Modulation of T Cell Compartment in a Preclinical CLL Murine Model By a Selective PI3K Delta Inhibitor, TGR-1202 (Abstract Number 3236)

This poster presentation included preclinical data describing the differential regulation of human T-cells by TGR-1202 in a preclinical CLL murine model. Highlights from this poster include:

Both TGR-1202 and duvelisib oral administration demonstrated comparable efficacy by reducing CLL burden over time in leukemic mice;
TGR-1202 and duvelisib both targeted the T cell population in vivo, however:
TGR-1202 relatively maintained the number of Tregs and Th17 cells and expression of functional markers on Tregs compared to duvelisib treatment in vivo and ex vivo; and
Duvelisib resulted in greater disruption of Treg/Th17 ratio compared to TGR-1202 in vivo, which may have implications for occurrence of autoimmune-like organ toxicity.
PRESENTATION DETAILS:
Copies of the above referenced presentations are available on the Company’s website at www.tgtherapeutics.com, located on the Publications page.

TG THERAPEUTICS INVESTOR & ANALYST EVENT DETAILS:
TG Therapeutics will also host an investor and analyst reception on Monday, December 5th, 2016 beginning at 8:00pm PT. The event will take place at the Marriott Gaslamp, in San Diego, California, in the Presidio AB Ballroom.
NOTE: This event will be webcast live and will be available on the Events page, located within the Investors & Media section of the Company’s website at www.tgtherapeutics.com, as well as archived for future review. This event will also be broadcast via conference call. In order to access the conference line, please call 1-877-407-8029 (U.S.), 1-201-689-8029 (outside the U.S.), and reference Conference Title: TG Therapeutics 2016 Investor & Analyst Event.