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News Article | February 22, 2017
Site: www.prweb.com

A cylindrical “pipeline” used for treating large brain aneurysms is just as effective on smaller and sometimes harder to reach ones, according to the results of a clinical trial announced Wednesday. The study’s findings were presented at the International Stroke Conference in Houston by Ricardo A. Hanel, MD, PhD, neurovascular surgeon with Baptist Health and Lyerly Neurosurgery and director of the Baptist Neurological Institute. Eric Sauvageau, MD, neurovascular surgeon and director of the Baptist Stroke & Cerebrovascular Center, was also a co-author and co-investigator on the study. “This study shows the benefit of this breakthrough technology for smaller aneurysms. It demonstrates that the Pipeline ™ Embolization Device is a safe and effective way of dealing with under 12 millimeter aneurysms,” Dr. Hanel said. “The good thing about the pipeline device is once the aneurysm is closed off and treated, the patient is cured, which is very empowering. “The Pipeline is likely more durable and, in the hands of experienced operators like the ones in the study, has low complication rates,” he added. A cerebral aneurysm (also known as an intracranial aneurysm) is a weak or thin spot on a blood vessel in the brain that balloons out and fills with blood. The Pipeline, a braided cylindrical mesh known as a flow diverter, is inserted through a microcatheter into an artery in the groin. The device is then threaded through the body to the brain to slow the flow of blood into the aneurysm and allow the diseased vessel to heal. The Pipeline is currently approved by the U.S. Food and Drug Administration for adults with large aneurysms (which are greater than 12 mm). The results of the clinical trial could open up the procedure for use on patients with small- and medium-sized, wide-necked, unruptured aneurysms, which make up the majority of the cases. "This study confirms that flow diversion is a valid alternative to complement our existing techniques to fix brain aneurysms,” Dr. Sauvageau said. Twenty-two sites in the United States and one in Canada participated in the PREMIER study and 141 patients, including 21 from Baptist Medical Center Jacksonville, which had the highest number enrolled. The study found that a high rate of aneurysms were completely healed at the one-year follow up, with no cases of recurrence. There were also no incidents of aneurysms rupturing one year after the procedure. These results will be submitted to the FDA for review. Dana Bean, of Fernandina Beach, was one of the first to participate in the study; Kristine Meyer, from Mandarin, was the last. Both had successful treatment and surgery at the Baptist Neurological Institute and the Stroke & Cerebrovascular Center at Baptist Medical Center Jacksonville and Lyerly Neurosurgery. Bean, now 54, had lived with a small, hard-to-reach brain aneurysm for six years. It was in the exact spot as the aneurysm that took her mother’s life when Bean was just 6. Her mother collapsed on the playground, as Bean and her brothers played nearby. An ambulance came and she never saw her mother again. She used to wake up in the middle of the night worrying that her aneurysm would burst. In 2014, she became just the second person in the world to be part of the Pipeline clinical trial. At her two-year follow up this past fall, Bean described life without the aneurysm. “Before I worried about dying or being a burden to other people,” she said. “I wanted to be here for graduations, weddings and new babies and the future. Now that I’m cured, I know to seize every day. I live every day to the fullest and I’m excited about the future.” The 42-year-old Meyer worried that her brain aneurysm would burst while driving in her car, with her young children in the back seat. She had the Pipeline procedure in November 2015. Last October, she learned that her aneurysm was gone after shrinking over time. “That was the best Thanksgiving gift I could have received. I don’t have to live with that fear anymore of what could go wrong,” Meyer said. More than a year earlier, she had been experiencing numbness in her arm, dizziness and headaches, which led to the discovery of her aneurysm. “My equilibrium was off, which wasn’t the norm for me. I felt like something was wrong,” Meyer said. The aneurysm was in a difficult location behind her eye and nose, and Meyer said she didn’t want to risk any complications from other more invasive brain surgeries. Using the Pipeline, Dr. Hanel was able to reach the aneurysm and redirect the blood flow away from the aneurysm. The commercial real estate broker was home the next day and was back to work in just two weeks. “Dr. Hanel really took time explaining the procedure and answering questions with not only me, but my husband and mother. We never felt rushed,” Meyer said. “I was excited I had the opportunity to participate [in the study], otherwise I would have had to live with it and not know if and/or when it was going to rupture.” For more information on Baptist Health and Lyerly Neurosurgery, go to lyerlyneuro.com. ### About Baptist Health Baptist Health is a faith-based, mission-driven system in Northeast Florida comprised of Baptist Medical Center Jacksonville; Baptist Medical Center Beaches; Baptist Medical Center Nassau; Baptist Medical Center South; Baptist Clay Medical Campus and Wolfson Children’s Hospital – the region’s only children’s hospital. All Baptist Health hospitals, along with Baptist Home Health Care, have achieved Magnet™ status for excellence in patient care. Baptist Health is part of Coastal Community Health, a regional affiliation between Baptist Health, Flagler Hospital and Southeast Georgia Health System forming a highly integrated hospital network focused on significant initiatives designed to enhance the quality and value of care provided to our contiguous communities. Baptist Health has the area’s only dedicated heart hospital; orthopedic institute; women’s services; neurological institute, including comprehensive neurosurgical services, a comprehensive stroke center and three primary stroke centers; a Bariatric Center of Excellence; a full range of psychology and psychiatry services; urgent care services; and primary and specialty care physicians’ offices throughout Northeast Florida. Baptist MD Anderson Cancer Center is a regional destination for multidisciplinary cancer care which is clinically integrated with MD Anderson Cancer Center, the internationally renowned cancer treatment and research institution in Houston. For more details, visit baptistjax.com.


TORONTO, ONTARIO--(Marketwired - Feb. 21, 2017) - Soricimed Biopharma Inc. ("Soricimed"), a clinical-stage pharmaceutical company discovering and developing peptide-based cancer therapeutics, is pleased to announce publication of their paper entitled, First-in-human phase I study of SOR-C13, a TRPV6 calcium channel inhibitor, in patients with advanced solid tumors. This peer-reviewed paper was published in the journal Investigational New Drugs, The Journal of New Anticancer Agents. This open-access publication can be viewed online at http://link.springer.com/article/10.1007/s10637-017-0438-z SOR-C13 is the first drug candidate targeting TRPV6 to enter human clinical trials. This publication describes the design and results of a multi-center Phase 1 clinical trial and shares the conclusion that SOR-C13 was safe and well tolerated, without evidence of the significant toxicities often observed with cytotoxic chemotherapy. Additionally, the study provided preliminary indication of anticancer activity, including promising activity in two patients with pancreatic cancer, who had failed three prior regimens of treatment. These findings follow recent announcements of SOR-C13 being granted orphan drug designation for the treatment of both ovarian and pancreatic cancer, by the U.S. Food and Drug Administration (FDA). "It is important for the advancement of novel approaches to address difficult to treat cancer and be able to share details of Soricimed's Phase I trial in such a well-respected peer-reviewed journal", stated Siqing Fu, M.D., Ph.D., Principal Investigator & Associate Professor, University of Texas, MD Anderson Cancer Center. "This trial involved 9 investigators and three clinical sites in the United States and Canada and was conducted under FDA and Health Canada regulations. The findings from this trial are very promising and warrant further study. My colleagues and I, at MD Anderson, look forward to working with Soricimed on future clinical trials of SOR-C13 as a new approach to treating solid-tumor cancer." "We are very pleased to be sharing our strong scientific and clinical data with the anticancer community", stated Professor Jack Stewart, Chief Scientific Officer, Soricimed Biopharma, Inc. "Anonymous peer review helps validate our methods, our data interpretation and our conclusions from this important study. These results, plus our two Orphan Drug Status designations, warrant developing this new drug to the next human trials. It's an exciting time for Soricimed." About SOR-C13: SOR-C13 is a first-in-class peptide in development for the treatment of cancer. SOR-C13 binds with high selectivity and affinity to TRPV6, a calcium channel that is highly elevated in prostate, breast, lung and ovarian cancer and correlates with poor outcomes. TRPV6-mediated Ca2+ entry is responsible for maintaining a high tumour proliferation rate, as well as increasing tumour cell survival, promoting metastases and fortifying mechanisms that withstand cell destruction. By binding to this channel, SOR-C13 starves cancer cells of calcium that is needed for cell growth and division. Due to the high specificity of SOR-C13 for its target and its unique mechanism of action this drug candidate may result in fewer and less severe side effects compared to standard cancer chemotherapy. SOR-C13 is the first drug candidate targeting TRPV6 to have entered clinical development anywhere in the world. About Soricimed Biopharma: Soricimed Biopharma Inc. is a private Canadian clinical-stage company developing novel cancer therapeutics and diagnostics. Soricimed's drug candidates have demonstrated a capability to reduce cancer cell viability, induce apoptosis and to reduce human tumour volume while minimizing side-effects in classic animal and in vitro tumour models. Soricimed recently announced positive results indicating safety, tolerability and potential activity in a Phase I trial of SOR-C13 in subjects with advanced solid tumour cancers. Additionally, Soricimed obtained two orphan drug statuses for treatment of ovarian and for pancreatic cancers with SOR-C13. Privately held, Soricimed is funded through private investors and various programs from the Governments of Canada and New Brunswick. For more information please visit, www.soricimed.com.


TORONTO, ONTARIO--(Marketwired - 21 fév. 2017) - Soricimed Biopharma Inc. (« Soricimed »), une compagnie pharmaceutique au stade clinique spécialisée dans la recherche et la mise au point de thérapies contre le cancer à partir de peptides, est heureuse d'annoncer la publication de l'article intitulé First-in-human phase I study of SOR-C13, a TRPV6 calcium channel inhibitor, in patients with advanced solid tumors (première étude de phase 1, chez l'humain, du SOR-C13, un inhibiteur des canaux calciques TRPV6, chez des patients présentant des tumeurs solides avancées). Cet article soumis à un comité de lecture a été publié dans la revue Investigational New Drugs, The Journal of New Anticancer Agents. Cette publication en libre accès peut être consultée sur le http://link.springer.com/article/10.1007/s10637-017-0438-z SOR-C13 est le premier médicament candidat ciblant le canal TRPV6 à faire l'objet d'essais cliniques chez des sujets humains. Cette publication décrit la conception et les résultats d'un essai clinique multicentrique de phase 1 et présente la conclusion selon laquelle le SOR-C13 s'est révélé sûr et bien toléré et sans les toxicités importantes souvent observées en ce qui concerne la chimiothérapie cytotoxique. En outre, l'étude a fourni des indications préliminaires liées à une activité anticancéreuse, dont une activité prometteuse chez deux patients atteints d'un cancer du pancréas qui n'avaient pas répondu à trois différents traitements. Peu de temps avant ces résultats, Soricimed avait annoncé que la U.S. Food and Drug Administration (FDA) avait accordé au SOR-C13 la désignation de médicament orphelin pour le traitement du cancer de l'ovaire et du pancréas. « Il est important, en ce qui concerne la progression des nouveaux traitements, que ces derniers ciblent les cancers difficiles à traiter, ainsi que de pouvoir présenter en détail l'essai de phase I de Soricimed dans une revue scientifique très respectée », a indiqué Siqing Fu, docteur en médecine, Ph. D., chercheur principal et professeur agrégé, Université du Texas, MD Anderson Cancer Center. « Cet essai a été mené par neuf chercheurs dans trois sites cliniques aux États-Unis et au Canada, conformément aux règlements de la FDA et de Santé Canada. Les résultats sont très prometteurs et justifient une étude plus approfondie. Mes collègues du MD Anderson Cancer Center et moi-même serons heureux de pouvoir collaborer avec Soricimed lors des prochains essais cliniques du SOR-C13 comme nouveau protocole de traitement des cancers avec tumeurs solides. » « Nous sommes très heureux de pouvoir partager nos données scientifiques et cliniques, qui sont solides, avec la communauté de recherche et de traitement du cancer », a indiqué le professeur Jack Stewart, directeur scientifique chez Soricimed Biopharma, Inc. « L'examen anonyme par des pairs permet de valider nos méthodes, l'interprétation que nous faisons des données ainsi que les conclusions de cette importante étude. Ces résultats, ainsi que nos deux désignations de médicament orphelin, justifient la poursuite du développement de ce nouveau médicament jusqu'aux prochains essais sur des humains. Il s'agit d'une période fort stimulante pour Soricimed. » À propos du SOR-C13 : Le SOR-C13 est un nouveau peptide en phase de développement pour le traitement du cancer. Le SOR-C13 se fixe avec une forte sélectivité et affinité au TRPV6, c'est-à-dire le canal calcique qui est très élevé dans le cancer de la prostate, du sein, du poumon et de l'ovaire, et pour lequel les résultats sont médiocres. L'entrée de Ca2+ médiée par le TRPV6 est responsable du maintien d'un taux élevé de prolifération tumorale ainsi que de l'augmentation de la survie des cellules tumorales, entraînant la formation de métastases et le renforcement des mécanismes qui résistent à la destruction des cellules. En se liant à ce canal, le SOR-C13 prive les cellules cancéreuses de calcium, lequel est nécessaire à la croissance et à la division cellulaires. En raison de l'activité très spécifique du SOR-C13 et de son mécanisme d'action unique, ce médicament candidat peut entraîner des effets secondaires moins nombreux et moins prononcés que la chimiothérapie classique. Le SOR-C13 est le premier médicament candidat qui cible le TRPV6 et qui fait l'objet d'essais cliniques; aucun autre essai de ce type n'a actuellement lieu ailleurs dans le monde. À propos de Soricimed Biopharma : Soricimed Biopharma Inc. est une société privée canadienne spécialisée dans le développement de thérapies et d'outils diagnostiques liés au cancer. Soricimed a montré que ses médicaments candidats ont la capacité de diminuer la viabilité des cellules cancéreuses, d'induire l'apoptose et de réduire le volume des tumeurs humaines tout en minimisant les effets secondaires dans les modèles tumoraux animaux classiques in vitro. Soricimed a récemment annoncé des premiers résultats positifs montrant la sécurité, la tolérabilité et l'activité potentielle du SOR-C13 en phase 1, chez des sujets atteints de cancers avancés avec tumeurs solides. Soricimed a de plus obtenu la désignation de médicament orphelin pour le traitement des cancers de l'ovaire et du pancréas avec le SOR-C13. Société privée, Soricimed est financée par des investisseurs privés et divers programmes des gouvernements du Canada et du Nouveau-Brunswick. Pour en savoir plus, veuillez visiter le site www.soricimed.com.


News Article | March 1, 2017
Site: www.eurekalert.org

It's what's missing in the tumor genome, not what's mutated, that thwarts treatment of metastatic melanoma with immune checkpoint blockade drugs, researchers at The University of Texas MD Anderson Cancer Center report in Science Translational Medicine. Whole exome sequencing of tumor biopsies taken before, during and after treatment of 56 patients showed that outright loss of a variety of tumor-suppressing genes with influence on immune response leads to resistance of treatment with both CTLA4 and PD1 inhibitors. The team's research focuses on why these treatments help 20-30 percent of patients -- with some complete responses that last for years - but don't work for others. Their findings indicate that analyzing loss of blocks of the genome could provide a new predictive indicator. "Is there a trivial or simple (genomic) explanation? There doesn't seem to be one," said co-senior author Andrew Futreal, Ph.D., professor and chair of Genomic Medicine and co-leader of MD Anderson's Moon Shots Program™. "There's no obvious correlation between mutations in cancer genes or other genes and immune response in these patients." "There are, however, pretty strong genomic copy loss correlates of resistance to sequential checkpoint blockade that also pan out for single-agent treatment," Futreal said. Doctoral candidate Whijae Roh, co-lead author, Futreal, and co-senior author Jennifer Wargo, M.D., associate professor of Surgical Oncology and Genomic Medicine, and colleagues analyzed the genomic data for non-mutational effects. "We found a higher burden of copy number loss correlated to response to immune checkpoint blockade and to lower immune scores, a measure of immune activation in the tumor's microenvironment," said Roh, a graduate student in the University of Texas MD Anderson UTHealth Graduate School of Biomedical Sciences. "We also found copy loss has an effect that is independent of mutational load in the tumors." Melanoma tumors with larger volumes of genetic alterations, called mutational load, provide more targets for the immune system to detect and are more susceptible to checkpoint blockade, although that measure is not conclusive alone. "Combining mutational load and copy number loss could improve prediction of patient response," Wargo said. When the team stratified patients in another data set of patients by whether they had high or low copy loss or high or low mutational load, they found that 11 of 26 patients with high mutational load and low copy loss had a clinical benefit, while only 4 or 26 with low mutational load and high copy loss benefited from treatment. In the trial, patients were treated first with the immune checkpoint inhibitor ipilimumab, which blocks a brake called CTLA4 on T cells, the immune system's specialized warriors, freeing them to attack. Patients whose melanoma did not react then went on to anti-PD1 treatment (nivolumab), which blocks a second checkpoint on T cells. Biopsies were taken, when feasible, before, during and after treatment for molecular analysis to understand response and resistance. To better understand the mechanisms at work, the team analyzed tumor genomes for recurrent copy loss among 9 tumor biopsies from patients who did not respond to either drug and had high burden of copy number loss. They found repeated loss of blocks of chromosomes 6, 10 and 11, which harbor 13 known tumor-suppressing genes. Analysis of a second cohort of patients confirmed the findings, with no recurrent tumor-suppressor loss found among any of the patients who had a clinical benefit or long-term survival after treatment. Ipilimumab sometimes wins when it fails The researchers also found a hint that treatment with ipilimumab, even if it fails, might prime the patient's immune system for successful anti-PD1 treatment. The team analyzed the genetic variability of a region of the T cell receptors, a feature of T cells that allows them to identify, attack and remember an antigen target found on an abnormal cell or an invading microbe. They looked for evidence of T cell "clonality," an indicator of active T cell response. Among eight patients with longitudinal samples taken before treatment with both checkpoint types, all three who responded to anti-PD1 therapy had shown signs of T cell activation after anti-CTLA treatment. Only one of the five non-responders had similar indicators of T cell clonality. "That's evidence that anti-CTLA4 in some cases primes T cells for the next step, anti-PD1 immunotherapy. It's well known that if you don't have T cells in the tumor, anti-PD1 won't do anything, it doesn't bring T cells into the tumor," Futreal says. Overall, they found that T cell clonality predicts response to PD1 blockade but not to CTLA-4 blockade. "Developing an assay to predict response will take an integrated analysis, thinking about genomic signatures and pathways, to understand the patient when you start therapy and what happens as they begin to receive therapy," Wargo said. "Changes from pretreatment to on-therapy activity will be important as well." The Science Translational Medicine paper is the third set of findings either published or presented at scientific meetings by the team, which is led by Futreal and Wargo, who also is co-leader of the Melanoma Moon Shot™. Immune-monitoring analysis showed that presence of immune infiltrates in a tumor after anti-PD1 treatment begins is a strong predictor of success. They also presented evidence that the diversity and composition of a patient's gut bacteria also affects response to anti-PD1 therapy. The serial biopsy approach is a hallmark of the Adaptive Patient-Oriented Longitudinal Learning and Optimization™ (APOLLO) platform of the Moon Shots Program™, co-led by Futreal that systematically gathers samples and data to understand tumor response and resistance to treatment over time. The Moon Shots Program™ is designed to reduce cancer deaths by accelerating development of therapies, prevention and early detection from scientific discoveries. Futreal holds the The Robert A. Welch Distinguished University Chair in Chemistry at MD Anderson. Co-authors with Roh, Futreal and Wargo are co-first authors Pei-Ling Chen, M.D., of Genomic Medicine and Pathology, and Alexandre Reuben, Ph.D., of Surgical Oncology; also Christine Spencer, Feng Wang, Ph.D., Zachary Cooper, Ph.D., Curtis Gumbs, Latasha Little, Qing Chang, Wei-Shen Chen, M.D., and Jason Roszik, Ph.D., of Genomic Medicine; Michael Tetzlaff, Ph.D., M.D., and Victor Prieto, M.D., Ph.D., of Pathology; Peter Prieto, M.D., Vancheswaran Gopalakrishnan, Jacob L. Austin-Breneman, Hong Jiang, Ph.D., and Jeffrey Gershenwald, M.D., of Surgical Oncology; John Miller, Ph.D., Oncology Research for Biologics and Immunotherapy Translation (ORBIT); Sangeetha Reddy, M.D., Division of Cancer Medicine; Khalida Wani, Ph.D., Mariana Petaccia De Macedo, M.D., Ph.D., Eveline Chen, and Alexander Lazar, M.D., Ph.D., of Translational Molecular Pathology; Michael Davies, M.D., Ph.D., Hussein Tawbi, M.D., Ph.D., Patrick Hwu, M.D., Wen-Jen Hwu, M.D., Ph.D., Adi Diab, M.D., Isabella Glitza, M.D., Ph.D., Sapna Patel, M.D., Scott Woodman, M.D., Ph.D., and Rodabe Amaria, M.D., of Melanoma Medical Oncology; Jianhua Hu, Ph.D., of Biostatistics; Padmanee Sharma, M.D., Ph.D., and James Allison, Ph.D., of Immunology; Lynda Chin, M.D., University of Texas System; and Jianhua Zhang Ph.D., of the Institute for Applied Cancer Science. Wargo, Sharma and Allison are all members of the Parker Institute for Cancer Immunotherapy. The research was funded by MD Anderson's Melanoma Moon Shot™, the Melanoma Research Alliance Team Science Award, the John G. and Marie Stella Kenedy Memorial Foundation, the University of Texas System STARS program; the Cancer Prevention and Research Institute of Texas; the American Society of Clinical Oncology; Conquer Cancer Foundation; the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation; and grants from the National Cancer Institute of the National Institutes of Health (U54CA163125, 1K08CA160692-01A1, T32CA009599, NIH T32 CA009666, R01 CA187076-02) and MD Anderson's Institutional Tissue Bank (2P30CA016672) Spencer and Gopalakrishnan are graduate students in The University of Texas Health Science Center at Houston School of Public Health.


WALTHAM, Mass. & VIENNA & LEBANON, N.H.--(BUSINESS WIRE)--Arsanis, Inc., a clinical-stage biopharmaceutical company developing targeted monoclonal antibodies for pre-emptive and post-infection treatment of serious infectious diseases, and Adimab, LLC, the global leader in the discovery and optimization of fully human monoclonal and bispecific antibodies, announced today they have entered into an agreement under which Arsanis has secured the exclusive, worldwide license to antibodies targeting respiratory syncytial virus (RSV) that were discovered by Adimab. Arsanis will initially focus on the selection of a lead RSV antibody candidate and has received a grant of up to $9.3 million from the Bill & Melinda Gates Foundation to advance the selected antibody to IND filing. “Arsanis’ partnerships with Adimab and the Gates Foundation will allow us to apply our deep expertise in the discovery and development of anti-infective antibodies to advance highly potent human monoclonal antibodies for the prevention of RSV infection,” said Rene Russo, Pharm.D., BCPS, President and Chief Executive Officer, Arsanis. “We believe this approach has the potential to address a significant global need for effective and accessible RSV therapeutics in both developed and developing countries.” Under the agreement with Adimab, Arsanis has exclusively licensed a panel of RSV antibodies for the purpose of evaluating and selecting the best therapeutic leads under an exclusive global development and commercialization license. Adimab will be entitled to receive license fees and development milestones, as well as a royalty on net sales. “We are very pleased that Arsanis and the Gates Foundation are collaborating on this important program. Through our B cell isolation approach, Adimab has identified highly potent antibodies against a number of infectious disease targets. The RSV antibodies licensed to Arsanis include some of the most potent RSV neutralizers reported to date,” said Guy Van Meter, VP of Business Development at Adimab. “This new agreement expands an already successful relationship with Arsanis, under which Arsanis’ lead program ASN100 for S. aureus pneumonia, currently in a Phase 2 clinical study, was discovered.” RSV is a highly contagious virus that causes infections in both the upper and lower respiratory tract. RSV infects nearly every child at least once by the age of two years and is a major cause of hospitalization due to respiratory infection in children, the elderly, and immunocompromised patients. RSV infection typically results in cold-like symptoms but can lead to more serious respiratory illnesses such as croup, pneumonia, bronchiolitis, and in extreme cases, death. RSV infection in the pediatric and adult populations account for more than 300,000 hospitalizations per year in the U.S. In the developing world, RSV is responsible for 30 million cases of acute respiratory tract infection and 200,000 deaths per year. As a result, there is a significant need for novel therapeutics to prevent RSV infection. Arsanis is a clinical-stage biotechnology company leading the development of targeted monoclonal antibodies (mAbs) for pre-emptive therapy and treatment of serious infectious diseases. The company’s current programs address pathogenic processes selectively, aiming to preserve the healthy microbiome and potentially allowing Arsanis to address critical infections without contributing to the problem of resistance. The company is building a broad product pipeline addressing the most important infectious diseases that threaten patients globally. Its lead clinical program, ASN100, is aimed at serious Staphylococcus aureus infections and is being evaluated in a Phase 2 clinical study for the prevention of S. aureus pneumonia in high-risk patients. Arsanis is a U.S. company headquartered in Waltham, Massachusetts, with European research and preclinical development operations headquartered in Vienna, Austria (Arsanis Biosciences GmbH). For more information, please visit the Arsanis website at www.arsanis.com. Adimab has established antibody discovery collaborations with many leading pharmaceutical companies, such as Merck, Novo Nordisk, Biogen, GSK, Roche, Novartis, Eli Lilly, Genentech, Celgene, Gilead, Kyowa Hakko Kirin, Takeda and Sanofi. In addition, Adimab has partnered with several smaller publicly traded companies, such as Acceleron, Merrimack Pharmaceuticals, Kite, Five Prime, as well as leading venture-backed companies including Jounce, Mersana, Alector, Surface Oncology, Potenza, Tizona, Tusk and several academic institutions such as Memorial Sloan Kettering and MD Anderson. The Adimab antibody discovery and optimization platform has also been internalized by several large pharma partners; Adi-inside partners include Merck, Novo Nordisk, Biogen and GSK. Adimab's integrated antibody discovery and optimization platform provides unprecedented speed from antigen to purified, full-length human IgGs. Adimab offers fundamental advantages by delivering diverse panels of therapeutically relevant antibodies that meet the most aggressive standards for affinity, epitope coverage, species cross-reactivity and developability. Adimab enables its partners to rapidly expand their biologics pipelines through a broad spectrum of technology access arrangements. For more information, please visit the Adimab website at http://www.adimab.com.


News Article | March 1, 2017
Site: www.eurekalert.org

HOUSTON ? Anyone who uses an employee badge to enter a building may understand how a protein called ENL opens new possibilities for treating acute myeloid leukemia (AML), a fast-growing cancer of bone marrow and blood cells and the second most common type of leukemia in children and adults. Findings from a study at The University of Texas MD Anderson Cancer Center revealed the leukemia-boosting abilities of ENL, which contains a protein component called YEATS that "reads" histone proteins. Histone proteins make up chromatin, large clusters of DNA- and RNA-containing molecules comprising our body's chromosomes. Just as a scanner "reads" data on an identification badge, ENL recognizes a type of histone modification known as acetylation. Research results, which build upon a previous MD Anderson study of histone-reading proteins, are published in the March 1 online issue of Nature. The findings indicated treatment against ENL with a class of experimental drugs called bromodomain and extra-terminal (BET) inhibitors may be effective for treating AML. "Our study showed that ENL is required for disease maintenance in AML," said Xiaobing Shi, Ph.D., associate professor of Epigenetics and Molecular Carcinogenesis. "Depletion of ENL led to anti-leukemic effects, suppressing growth both in vivo and in vitro. Notably, disrupting ENL further sensitized leukemia cells to BET inhibitors." Histone modifications like acetylation serve as docking sites for reader proteins which recognize specific modifications, influencing downstream biological outcomes. While many such reader proteins have been identified for histone modifications called methylation, few are known to recognize histone acetylation. Shi's team employed CRISPR, a gene-editing tool, to deplete ENL and suppress cancer gene expression, which was crucial given that cancer cells often co-opt chromatin regulatory pathways. "Targeting epigenetic readers represents a class of anti-cancer therapy that we believe holds clinical promise," said Hong Wen, Ph.D., research assistant professor of Epigenetics and Molecular Carcinogenesis and co-first author of the paper. "Our study revealed ENL as a chromatin reader that regulates oncogenic programs, thus establishing ENL as a potential drug target for AML." MD Anderson study team members included Xiaolu Wang of the Department of Epigenetics and Molecular Carcinogenesis. Other participating institutions included The Rockefeller University, New York; Memorial Sloan Kettering Cancer Center, New York; Dana-Farber Cancer Institute, Boston; Tsinghua University, Beijing; Baylor College of Medicine, Houston; Icahn School of Medicine at Mount Sinai, New York; and Harvard Medical School; Boston. The study was funded by the National Institutes of Health (P30CA016672, RO1CA204639-01, CA66996, CA140575, 1R01CA204020, R01HG007538 and R01CA193466), the Cancer Prevention Research Institute of Texas (RP160237 and RP170285), the Leukemia and Lymphoma Society (LLS-SCOR 7006-13), the Robert A. Welch Foundation (G1719), the Major State Basic Research Development Program in China (2016FA0500700 and 2015CB910503), and the Tsinghua University Initiative Research program.


News Article | February 24, 2017
Site: www.eurekalert.org

Orlando- In a significant advance in improving the safety of donor stem cell transplants, a major clinical trial led by researchers at Dana-Farber Cancer Institute and Brigham and Women's Hospital (BWH) has shown that a novel agent can protect against the most common viral infection that patients face after transplantation. The results represent a breakthrough in a decade-long effort to identify an effective drug for the prevention of CMV infection in transplant patients that doesn't produce side effects that negate the benefit of the drug itself, the study authors said. The findings, from an international phase 3 clinical trial of the drug letermovir for preventing cytomegalovirus (CMV) infection in transplant patients, will be presented at the 2017 Bone Marrow Transplant Tandem Meetings of the American Society for Blood and Marrow Transplantation (ASBMT) and the Center for International Blood and Marrow Transplant Research (CIBMTR) in Orlando, Florida, February 22, 2017. The study, which involved 565 adult patients at 67 research centers in 20 countries, compared letermovir to placebo in preventing an active CMV infection following transplant with donor stem cells. The patients, who were undergoing transplant as treatment for blood-related cancers or other disorders, all carried a CMV infection from earlier in life that had been wrestled into dormancy by their immune system. Twenty-four weeks after completing up to 14 weeks of treatment, 61 percent of the patients receiving a placebo had developed a CMV infection serious enough to require treatment or had discontinued the trial. By contrast, only 38 percent of those treated with letermovir developed that level of CMV infection or did not complete the trial. Unlike other drugs able to forestall active CMV infection in stem cell transplant patients, letermovir did so without producing unacceptable toxicities. Most of the side effects associated with letermovir were tolerable, including mild cases of nausea or vomiting, and some swelling, investigators found. Letermovir also conferred a survival benefit: at the 24-week mark, 15 percent of the placebo patients had died, compared to 10 percent of those receiving letermovir. "For the first time, we seem to have a drug that is a true safe and effective preventive for CMV infection in stem cell transplant patients," said the study's lead author, Francisco Marty, MD, an infectious disease specialist at Dana-Farber and BWH. "Letermovir will allow many patients to avoid infection, usually with no or mild side effects, and seems to provide a survival benefit in the first six months post-transplant." Transplantation of donor hematopoietic stem cells - which give rise to all types of blood cells, including white blood cells of the immune system - is used to treat blood-related cancers such as leukemia, lymphoma, and myeloma, as well as several types of non-cancerous blood disorders. Patients typically receive chemotherapy to wipe out or reduce the bone marrow, where blood cells are formed, followed by an infusion of donor stem cells to rebuild their blood supply and reconstitute their immune system. While refinements in transplant techniques have sharply improved the safety of the procedure, the reactivation of CMV infection following a transplant has been a longstanding problem. Infection with CMV, a type of herpes virus, is one of the most common viral infections in the world. In the United States, it's estimated that over 50 percent of people are infected before adulthood. In other parts of the world, infection rates can be significantly higher. The effects of CMV infection can range from no symptoms to a flu-like fever or mononucleosis ("mono") syndrome. Once the immune system has brought the infection under control, the virus persists unobtrusively in the body. The jolt of a stem cell transplant - the rapid erasure or diminishment of the immune system produced by pre-transplant chemotherapy, as well as measures to prevent graft-versus-host disease - can give CMV a chance to reawaken and run amok before the newly reconstituted immune system takes hold. In the early years of bone marrow transplant therapy, 60 to 70 percent of transplant recipients developed CMV infection, Marty recounts. Of those, 20 to 30 percent contracted CMV pneumonia, and of those, 80 percent died of the disease. In previous clinical trials, several drugs aimed at preventing CMV infection in stem cell transplant patients either were not effective or produced intolerable side effects. In the absence of safe preventive drugs, physicians worked out a "surveillance" approach in which they provide treatment only when patients develop CMV infection, and only for a short period of time. This strategy has largely been a success: patients now have just a 2 or 3 percent chance of getting CMV disease affecting the lungs or other organs. Still, the often harsh side effects of current drugs were reason to continue the search for a useful preventive agent. Letermovir works by a different mechanism from previously tested agents, which block an enzyme known as DNA polymerase, which viruses use to duplicate their DNA. (Human cells use the same process to replicate their own DNA.) By contrast, letermovir blocks a process by which CMV is "packaged" inside infected cells - a wrapping that allows it to go on and infect other cells. The fact that this process does not occur in human cells may explain in part why letermovir usually gives rise to only mild side effects, researchers say. In the trial, patients received letermovir or a placebo beginning an average of nine days after transplant. "The goal was to suppress the virus before it has a chance to become active," Marty remarked. "The results of this trial offer encouragement that letermovir can offer a new strategy for donor stem cell transplant patients in preventing the emergence of CMV infection following transplant." The senior author of the study is Cyrus Badshah, MD, PhD, of Merck & Co., the developer of letermovir. Co-authors are Per T. Ljungman, MD, PhD, of Karolinska University Hospital, Stockholm, Sweden; Roy F. Chemaly, MD, MPH, of MD Anderson Cancer Center; Johan A. Maertens, MD, PhD, of Universitaire Ziekenhuizen, Leuven, Belgium; David R. Snydman, MD, of Tufts Medical Center; Rafael F. Duarte, MD, PhD, of Hospital Universitario Puerta de Hierro, Madrid, Spain; Emily A. Blumberg, MD, of the University of Pennsylvania; Hermann Einsele, MD, of Universitätsklinikum Würzburg, Würzburg, Germany; Michael J. Boeckh, MD, of Fred Hutchinson Cancer Research Center; and Valerie L. Teal, MS, Hong Wan, PhD, Nicholas A. Kartsonis, MD, and Randi Y. Leavitt, MD, PhD, of Merck & Co.


News Article | February 15, 2017
Site: www.businesswire.com

WALTHAM, Mass.--(BUSINESS WIRE)--X-Chem, Inc. (X-Chem) announced today that it has expanded its collaboration with Janssen Biotech, Inc., one of the Janssen Pharmaceutical Companies of Johnson & Johnson, to discover new drug leads for the treatment of inflammatory disease. The multi-target expansion builds on the parties’ existing discovery and license partnership, entered into in December 2014, and was facilitated by Johnson & Johnson Innovation. This latest agreement will apply X-Chem’s DEX™ platform to the identification of novel modulators for challenging disease targets, following the licensing of multiple series of X-Chem-discovered small molecules by Janssen in 2016. Under the terms of the agreement, X-Chem receives an upfront payment and research funding, and is eligible to receive additional payments and royalties based on the achievement of clinical, regulatory and commercial milestones. “We are pleased with this research alliance and the decision to increase the scope of the original agreement,” said Rick Wagner, Ph.D., Chief Executive Officer and Founder of X-Chem. “We are excited to continue our work with Janssen and discover the next generation of anti-inflammatory therapies.” About the DNA-Encoded X-Chem (DEX™) Library and Platform Due to the size and diversity of the DEX™ library, X-Chem can discover multiple series of novel, potent and selective lead compounds at an unprecedented rate of success against a wide range of targets, including some that previously failed using conventional screening methods. A number of proprietary innovations in library design, screening methodology and bioinformatics underlie the exceptional performance of the DEX™ platform. In particular, X-Chem’s approach to library construction allows for additional chemical reactions to become useable in DNA-encoded library synthesis. Together, these developments result in a much greater repertoire of diversity for small molecules, which cover a range of categories including fragment molecules, small molecular weight heterocyclic compounds, and macrocyclic structures. This diverse library, combined with a heightened ability to detect active molecules, has yielded a robust process that has been highly successful against targets categorized as difficult or intractable. The X-Chem drug discovery engine is based on a library, currently in excess of 120 billion compounds and growing, generated by iterative combinatorial synthesis of small molecules tethered to DNA tags that record the synthetic history of the small molecule. Every small molecule in the library has a unique DNA barcode attached to it. The library is screened as a mixture using affinity-based binding to a target of interest. Certain rare molecules in the library that bind to the target can be “fished out,” while the rest of the molecules are washed away. DNA sequencing methods are then used to detect molecules that are enriched when bound to the target. The diverse nature of the library produces multiple families or clusters of related molecules that bind to the target, forming a basis for emergent structure-activity relationships. Structure-activity relationships are typically used by medicinal chemists to guide iterative chemical maturation of a molecule into a drug. Based on the synthetic history encoded in the DNA sequence information, molecules are then made without the DNA tag attached, and tested for activity in conventional assays. X-Chem, Inc. is a privately-owned biotechnology company based in Waltham, Mass. The company’s mission is to apply its powerful product engine to the discovery of small molecule compounds against high-value therapeutic targets. X-Chem has established partnerships with Roche, AstraZeneca, Bayer, Pfizer, Alexion, MD Anderson Cancer Center, Sanofi, Abbvie and several other leading pharmaceutical companies, biotechnology organizations, and academic centers. For further information on X-Chem, please visit: http://www.x-chemrx.com/.


News Article | February 23, 2017
Site: news.yahoo.com

It’s safe to say that any breast cancer survivor who’s been through treatment wants to avoid having to go through it again. The risk of breast cancer recurrence is highly individual and varies according to the type and the stage of breast cancer you had. But a new research review published in the Canadian Medical Association Journal, or CMAJ, sheds light on how various lifestyle changes may be able to improve anyone’s odds of preventing a breast cancer recurrence. The most important one: exercise. The review authors found it can reduce a breast cancer recurrence by 40 percent. According to the study authors, "physical activity has the most robust effect of all lifestyle factors on reducing breast cancer recurrence." “Exercise has a benefit that’s separate from weight control. It regulates hormone levels, improves insulin resistance, and reduces inflammation,” says study co-author Ellen Warner, M.D., a professor of medicine at the University of Toronto and a medical oncologist at Toronto’s Sunnybrook Odette Cancer Centre. Exercise can also help the depression, fatigue, lymphedema (swelling in the arm caused by removing lymph nodes), and stress that might accompany diagnosis and treatment, according to Susan Gilchrist, M.D., an associate professor of clinical cancer prevention and cardiology at the University of Texas MD Anderson Cancer Center in Houston. In the study, the researchers say that breast cancer survivors should be encouraged to get at least 150 minutes of moderate-intensity or 75 minutes of vigorous aerobic exercise (brisk walking, cycling, running, or aerobic classes) in addition to at least two strength-training sessions weekly. That's the same amount of exercise the U.S. Department of Health and Human Services guidelines recommended for all of us. Always get your doctor’s clearance before you begin an exercise program, especially if you’ve had breast surgery. Work with a physical therapist at first to make sure your workout is appropriate for your range of motion, Gilchrist advises. Walking, says Gilchrist, is a great place to start for most breast cancer patients. (You can find a personal trainer who’s certified to work with cancer patients at the American College of Sports Medicine website.) The study authors also point out that many hospitals and cancer-care centers now offer exercise programs for breast cancer survivors, so check with your doctor. The study authors found that keeping your weight steady is important. Unfortunately, most breast cancer survivors do put on pounds. “There are a variety of factors at play, but there is something about breast cancer that makes patients more likely to gain weight,” says Warner. “Plus, chemotherapy slows the metabolism. If you eat and exercise the same way you always have, you will get heavier.” "On average, a woman will gain 10 to 12 pounds,” Gilchrist says. Exercise will help, she says, but you might need to do 200 minutes or more per week. Dietary changes (such as following the Mediterranean diet) didn’t seem to make a difference in breast cancer recurrence rates, according to the researchers, although eating foods high in saturated fat was related to an increased risk of dying from breast cancer. In addition, the researchers found that eating soy products was not linked to breast cancer recurrence. There is also some preliminary evidence that low blood levels of vitamin D might increase death rates and that getting more vitamin C could help prevent breast cancer recurrence, but the authors note more research is needed. More from Consumer Reports: Top pick tires for 2016 Best used cars for $25,000 and less 7 best mattresses for couples Consumer Reports has no relationship with any advertisers on this website. Copyright © 2006-2017 Consumers Union of U.S.


News Article | March 1, 2017
Site: globenewswire.com

SOUTH SAN FRANCISCO, Calif., March 01, 2017 (GLOBE NEWSWIRE) -- CytomX Therapeutics, Inc. (Nasdaq:CTMX), a biopharmaceutical company developing investigational Probody™ therapeutics for the treatment of cancer, plans to report full-year 2016 financial results on March 2, 2017, after the NASDAQ market close. The company will not conduct a conference call in conjunction with this financial results press release. About CytomX Therapeutics CytomX is a clinical-stage, oncology-focused biopharmaceutical company pioneering a novel class of investigational antibody therapeutics based on its Probody technology platform. The company uses the platform to create proprietary cancer immunotherapies against clinically-validated targets, such as PD-L1, and first-in-class cancer therapeutics against novel targets, such as CD166, that are difficult to drug without causing damage to healthy tissues. Probody therapeutics are designed to take advantage of unique conditions in the tumor microenvironment to enhance the tumor-targeting features of an antibody and reduce drug activity in healthy tissues.  The company’s lead program, CX-072, a wholly-owned PD-L1-targeting Probody therapeutic, is being evaluated in a Phase 1/2 study. The Investigational New Drug filing for CX-2009 is slated for the first half of 2017.  CX-2009 is a first-in-class Probody drug conjugate targeting the highly expressed tumor antigen, CD166.  Both clinical trials are modules within PROCLAIM (Probody Clinical Assessment In Man), an international umbrella clinical trial program that provides clinical trial sites with access to the company’s novel therapies under one central protocol. In addition to its proprietary programs, CytomX is collaborating with strategic partners including AbbVie, Bristol-Myers Squibb Company, Pfizer Inc., MD Anderson Cancer Center and ImmunoGen, Inc. For more information, visit www.cytomx.com or follow us on Twitter. CytomX Therapeutics Forward-Looking Statements This press release includes forward-looking statements. Such forward-looking statements involve known and unknown risks, uncertainties and other important factors that are difficult to predict, may be beyond our control, and may cause the actual results, performance or achievements to be materially different from any future results, performance or achievements expressed or implied in such statements. Accordingly, you should not rely on any of these forward-looking statements. Our Probody platform is beginning clinical development, and the process by which clinical development could potentially lead to an approved product is long and subject to significant risks and uncertainties. Projected net cash utilization and capital resources are subject to substantial risk of variance based on a wide variety of factors that can be difficult to predict.  Applicable risks and uncertainties include those relating to our preclinical research and development, clinical development, and other risks identified under the heading "Risk Factors" included in our filings with the SEC. The forward-looking statements contained in this press release are based on information currently available to CytomX and speak only as of the date on which they are made. CytomX does not undertake and specifically disclaims any obligation to update any forward-looking statements, whether as a result of any new information, future events, changed circumstances or otherwise.

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