On April 18, 2016 Agenus Inc. (NASDAQ: AGEN), an immuno-oncology company developing checkpoint modulator antibodies and cancer vaccines, reported that three abstracts on the Company’s checkpoint modulator product candidates were accepted for poster presentations at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) 2016 Annual Meeting (Press release, Agenus, APR 18, 2016, View Source [SID:1234510982]). The conference is taking place in New Orleans from April 16-20, 2016.

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Poster Details:

OX40
Poster Title: INCAGN01949: A Novel Anti-OX40 Agonist Antibody with the Potential to Enhance Tumor Specific T-cell Responsiveness, while Selectively Depleting Intratumoral Regulatory T Cells
Poster Number: #3204
Session Date: Tuesday, April 19, 2016
Session Time: 8:00 AM -12:00 PM CDT

GITR
Poster Title: A Novel Agonist Antibody (INCAGN01876) that Targets the Costimulatory Receptor GITR
Poster Number: #3220
Session Date: Tuesday, April 19, 2016
Session Time: 8:00 AM -12:00 PM CDT

CTLA-4
Poster Title: AGEN1884 and AGEN2041: Two Functionally Distinct Anti-CTLA-4 Antagonist Antibodies
Poster Number: #5005
Session Date: Wednesday, April 20, 2016
Session Time: 7:30 AM -11:00 AM CDT

Agenus is partnered with Incyte Corporation for the development of INCAGN1949 and INCAGN1876, and is partnered with Recepta Biopharma SA for certain South American rights for AGEN1884 and AGEN2041. Abstracts and posters will become available on the Company’s website at View Source following the poster sessions.

On April 18, 2016 TG Therapeutics, Inc. (Nasdaq:TGTX) reported the presentation of preclinical data describing the differential regulation of human T-cells by TGR-1202 in a poster presentation at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2016, which is being held April 16 – 20, 2016 at the Ernest N. Morial Convention Center in New Orleans, Louisiana (Press release, TG Therapeutics, APR 18, 2016, View Source [SID:1234510981]).

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As part of an ongoing research collaboration with the H. Lee Moffitt Cancer Center and Research Institute in Tampa, FL, data was generated comparing TGR-1202 with the PI3K-delta inhibitors idelalisib and duvelisib in in-vitro models assessing the impact on T-cell subsets. Key conclusions from the poster are as follows:

TGR-1202 exhibits dose dependent cytotoxicity against human T cells beginning 25uM, comparable to the PI3K-delta inhibitors idelalisib and duvelisib,
TGR-1202 allows relative conservation of TH2 cytokine expression and GATA-3 mRNA compared to other PI3K-delta inhibitors idelalisib and duvelisib
Regulatory T cell (Treg) population number and function is reduced overall after treatment with all three agents but to a lesser degree in TGR-1202 treated samples
TGR-1202 does not robustly reduce the expression of PD-1 and CTLA-4 on Tregs, suggesting that a suppressive phenotype is maintained to a greater extent compared to idelalisib and duvelisib.
Michael S. Weiss, the Company’s Executive Chairman and Interim Chief Executive Officer, stated, "Many of the adverse events associated with existing PI3K-delta inhibitors such as colitis and hepatic toxicity, and most recently with opportunistic infections, are thought to be related to T-cell immune mediated mechanisms. This pre-clinical data now begins to elucidate key differences in the impact of these inhibitors on human T-cell subsets, which may explain the differentiated safety profile observed with TGR-1202 to date in the clinic. These data represent the first step in improving our understanding and we look forward to continuing our research collaboration with the team at Moffitt."

PRESENTATION DETAILS

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

On April 18, 2016 Seattle Genetics, Inc. (NASDAQ: SGEN) reported multiple data presentations that support several of the company’s antibody-drug conjugate (ADC) and immuno-oncology programs featured at the upcoming 107th Annual Meeting of the American Association for Cancer Research (AACR) (Free AACR Whitepaper) being held April 16 through 20, 2016 in New Orleans, LA (Press release, Seattle Genetics, APR 18, 2016, View Source;p=RssLanding&cat=news&id=2157809 [SID:1234510980]). The presentations describe preclinical data with SGN-LIV1A and SEA-CD40, which are in ongoing clinical trials, and highlight two preclinical programs, a novel ADC for the treatment of multiple myeloma (SGN-CD352A) and a small molecule that enhances T-cell mediated antitumor activity (2-fluorofucose). Additional data highlight the growing body of knowledge regarding the ability of auristatin-based ADCs, including ADCETRIS (brentuximab vedotin), to initiate immunogenic cell death, supporting evaluation in combination with checkpoint inhibitors.

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"Our ADC expertise currently empowers a robust pipeline of more than a dozen clinical and preclinical programs," said Jonathan Drachman, M.D., Chief Medical Officer and Executive Vice President, Research and Development at Seattle Genetics. "At AACR (Free AACR Whitepaper), we will be presenting preclinical data that demonstrate encouraging activity with SGN-LIV1A, an ADC in phase 1 clinical development for breast cancer, and the preclinical development of a novel ADC for multiple myeloma, SGN-CD352A, which uses our newest ADC technology. We will also highlight the progress we have made in the important field of immuno-oncology, demonstrating that auristatin-based ADCs may be particularly well suited for combination with checkpoint inhibitors and presenting exciting preclinical data for SEA-CD40 and a small molecule, 2-fluorofucose."

Multiple presentations are being featured at AACR (Free AACR Whitepaper) that highlight advances with Seattle Genetics’ proprietary ADC and empowered antibody pipeline and research programs. Abstracts can be found at www.aacr.org and include the following:

Preclinical data from a novel ADC candidate SGN-CD352A for multiple myeloma will be highlighted in a poster presentation on Monday, April 18, 2016 (Abstract #1195). SGN-CD352A utilizes Seattle Genetics’ newest ADC technology and is composed of an anti-CD352 antibody attached to a highly potent cytotoxic DNA-crosslinking agent called a pyrrolobenzodiazepine (PBD) dimer via a proprietary site-specific conjugation technology to a monoclonal antibody with engineered cysteines (EC-mAb).
SGN-LIV1A will be highlighted in a poster presentation on Tuesday, April 19, 2016 (Abstract #2966) focusing on the potential of combination use with standard of care chemotherapeutic agents, including doxorubicin, paclitaxel (Abraxane), carboplatin and various kinase inhibitors, for the treatment of breast cancer. SGN-LIV1A is in a phase 1 trial for the treatment of LIV-1-expressing metastatic breast cancer.
A preclinical analysis will highlight the novel small molecule, 2-fluorofucose (2FF) in a poster presentation on Tuesday, April 19, 2016 (Abstract #4005). 2FF blocks cellular incorporation of a sugar (fucose) and has been shown in preclinical studies to stimulate T-cell receptor signaling leading to enhanced activation of dendritic cells.
The path of SEA-CD40 from research to clinical development will be highlighted in a poster presentation on Wednesday, April 20, 2016 (Abstract #4994). SEA-CD40 is in an ongoing phase 1 trial for patients with advanced malignancies. SEA-CD40 is a novel immuno-oncology agent targeted to CD40 utilizing Seattle Genetics’ proprietary sugar-engineered antibody (SEA) technology to produce a non-fucosylated antibody.
Preclinical data evaluating brentuximab vedotin (ADCETRIS) immune activity will be presented in a poster presentation on Wednesday, April 20, 2016 (Abstract #4914). The preclinical data being presented demonstrate that brentuximab vedotin treated tumor cells may initiate an antitumor immune response and supports combination strategies with immuno-oncology regimens, such as the ongoing phase 1/2 clinical trials evaluating ADCETRIS and nivolumab (Opdivo) in relapsed Hodgkin and non-Hodgkin lymphoma.
About Seattle Genetics

On April 18, 2016 OncoSec Medical Incorporated ("OncoSec") (NASDAQ: ONCS), a company developing DNA-based intratumoral cancer immunotherapies, reported that preclinical data from its collaboration with Heat Biologics, Inc (Press release, OncoSec Medical, APR 18, 2016, View Source [SID:1234510979]). ("Heat") focused on evaluating the combination of immunotherapy platforms were presented yesterday at the American Conference for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting (www.aacr.org).

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In the poster entitled "In vivo intra-tumoral electroporation of gp96-Ig/Fc-OX40L stimulates CD8+ T cell cross-priming to tumor specific neoantigens" (Abstract #567), researchers concluded that combining Heat’s ComPACT vaccine with OncoSec’s intratumoral DNA electroporation delivery platform stimulated an expansion of neoantigen-specific CD8+ T cells, leading to a regression in both treated and untreated cancer lesions in two mouse studies (melanoma and colorectal cancer). OncoSec and Heat announced their collaboration last year to evaluate the preclinical efficacy of delivering Heat’s immunotherapy vaccines via OncoSec’s ImmunoPulse platform.

"We are excited by our collaboration with Heat and by these initial findings. The ability of the tumor’s microenvironment to evade immune recognition and remain non-immunogenic is a significant challenge, which we believe needs to be addressed when designing new immuno-therapies," said Robert H. Pierce, MD, OncoSec’s Chief Scientific Officer. "The initial feasibility data between our two platforms are encouraging and we are currently exploring the potential synergy between our platforms with both ComPACT and interleukin-12 expressing plasmids."

"In this first preclinical study demonstrating the feasibility of electroporating ComPACT DNA plasmids, we saw robust neoantigen T cell response and tumor regression in both treated and untreated tumors, indicating a systemic anti-tumor response that could be reflective of what we might see in metastatic lesions," said Taylor Schreiber, MD, PhD, Heat’s Chief Scientific Officer. "We believe that this approach is promising and that further studies are merited, especially as this combination approach has the potential to stimulate shared and private tumor antigens without introducing the complexities associated with personalized therapies."

Copies of the abstract are available and can be viewed online through the AACR (Free AACR Whitepaper) website at www.aacr.org. The poster is available in the Publications section of OncoSec’s website.

On April 18, 2016 Oncolytics Biotech Inc. ("Oncolytics" or the "Company") (TSX: ONC) (OTCQX: ONCYF) (FRA: ONY) reported that two poster presentations covering preclinical work in multiple myeloma and colorectal cancer are being made by the Company’s research collaborators at the 2016 American Association of Cancer Research annual meeting being held from April 16th to 20th, 2016 in New Orleans, LA (Filing, 6-K, Oncolytics Biotech, APR 18, 2016, View Source [SID:1234510978]).

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"Both multiple myeloma and colorectal cancer are target indications for later-stage clinical testing of REOLYSIN," said Dr. Brad Thompson, President and CEO of Oncolytics. "These important preclinical findings continue to advance our understanding of how REOLYSIN interacts with the immune system and how immunomodulatory interventions could improve its cancer cell killing capabilities."

The first abstract/poster is titled "Successful oncolytic virotherapy in a bortezomib resistant syngeneic mouse model of multiple myeloma: implications for translation significance," and was authored by Thirukkuamaran, et al. Using the VK*MYC bortezomib resistant transplantable multiple myeloma mouse model, the authors demonstrated that mice harboring bortezomib insensitive multiple myeloma tumors significantly responded to reovirus treatment. These data are supportive of previous and ongoing preclinical and clinical work in this indication and the Company is currently enrolling patients in a Phase 1b study of REOLYSIN in combination with bortezomib in patients with relapsed or refractory multiple myeloma.

The second abstract/poster is titled "Toll like receptor 3 as an immunotherapeutic target for Kras mutated colorectal cancer," and was authored by Goel, et al. The authors hypothesized that effective expression of toll like receptors 3 ("TLR3") would dampen the infection potential of reovirus through the mounting of an innate immune response. Using a xenograft model with HCT116 colorectal cancer cells, those with TLR3 downregulated cells showed improved control of tumor growth with reovirus treatment compared to those expressing TLR3 (p=0.04). Down regulation of the host immune response improved virus mediated cell cytotoxicity and the findings could result in improved and beneficial killing of cancer cells by reovirus.