On April 11, 2018 Lytix Biopharma Reported that it will present data at the 2018 American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting taking place from 14th – 18th April 2018 at McCormick Place North/South, Chicago, Illinois, US (Press release, Lytix Biopharma, APR 11, 2018, View Source
[SID1234525270]).

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Dr Mikael J. Pittet, Associate Professor at Harvard Medical School, Senior Faculty of the Center for Systems Biology (CSB) at Massachusetts General Hospital (MGH) and Director of the CSB Cancer Immunology Program will present the data in a poster presentation from 8-12 am on Wednesday April 18. Previous experimental studies identified LTX-315’s ability to control cancer in mice grafted with various tumor cell lines triggering tumor-specific T cells. The analyses has now been extended to conditional genetic mouse models of both melanoma (driven by Braf and Pten alterations) and soft tissue sarcoma (driven by Kras and P53 alterations). In these genetic models, cancer cells are derived from somatic cells that are transformed in their normal tissue microenvironment and progress to high-grade tumors that are poorly infiltrated by T cells and typically resist prescribed chemo- and immunotherapeutic treatments.

"We are excited to present this data at AACR (Free AACR Whitepaper) in conjunction with Dr Pittet’s team which shows that LTX-315 not only delays tumor progression substantially in both models, but also profoundly alters the tumor microenvironment, most notably characterized with CD8+ T cell, NK cell and dendritic cell infiltration. A similar transition from a ‘cold’ to a ‘hot’ tumor microenvironment is seen in patients with melanoma, sarcoma and breast cancer after treatment with LTX-315. Furthermore, CD8+ T cell depletion in mice abrogated long-term antitumor efficacy of LTX-315, indicating that these cells are required for drug-induced tumor control. Importantly, the ability to convert non-T-cell-infiltrated tumors into ones that display antitumor T cell immunity opens the possibility to prime and make unresponsive tumors sensitive for systemic immune treatments," commented Dr Edwin Klumper, CEO of Lytix Biopharma.

View Source!/4562/presentation/8122

April 18, 2018, 8:00 AM – 12:00 PM
Section 25 Session PO.CL06.08 – Immunomodulatory Agents and Interventions 3

5549 / 5 – Antitumor efficacy of the oncolytic peptide LTX-315 in genetic mouse models that resist conventional chemo- and immunotherapeutic treatments

M. J. Pittet1, H-W. Liao1, B. Sveinbjørnsson2, Ø. Rekdal2; 1Massachusetts Gen. Hosp., Boston, MA, 2Lytix Biopharma, Tromso, Norway

On April 11, 2018 ADC Therapeutics (ADCT), an oncology drug discovery and development company that specializes in the development of proprietary Antibody Drug Conjugates (ADCs) targeting major cancers, reported its presence at the Annual Meeting of the American Association for Cancer Research (AACR) (Free AACR Whitepaper) taking place April 14-18, 2018 in Chicago, USA (Press release, ADC Therapeutics, APR 11, 2018, View Source [SID1234525271]). Two poster presentations will highlight strong preclinical data for its two new investigational programs ADCT-601 targeting AXL and ADCT-701 targeting DLK-1. In addition, Dr. Jaewoong Lee, of The Beckman Institute of the City of Hope will make an oral presentation on novel preclinical data for ADCT-301 targeting CD25.

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"Our two new investigational programs show compelling efficacy and safety in preclinical studies," said Dr. Jay Feingold, Chief Medical Officer and Senior Vice President of Clinical Development at ADCT. "These results provide an important step to advance ADCT-601 and ADCT-701 into the clinic and enlarge our pipeline of PBD-based ADCs in multiple ongoing clinical trials for the treatment of both solid and hematological cancers."

Poster titles and highlights of the data that will be presented are available on the AACR (Free AACR Whitepaper) conference website at www.aacr.org and include the following:

ADCT-701, a novel pyrrolobenzodiazepine (PBD) dimer-based antibody-drug conjugate (ADC) targeting DLK1-expressing tumors Abstract #744, April 15, 1:00 pm – 5:00 pm CT

– ADCT-701 is an ADC composed of a humanized IgG1 antibody against human DLK1, site-specifically conjugated using GlycoConnectTM technology to PL1601, which contains a valine-alanine cleavable linker and the PBD dimer cytotoxin SG3199.

– ADCT-701 demonstrated potent and specific in vitro and in vivo anti-tumor activity in DLK1-expressing cancer-derived models and it was stable and well tolerated in rats.

Preclinical activity of ADCT-601, a novel pyrrolobenzodiazepine (PBD) dimer-based antibody-drug conjugate (ADC) targeting AXL-expressing tumors Abstract #2792A, April 16, 1:00 pm – 5:00 pm CT

– ADCT-601 is an ADC composed of a humanized IgG1 antibody against human AXL, site-specifically conjugated using GlycoConnectTM technology to PL1601, which contains a valine-alanine cleavable linker and the PBD dimer cytotoxin SG3199.

– ADCT-601 demonstrated potent and specific in vitro and in vivo anti-tumor activity in various cancer-derived models with different levels of membranous AXL, and it was stable and well tolerated in rats.

CD25 enables oncogenic BCR- and TCR-signaling and represents a therapeutic target in lymphoblastic malignancies Abstract #2983, April 16, 2018, 4:05 PM – 4:20 PM

– Novel data identifies CD25 as a previously unrecognized feedback regulator of oncogenic B/TCR-signaling supporting CD25 as a therapeutic target in refractory lymphoid malignancies.

– ADCT-301 demonstrated durable remissions in patient-derived Ph+ ALL cells PDX models

On April 11, 2018 Tarveda Therapeutics, Inc., a clinical stage biopharmaceutical company discovering and developing Pentarins as a new class of potent and selective cancer medicines, reported that the company will present preclinical data related to PEN-866 at the 2018 American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting, occurring April 14-18, 2018 in Chicago, IL (Press release, Tarveda Therapeutics,APR 11, 2018, View Source [SID1234525272]). PEN-866 is a miniature drug conjugate designed to treat patients with solid tumor types known to be sensitive to topoisomerase 1 inhibitors such as SN-38, the payload of PEN-866. The presentation will address the combination of PEN-866 with PARP inhibitors in models of ovarian cancer, lung cancer and colorectal cancer.

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Details of the poster presentation are as follows:

Title: Combination of the miniature drug conjugate PEN-866 with PARP inhibitors as a rational approach to overcoming limitations of PARP inhibitor monotherapy
Date:

April 18, 2018
Time:

8:00 AM – 12:00 PM CT
Location:

Section 37, McCormick Place North/South, Chicago, IL

About PEN-866
PEN-866 exploits the activation of Heat Shock Protein 90 (HSP90) in tumors to accumulate and release its potent anti-cancer payload, SN-38. PEN-866 is a miniature conjugate that comprises a small molecule, HSP90-targeting ligand linked to SN-38, the active metabolite of irinotecan. The conjugate accumulates and is retained in tumors, and by way of a sustained release of SN-38, causes prolonged DNA damage and tumor regressions in multiple patient-derived and other xenograft tumor models.

About Pentarins
Tarveda is developing Pentarins, potent and selective miniature drug conjugates with high affinity for specific cell surface and intracellular targets. Pentarins are engineered to bind to their tumor cell targets and provide sustained release of their potent therapeutic payloads deep into solid tumor tissue. Comprised of a targeting ligand conjugated to a potent cancer cell killing agent through a tuned chemical linker, Pentarins are designed to overcome the deficits of both larger antibody drug conjugates and small molecules that limit their therapeutic effectiveness against solid tumors. Together, the components of Tarveda’s Pentarins have distinct, yet synergistic, anticancer attributes: the small size of Pentarins allows for rapid and deep penetration into the tumor tissue, the ligand’s targeting ability allows for specific binding and retention in tumor cells, and the chemical linker is tuned to optimize the release of the potent, cell killing payload inside the cancer cells for efficacy.

On April 10, 2018 Illumina, Inc. (NASDAQ:ILMN) reported that it will issue results for first quarter 2018 following the close of market on Tuesday, April 24, 2018 (Press release, Illumina, APR 10, 2018, View Source [SID1234525252]).

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On the same day, at 2:00 pm Pacific Time (5:00 pm Eastern Time), Francis deSouza, President and Chief Executive Officer, and Sam Samad, Senior Vice President and Chief Financial Officer, will host a conference call with analysts, investors, and other interested parties to discuss financial and operating results.

Conference Call Details

The conference call will begin at 2:00 pm Pacific Time (5:00 pm Eastern Time) on Tuesday, April 24, 2018. Interested parties may access the live teleconference through the Investor Relations section of Illumina’s web site under the "company" tab at www.illumina.com. Alternatively, individuals can access the call by dialing 800-708-4539, or 1-847-619-6396 outside North America, both with passcode 46755682.

A replay of the conference call will be available from 4:30 pm Pacific Time (7:30 pm Eastern Time) on April 24, 2018 through May 1, 2018 by dialing 888-843-7419, or 1-630-652-3042 outside North America, both with passcode 46755682.

On April 10, 2018 Asana BioSciences, LLC, an oncology focused, clinical stage biopharmaceutical company, reported that it will present updates for two of its lead molecules in clinical development at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting being held in Chicago, IL, April 14-18, 2018 (Press release, Asana BioSciences, APR 10, 2018, View Source [SID1234525253]).

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The presentation details are as follows:

1. ASN003, a novel highly selective BRAF and PI3K dual inhibitor: Phase I PK/PD results in patients with advanced solid tumors.

Authors: D. Rasco1, N. Lakhani2, R. Sullivan3, M. Mita4, J. Shah5, H. Usansky5, S. Reddy5, N. S. Rao5, L. Denis5, K. Flaherty3, Anthony Tolcher6. 1START Med. Oncology, San Antonio, TX; 2START Med. Oncology, Grand Rapids, MI; 3MGH, Boston, MA; 4Cedars Sinai Med. Oncology, Los Angeles, CA; 5Asana BioSciences, Lawrenceville, NJ, 6NEXT Oncology, San Antonio, TX.
Session: PO.CT01 – Phase I Clinical Trials 1; Section 42
Abstract: #CT019 / 12
Date/Time: Sunday, April 15 at 1:00pm – 5:00pm

2. Strong antitumor activity of ASN007, an oral ERK1/2 inhibitor, in PDX tumor models with MAP kinase pathway alterations including KRAS mutations.

Authors: Sanjeeva P. Reddy, Niranjan S. Rao, Roger A. Smith, Scott K. Thompson, Sarper
Toker. Asana BioSciences, Lawrenceville, NJ.
Session: PO.ET06.10 – Canonical Targets 2; Section 36
Abstract: #5783 / 9
Date/Time: Wednesday, April 18 at 8:00am – 12:00pm

ASN003 is a potent and highly selective inhibitor of both B-RAF and PI3 kinases. RAS-RAF-MEK and PI3K-AKT-mTOR are two major pathways involved in tumor cell signaling and growth. Components of these pathways are frequently mutated in a broad range of tumors. Selective BRAF inhibitors induce dimerization of RAF proteins, leading to paradoxical activation of the RAF-MEK-ERK cascade. This activation is a major limitation for the clinical use of selective RAF inhibitors, as it leads to resistance and results in side effects in the skin limiting their use in patients with BRAF mutant tumors. In addition, elevated signaling through the PI3K/AKT pathway, with or without concomitant MAPK reactivation, represents an alternative path to resistance to BRAF inhibitors. ASN003 demonstrates broad anti-proliferative activity in tumor cell lines and strong tumor growth inhibition in tumor xenograft models, including BRAF inhibitor resistant models. ASN003 is currently in Phase I clinical development in patients with advanced solid tumors, including melanoma, colorectal cancer and non-small cell lung cancer (clinicaltrials.gov NCT02961283). ASN003 is well tolerated and shows the potential to be developed as a monotherapy or in combination with checkpoint inhibitors or other standard of care.

ASN007 is a potent inhibitor of the extracellular-signal-regulated kinases, ERK1 and ERK2 (ERK1/2), key players in the RAS/RAF/MEK (MAPK) signaling pathway. This pathway is frequently hyper-activated in a wide range of cancers through mutations in upstream targets such as BRAF and RAS proteins. Inhibition of ERK1/2 offers a promising therapeutic strategy for such cancers. ASN007 shows potent and selective anti-proliferative activity in cancer cell lines that are driven by the MAPK-pathway, including RAS mutant cell lines. Furthermore, ASN007 demonstrates strong inhibition of tumor growth in multiple BRAF and KRAS mutant patient-derived and cell-line-derived xenograft models, including those that are resistant to BRAF and MEK inhibitors. ASN007 is currently in Phase I clinical development in patients with advanced solid tumors, including melanoma, colorectal cancer, non-small cell lung cancer and pancreatic cancer (clinicaltrials.gov NCT03415126).