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— Chronic Lymphocytic Leukemia (CLL) Pipeline Market Companies Involved in Therapeutics Development are 4SC AG, AbbVie Inc, Acetylon Pharmaceuticals Inc, Aeglea BioTherapeutics Inc, Altor BioScience Corp, Amgen Inc, Aprea AB, Aptevo Therapeutics Inc, Arno Therapeutics Inc, ArQule Inc, Astellas Pharma Inc, Astex Pharmaceuticals Inc, Baliopharm AG, Bayer AG, BeiGene Ltd, Bellicum Pharmaceuticals Inc, Biogen Inc, Bionomics Ltd, Bionovis SA, Biothera Pharmaceutical Inc, Boehringer Ingelheim GmbH, Bristol-Myers Squibb Company, Celgene Corp, Cellectis SA, Cellular Biomedicine Group Inc, Coherus BioSciences Inc, CrystalGenomics Inc, Cyclacel Pharmaceuticals Inc, Daiichi Sankyo Company Ltd, Eli Lilly and Company, F. Hoffmann-La Roche Ltd, GeneaMed Ltd, Genentech Inc, Genor BioPharma Co Ltd, Gilead Sciences Inc, Grupo Ferrer Internacional SA, Hutchison MediPharma Ltd, Hybrigenics SA, Igenica Biotherapeutics Inc, Immatics Biotechnologies GmbH, ImmunoGen Inc, Immunomedics Inc, Incyte Corp, Inflection Biosciences Ltd, Innate Pharma SA, Innovent Biologics Inc, Johnson & Johnson, Juno Therapeutics Inc, Kancera AB, Karyopharm Therapeutics Inc, Kite Pharma Inc, Les Laboratoires Servier SAS, LFB SA, Lymphocyte Activation Technologies SA, Medicenna Therapeutics Inc, MENTRIK Biotech LLC, Merck & Co Inc, Merck KGaA, Mesoblast Ltd, Millennium Pharmaceuticals Inc, MorphoSys AG, NantKwest Inc, Nordic Nanovector ASA, Novartis AG, Oncternal Therapeutics, Inc., Ono Pharmaceutical Co Ltd, Panacea Biotec Ltd, PEP-Therapy SAS, Pfizer Inc, Pharmacyclics Inc, PIQUR Therapeutics AG, Portola Pharmaceuticals Inc, Redx Pharma Plc, Respiratorius AB, Revitope Oncology, Inc., Rhizen Pharmaceuticals SA, Sandoz International GmbH, Sanofi, Selvita SA, Simcere Pharmaceutical Group, Sorrento Therapeutics Inc, Supratek Pharma Inc, Takeda Pharmaceutical Company Ltd, Targazyme Inc, TG Therapeutics Inc, The International Biotechnology Center (IBC) Generium, Theravectys SA, Tolero Pharmaceuticals Inc, TRACON Pharmaceuticals Inc, Tragara Pharmaceuticals Inc, Trillium Therapeutics Inc, United BioPharma, Inc., Unum Therapeutics Inc, Verastem Inc, VioQuest Pharmaceuticals Inc, Viralytics Ltd, Xencor Inc, ZIOPHARM Oncology Inc and Zymeworks Inc. This research provides comprehensive information on the therapeutics under development for Chronic Lymphocytic Leukemia (CLL) (Oncology), complete with analysis by stage of development, drug target, mechanism of action (MoA), route of administration (RoA) and molecule type. The guide covers the descriptive pharmacological action of the therapeutics, its complete research and development history and latest news and press releases. Inquire more about this research report at http://www.reportsnreports.com/contacts/inquirybeforebuy.aspx?name=774108 The Chronic Lymphocytic Leukemia (CLL) (Oncology) pipeline guide also reviews of key players involved in therapeutic development for Chronic Lymphocytic Leukemia (CLL) and features dormant and discontinued projects. The guide covers therapeutics under Development by Companies /Universities /Institutes, the molecules developed by Companies in Pre-Registration, Phase III, Phase II, Phase I, Phase 0, IND/CTA Filed, Preclinical, Discovery and Unknown stages are 5, 5, 43, 45, 1, 3, 54, 13 and 1 respectively. Similarly, the Universities portfolio in Phase II, Phase I, Preclinical and Discovery stages comprises 4, 6, 8 and 7 molecules, respectively. Chronic Lymphocytic Leukemia (CLL) (Oncology) pipeline guide helps in identifying and tracking emerging players in the market and their portfolios, enhances decision making capabilities and helps to create effective counter strategies to gain competitive advantage. The guide is built using data and information sourced from Global Markets Directs proprietary databases, company/university websites, clinical trial registries, conferences, SEC filings, investor presentations and featured press releases from company/university sites and industry-specific third party sources. Additionally, various dynamic tracking processes ensure that the most recent developments are captured on a real time basis. Note: Certain content / sections in the pipeline guide may be removed or altered based on the availability and relevance of data. Buy a copy of this research report at http://www.reportsnreports.com/purchase.aspx?name=774108 • The pipeline guide provides a snapshot of the global therapeutic landscape of Chronic Lymphocytic Leukemia (CLL) (Oncology). • The pipeline guide reviews pipeline therapeutics for Chronic Lymphocytic Leukemia (CLL) (Oncology) by companies and universities/research institutes based on information derived from company and industry-specific sources. • The pipeline guide covers pipeline products based on several stages of development ranging from pre-registration till discovery and undisclosed stages. • The pipeline guide features descriptive drug profiles for the pipeline products which comprise, product description, descriptive licensing and collaboration details, R&D brief, MoA & other developmental activities. • The pipeline guide reviews key companies involved in Chronic Lymphocytic Leukemia (CLL) (Oncology) therapeutics and enlists all their major and minor projects. • The pipeline guide evaluates Chronic Lymphocytic Leukemia (CLL) (Oncology) therapeutics based on mechanism of action (MoA), drug target, route of administration (RoA) and molecule type. • The pipeline guide encapsulates all the dormant and discontinued pipeline projects. • The pipeline guide reviews latest news related to pipeline therapeutics for Chronic Lymphocytic Leukemia (CLL) (Oncology) • Procure strategically important competitor information, analysis, and insights to formulate effective R&D strategies. • Recognize emerging players with potentially strong product portfolio and create effective counter-strategies to gain competitive advantage. • Find and recognize significant and varied types of therapeutics under development for Chronic Lymphocytic Leukemia (CLL) (Oncology). • Classify potential new clients or partners in the target demographic. • Develop tactical initiatives by understanding the focus areas of leading companies. • Plan mergers and acquisitions meritoriously by identifying key players and it’s most promising pipeline therapeutics. • Formulate corrective measures for pipeline projects by understanding Chronic Lymphocytic Leukemia (CLL) (Oncology) pipeline depth and focus of Indication therapeutics. • Develop and design in-licensing and out-licensing strategies by identifying prospective partners with the most attractive projects to enhance and expand business potential and scope. • Adjust the therapeutic portfolio by recognizing discontinued projects and understand from the know-how what drove them from pipeline. For more information, please visit http://www.reportsnreports.com/reports/774108-chronic-lymphocytic-leukemia-cll-pipeline-review-h2-2016.html


News Article | October 27, 2016
Site: www.eurekalert.org

Acute myeloid leukemia (AML) is an aggressive cancer known for drug resistance and relapse. In an effort to uncover new treatment strategies, researchers at University of California San Diego School of Medicine and Moores Cancer Center discovered that a cell surface molecule known as CD98 promotes AML. The study, published October 27 by Cancer Cell, also shows that inhibiting CD98 with the therapeutic antibody IGN523 blocks AML growth in patient-derived cells and mouse models. "To improve therapeutic strategies for this disease, we need to look not just at the cancer cells themselves, but also at their interactions with surrounding cells, tissues, molecules and blood vessels in the body," said co-senior author Tannishtha Reya, PhD, professor of pharmacology at UC San Diego School of Medicine and Moores Cancer Center. "In this study, we identified CD98 as a critical molecule driving AML growth. We showed that blocking CD98 can effectively reduce leukemia burden and improve survival by preventing cancer cells from receiving support from the surrounding environment." Reya led the study together with Mark Ginsberg, MD, professor of medicine at UC San Diego School of Medicine and Moores Cancer Center. Co-author Edward van der Horst, PhD, senior director at Igenica Biotherapeutics Inc., provided the anti-CD98 antibody IGN523. AML is a type of cancer in which the bone marrow makes abnormal white blood cells, red blood cells or platelets. Reya's team and others have previously shown that leukemia cells interact with their surroundings in the body via molecules on their cell surfaces, and that these interactions can help the cancer cells divide, replicate and metastasize. CD98 is a molecule found on the surface of cells, where it controls how cells stick to one another. CD98 is known to play a role in the proliferation and activation of certain immune cells. CD98 levels are also known to be elevated in some solid tumors, and linked to poor prognosis. To determine CD98's role in AML, in this latest study Reya's team engineered mouse models that lack the molecule. They found that the loss of CD98 blocked AML growth and improved survival. CD98 loss largely spared normal blood cells, which the researchers said indicates a potential therapeutic window. Further experiments revealed that leukemia cells lacking CD98 had fewer stable interactions with the lining of blood vessels -- interactions that were needed to fuel AML growth. Next, the researchers wanted to see what would happen if they blocked CD98 in AML with a deliverable inhibitor. In 2015, Igenica Biotherapeutics Inc. tested IGN523, a humanized antibody that specifically binds and inhibits CD98, in a phase 1 clinical trial at Moores Cancer Center and elsewhere. The trial's goal was to determine a safe dose for IGN523 administration in AML patients. In this study, Reya and team tested IGN523 in their own AML models. The researchers found that IGN523 blocks CD98's AML-promoting activity in both mouse models of AML and human cells in the laboratory. They also transplanted human patient-derived AML cells into mice and treated the recipients soon after with either IGN523, the anti-CD98 antibody, or with a control antibody. Anti-CD98-treatment effectively eliminated AML cells. In contrast, AML in control mice expanded more than 100-fold. "This study suggests that human AML can't get established without CD98, and that blocking the molecule with anti-CD98 antibodies could be beneficial for the treatment of AML in both adults and children," Reya said. Moving forward, Reya and team are working to further define whether CD98 could be targeted to treat pediatric AML. "Many of the models we used in this work were based on mutations found in childhood AML," she said. "While many childhood cancers have become very treatable, childhood AML continues to have a high rate of relapse and death. We plan to work with pediatric oncologists to test if anti-CD98 agents can be effective against pediatric AML, and whether it can improve responses to current treatments. I think this is particularly important to pursue since the anti-CD98 antibody has already been through phase I trials, and could be more easily positioned to test in drug-resistant pediatric AML." The American Cancer Society estimates that there will be about 19,950 new cases of AML and about 10,430 deaths from the disease in the United States in 2016, mostly adults. Approximately 500 children are diagnosed with AML in the U.S. each year, and it's the most common second cancer among children treated for other cancers, according to St. Jude Children's Research Hospital.


News Article | October 29, 2016
Site: www.sciencedaily.com

Acute myeloid leukemia (AML) is an aggressive cancer known for drug resistance and relapse. In an effort to uncover new treatment strategies, researchers at University of California San Diego School of Medicine and Moores Cancer Center discovered that a cell surface molecule known as CD98 promotes AML. The study, published October 27 by Cancer Cell, also shows that inhibiting CD98 with the therapeutic antibody IGN523 blocks AML growth in patient-derived cells and mouse models. "To improve therapeutic strategies for this disease, we need to look not just at the cancer cells themselves, but also at their interactions with surrounding cells, tissues, molecules and blood vessels in the body," said co-senior author Tannishtha Reya, PhD, professor of pharmacology at UC San Diego School of Medicine and Moores Cancer Center. "In this study, we identified CD98 as a critical molecule driving AML growth. We showed that blocking CD98 can effectively reduce leukemia burden and improve survival by preventing cancer cells from receiving support from the surrounding environment." Reya led the study together with Mark Ginsberg, MD, professor of medicine at UC San Diego School of Medicine and Moores Cancer Center. Co-author Edward van der Horst, PhD, senior director at Igenica Biotherapeutics Inc., provided the anti-CD98 antibody IGN523. AML is a type of cancer in which the bone marrow makes abnormal white blood cells, red blood cells or platelets. Reya's team and others have previously shown that leukemia cells interact with their surroundings in the body via molecules on their cell surfaces, and that these interactions can help the cancer cells divide, replicate and metastasize. CD98 is a molecule found on the surface of cells, where it controls how cells stick to one another. CD98 is known to play a role in the proliferation and activation of certain immune cells. CD98 levels are also known to be elevated in some solid tumors, and linked to poor prognosis. To determine CD98's role in AML, in this latest study Reya's team engineered mouse models that lack the molecule. They found that the loss of CD98 blocked AML growth and improved survival. CD98 loss largely spared normal blood cells, which the researchers said indicates a potential therapeutic window. Further experiments revealed that leukemia cells lacking CD98 had fewer stable interactions with the lining of blood vessels -- interactions that were needed to fuel AML growth. Next, the researchers wanted to see what would happen if they blocked CD98 in AML with a deliverable inhibitor. In 2015, Igenica Biotherapeutics Inc. tested IGN523, a humanized antibody that specifically binds and inhibits CD98, in a phase 1 clinical trial at Moores Cancer Center and elsewhere. The trial's goal was to determine a safe dose for IGN523 administration in AML patients. In this study, Reya and team tested IGN523 in their own AML models. The researchers found that IGN523 blocks CD98's AML-promoting activity in both mouse models of AML and human cells in the laboratory. They also transplanted human patient-derived AML cells into mice and treated the recipients soon after with either IGN523, the anti-CD98 antibody, or with a control antibody. Anti-CD98-treatment effectively eliminated AML cells. In contrast, AML in control mice expanded more than 100-fold. "This study suggests that human AML can't get established without CD98, and that blocking the molecule with anti-CD98 antibodies could be beneficial for the treatment of AML in both adults and children," Reya said. Moving forward, Reya and team are working to further define whether CD98 could be targeted to treat pediatric AML. "Many of the models we used in this work were based on mutations found in childhood AML," she said. "While many childhood cancers have become very treatable, childhood AML continues to have a high rate of relapse and death. We plan to work with pediatric oncologists to test if anti-CD98 agents can be effective against pediatric AML, and whether it can improve responses to current treatments. I think this is particularly important to pursue since the anti-CD98 antibody has already been through phase I trials, and could be more easily positioned to test in drug-resistant pediatric AML." The American Cancer Society estimates that there will be about 19,950 new cases of AML and about 10,430 deaths from the disease in the United States in 2016, mostly adults. Approximately 500 children are diagnosed with AML in the U.S. each year, and it's the most common second cancer among children treated for other cancers, according to St. Jude Children's Research Hospital.

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