Foster City, CA, United States
Foster City, CA, United States

Gilead Sciences is an American biotechnology company that discovers, develops and commercializes therapeutics. For many years since the company was founded, the company concentrated primarily on antiviral drugs to treat patients infected with HIV, hepatitis B or influenza. In 2006, Gilead acquired two companies that were developing drugs to treat patients with pulmonary diseases. The company has fourteen commercially available products. Wikipedia.

SEARCH FILTERS
Time filter
Source Type

News Article | April 8, 2017
Site: www.techtimes.com

The U.S. Food and Drug Administration has given the green signal to two new drugs manufactured especially for pediatric patients suffering from the hepatitis C virus. On Friday, April 7, the FDA granted approval to Gilead Sciences' new drugs — Harvoni and Sovaldi — for treatment of chronic hepatitis C infections in children between 12 years and 17 years. These drugs were previously used to treat hepatitis C virus, or HCV, infections in adults. The FDA shared that the newly-approved drugs were the world's first direct-acting antiviral medications, which have received approval for kids and adolescents suffering from HCV. A direct-acting antiviral drug essentially reduces the quantity of HCV present in the body. It does so by stopping the virus from reproducing. In most cases, application of these drugs goes on to cure HCV completely. "These approvals will help change the landscape for HCV treatment by addressing an unmet need in children and adolescents," said FDA's Edward Cox. The approved drug will be now able to treat six major infections of HCV present in the body. Harvoni will be used to treat kids 12 years or older diagnosed with HCV infection 1, 4, 5, or 6. To be eligible for receiving the medicine, these kids will have to weigh at least 77 pounds. Moreover, they should not be suffering from cirrhosis or even mild cirrhosis. The efficiency, safety, and pharmacokinetics of the Harvoni drug for HCV strain 1 infection was proved and confirmed in an open-label, clinical trial that took place in various centers. The trial included 100 children aged 12 years and older, suffering from the above-mentioned strain. The results that were determined in the pediatric patients were compared to the outcome of the drug observed in adults. It was seen that 98 percent children were cured of the infection after undergoing the trial for 12 weeks. With regard to the efficacy and safety of Harvoni for HCV genotypes 4, 5, or 6, in children aged 12 years and above, similar results were determined for the drugs. Fatigue and headache were the most common side effects observed in the treatments where Harvoni was administered. For the evaluation of Sovaldi, combined with ribavirin, nearly 50 pediatric patients aged 12 years and above were put under a clinical trial spanning 12 weeks. These patients too had to weigh at least 77 pounds and did not suffer from cirrhosis or mild liver cirrhosis. At the end of the trial, it was observed that all the patients suffering from HCV strain 2 infection, and 97 percent of kids suffering from HCV 3 genotype, were cured of their respective ailments. The FDA stated that the patients who will be treated with Sovaldi in combination with ribavirin, may experience headache and fatigue. Gilead's VP Norbert Bischofberger said that the company's goal was to provide patients suffering from HCV with a treatment, which has the potential to cure them completely. © 2017 Tech Times, All rights reserved. Do not reproduce without permission.


News Article | April 20, 2017
Site: www.eurekalert.org

ILC 2017: Eight studies being presented at The International Liver Congress™ 2017 demonstrate contrasting evidence on the potential link between direct-acting antiviral treatment for hepatitis C and liver cancer According to data from eight studies being presented at The International Liver Congress™ 2017 in Amsterdam, The Netherlands, there remains continued debate on whether patients are at risk of developing liver cancer after achieving sustained virologic response (SVR) with a direct-acting antiviral (DAA) regimen for Hepatitis C virus (HCV). Investigators will present the results of their studies that show both sides of the argument - DAA therapy is associated with a higher risk of liver cancer compared with interferon-based therapy, versus there is no difference in liver cancer risk following cure with either therapy. Whilst remarkable progress has been made in the development of successful antiviral therapies for HCV infection, some recent studies suggest that curing patients does not eliminate the risk of developing liver cancer. There also appears to be an unexpectedly high rate of liver cancer (also known as hepatocellular carcinoma [HCC]) recurrence in patients who previously had their tumour treated successfully and had received DAAs.1 This claim was further supported by a Spanish study led by Dr Maria Reig and Dr Mariño, Hospital Clinic Barcelona, Spain in which patients with HCV and HCC who had previously been cured of HCC received DAA therapy. After a median 12.4 month follow-up, following treatment with DAAs, the rate of HCC coming back (recurrence) was 31.2% (24/77) and of those who received HCC treatment at recurrence, 30% (6/20) of patients presented progression in the immediate 6-month follow-up. This is an update of the study that will be published in the May 2017 issue of Seminars in Liver Disease, and is available here: https:/ . "Our study offers further support to previous findings that there is an unexpected high recurrence rate of hepatocellular carcinoma associated with DAAs, and that this association may result in a more aggressive pattern of recurrence and faster tumour progression," said Dr Maria Reig, Barcelona Clinic Liver Cancer Group, Hospital Clinic Barcelona, Spain, and lead author of the study. "These data indicate that there needs to be further research conducted in this area, clarifying the mechanism for the association between liver cancer recurrence and DAA therapy." Identifying those patients at risk of liver cancer is essential, a task that Dr Etienne Audureau, Public Health, Henri Mondor University Hospital, Créteil, France, and colleagues attempted to achieve by developing a prognostic tool for HCC. They found that in patients with severe scarring of the liver due to HCV (compensated cirrhosis), failure to achieve SVR was the most influential factor in predicting liver cancer. In addition, risk factors for liver cancer differ according to SVR status. The investigators recommend that in patients with compensated cirrhosis, eradication of HCV should be achieved before liver function is impaired and people who have achieved SVR should be monitored for liver cancer after 50 years of age. The mechanisms behind the development of liver cancer following HCV cure are not yet understood. One group of investigators led by Prof Thomas Baumert, Inserm Institute for Viral and Liver Diseases, University of Strasbourg, France, aimed to investigate if HCV infections produce epigenetic and transcriptional changes that persist after the infection is cured, and whether these epigenetic changes drive liver disease and HCC following cure. They found that the epigenetic and transcriptional changes are only partially reversed by DAAs and persist after HCV cure, suggesting that these changes are a driver for liver cancer that develops after HCV infection has been cured. The investigators concluded that these findings open a new perspective to develop novel biomarkers to identify patients at high risk of HCC and provide an opportunity to develop urgently needed strategies for HCC prevention. On the other side of the debate, a systematic review, meta-analyses, and meta-regression study, by Prof Gregory Dore and Dr Reem Waziry from The Kirby Institute, UNSW Sydney, and colleagues, found no evidence for higher risk of HCC occurrence or recurrence following DAA treatment, compared with interferon-based HCV therapy. A total of 41 studies, including 26 on HCC occurrence and 15 on HCC recurrence (in total, n=13,875 patients) were included. In studies assessing HCC occurrence, average follow up was shorter and average age was higher in DAA studies compared to interferon studies; incidence was lower with longer follow-up and younger age. In studies assessing HCC recurrence, average follow up was also shorter. Ultimately, in the meta-regression analysis, no evidence in favour of a differential HCC occurrence or recurrence was found between DAA and interferon regimens, after adjusting for study follow-up and age. "Recent studies have reported contradicting evidence on risk of hepatocellular carcinoma following direct-acting antiviral therapy; our aim was to bring some clarity to this," said Prof Gregory Dore, Kirby Institute and lead author of the study. "These data show the higher incidence of HCC observed following DAA therapy can be explained by the shorter duration of follow-up and older age of participants, rather than the DAA treatment regimen." A Scottish study, led by Dr Hamish Innes, School of Health and Life Sciences, Glasgow Caledonian University, Scotland, found that the risk of liver cancer following SVR was not associated with the use of DAAs, but baseline risk factors. Furthermore, risk of HCC development was similar in patients taking interferon-free regimens versus interferon-containing regimens, following a multivariate adjustment (IRR: 0.96, p=0.929) and no significant differences in HCC risk were found when treatment regimen was defined in terms of DAA containing regimens versus DAA free regimens. These data indicate that rather than the treatment regimens themselves, it is the baseline risk factors that determine risk of hepatocellular carcinoma. Another interesting study in Japanese patients with HCV genotype 1 infection, found a reduced incidence of liver cancer following achievement of SVR after 12 weeks of therapy with an interferon-free regimen (ledipasvir plus sofosbuvir) to a similar degree as that obtained with an interferon-containing regimen (simeprevir with peginterferon plus ribavirin). This study, which was conducted by Dr Masaaki Korenaga, Kohnodai Hospital, National Center for Global Health and Medicine, Chiba, Japan, and colleagues, also found that unexpected development of liver cancer following SVR in patients without previous liver cancer could potentially be predicted by imaging procedures (computer tomography or enhanced magnetic resonance imaging). Similarly, a Chinese study led by Dr George Lau, from the Beijing 302-Hong Kong Humanity and Health Hepatitis C Diagnosis and Treatment Centre, in Beijing, China, found no increase in the incidence of liver cancer in patients who achieved SVR12 with DAA compared to peginterferon plus ribavirin. A Sicilian study conducted by Dr Vincenza Calvaruso, University of Palermo, Palermo, Italy, and colleagues, demonstrated that patients who achieved SVR with DAAs had a similar risk of developing liver cancer when compared to historical controls of patients with compensated cirrhosis who achieved SVR after interferon-based therapy. In addition, those who achieved SVR with DAAs had a lower risk of developing liver cancer than those patients whose HCV infection was not cured. "The original observations made by researchers from the Barcelona Clinic Liver Cancer Group have sparked a huge number of studies aimed at verifying the potential association between DAA treatment and increased HCC recurrence after cure," said Prof Francesco Negro, Divisions of Gastroenterology and Hepatology of Clinical Pathology, University Hospital of Geneva, and EASL Governing Board Member. "At this stage, there is no reason to alter treatment guidelines until the issue is definitively clarified. We cannot exclude, however, that we may have to revise post-SVR surveillance in some specific patient subgroups." This annual congress is the biggest event in the EASL calendar, attracting scientific and medical experts from around the world to learn about the latest in liver research. Attending specialists present, share, debate and conclude on the latest science and research in hepatology, working to enhance the treatment and management of liver disease in clinical practice. This year, the congress is expected to attract approximately 10,000 delegates from all corners of the globe. The International Liver Congress™ 2017 will take place from April 19 - 23, at the RAI Amsterdam, Amsterdam, The Netherlands. About The European Association for the Study of the Liver (EASL) Since its foundation in 1966, this not-for-profit organisation has grown to over 4,000 members from all over the world, including many of the leading hepatologists in Europe and beyond. EASL is the leading liver association in Europe, having evolved into a major European Association with international influence, with an impressive track record in promoting research in liver disease, supporting wider education and promoting changes in European liver policy. Contact For more information, please contact the ILC Press Office at: Session title: Parallel session: Liver tumours: from patient stratification to management Time, date, and location of session: 16:00 - 18:00, Thursday 20 April, Elicium 2 Abstract: No evidence for higher risk of hepatocellular carcinoma occurrence or recurrence following direct-acting antiviral HCV therapy: A systematic review, meta-analyses, and meta-regression (PS160), 16:00 - 16:15 Gregory Dore, Australia Session title: Parallel session: HCV: post SVR management and complications Time, date, and location of session: 16:00 - 18:00, Thursday 20 April, Hall 5 Abstracts presented in order of appearance in press release: Tumour recurrence after Interferon-free treatment for hepatitis C in patients with previously treated hepatocellular carcinoma discloses a more aggressive pattern and faster tumour growth (PS031), 16:00 - 16:15 Maria Reig, Spain Identifying residual risk of hepatocellular carcinoma following hepatitis C virus eradication in compensated cirrhosis: decision-tree and random forest models developed in the French multicenter prospective ANRS CO12 CirVir cohort (PS034), 16:45 - 17:00 Etienne Audureau, France Hepatitis C virus-induced epigenetic and transcriptional changes persist post cure (PS033), 16:30 - 16:45 Thomas Baumert, France Among cirrhotic patients with a hepatitis C sustained viral response, the risk of de-novo hepatocellular carcinoma relates to baseline factors and not the use of direct acting antivirals: results from a nationwide cohort (PS035), 17:00 - 17:15 Hamish Innes, United Kingdom Sustained virologic response by ledipasvir/sofosbuvir reduces the incidence of hepatocellular carcinoma in Japanese patients with HCV genotype 1 infection. - Comparison with Simeprevir with peginterferon plus ribavirin (PS036), 17:15 - 17:30 Masaaki Korenaga, Japan No increase in the occurrence rate of hepatocellular carcinoma in Chinese treated by direct-acting antivirals compared to Interferon after eradication of hepatitis c virus: A long-term follow-up (PS037), 17:30 - 17:45 George Lau, China Occurrence of hepatocellular carcinoma in patients with hepatitis C virus related liver disease treated with direct-acting antivirals (PS038), 17:45 - 18:00 Vincenza Calvaruso, Italy Gregory Dore: Advisory board member and receives honorarium from Gilead, Merck, Abbvie, Bristol-Myers Squibb, Janssen, has received research grant funding from Gilead, Merck, Abbvie, Bristol-Myers Squibb, Janssen, and travel sponsorship from Gilead, Merck, Abbvie, and Bristol-Myers Squibb Vincenza Calvaruso: Advisory Board for AbbVie, BMS, Gilead Sciences and Intercept. Grant and research support for MSD 1 Reig M et al. Unexpected early tumor recurrence in patients with HCV-related HCC undergoing interferon-free therapy; a note of caution. J Hepatol. 2016;65:719-726.


FOSTER CITY, Calif.--(BUSINESS WIRE)--Gilead Sciences, Inc. (Nasdaq: GILD) today announced that Kevin Young CBE, Gilead’s Chief Operating Officer, and Norbert W. Bischofberger, PhD, Gilead’s Executive Vice President, R&D and Chief Scientific Officer, will participate in a fireside chat at the Bank of America Merrill Lynch Healthcare Conference in Las Vegas on Thursday, May 18 at 9:20 a.m. Pacific Time. The audio portion of the fireside chat will be accessible live through the company’s Investors page at www.gilead.com/investors. Please connect to the company’s website at least 15 minutes prior to the start of the presentation to ensure adequate time for any software download that may be required to listen to the webcast. The replay will be available for 14 days following the presentation. Gilead Sciences is a biopharmaceutical company that discovers, develops and commercializes innovative therapeutics in areas of unmet medical need. The company’s mission is to advance the care of patients suffering from life-threatening diseases. Gilead has operations in more than 30 countries worldwide, with headquarters in Foster City, California. For more information on Gilead Sciences, please visit the company’s website at www.gilead.com, follow Gilead on Twitter (@GileadSciences) or call Gilead Public Affairs at 1-800-GILEAD-5 or 1-650-574-3000.


News Article | May 2, 2017
Site: www.businesswire.com

FOSTER CITY, Calif.--(BUSINESS WIRE)--Gilead Sciences, Inc. (Nasdaq:GILD) today announced that the company’s Board of Directors has declared a cash dividend of $0.52 per share of common stock for the second quarter of 2017. The dividend is payable on June 29, 2017, to stockholders of record at the close of business on June 16, 2017. Future dividends will be subject to Board approval. Gilead Sciences is a biopharmaceutical company that discovers, develops and commercializes innovative therapeutics in areas of unmet medical need. The company’s mission is to advance the care of patients suffering from life-threatening diseases. Gilead has operations in more than 30 countries worldwide, with headquarters in Foster City, California. For more information on Gilead Sciences, please visit the company’s website at www.gilead.com, follow Gilead on Twitter (@GileadSciences) or call Gilead Public Affairs at 1-800-GILEAD-5 or 1-650-574-3000.


FOSTER CITY, Calif.--(BUSINESS WIRE)--Gilead Sciences, Inc. (Nasdaq: GILD) today announced 96-week results from two ongoing Phase 3 studies evaluating the safety and efficacy of daily Vemlidy® (tenofovir alafenamide, TAF 25mg) in immune active patients and in patients switching from Gilead’s Viread® (tenofovir disoproxil fumarate, TDF 300mg). Vemlidy is a once-daily treatment approved for adults with chronic hepatitis B virus (HBV) infection with compensated liver disease. In addition, Gilead presented data from preclinical studies of investigational compounds being studied for their potential role in HBV cure strategies. Data are being presented this week at The International Liver Congress™ 2017 in Amsterdam. Vemlidy is a novel, targeted prodrug of tenofovir that has demonstrated antiviral efficacy that is noninferior to that of Viread at Week 48 in patients with chronic HBV. Vemlidy treatment at the same time point also demonstrated a beneficial impact on renal and bone laboratory safety parameters compared to Viread. Analyses now conducted at Week 96 of treatment demonstrate continued benefits of Vemlidy including high rates of viral suppression, with no evidence of resistance, and less impact on renal and bone safety parameters as compared to Viread (#PS-042, #FRI-153). Additionally, patients switching from Viread to Vemlidy after Week 96 demonstrated maintenance of viral suppression, improvement in serum alanine aminotransferase (ALT) normalization rates, and improvement in bone and renal parameters 24 weeks after switching to Vemlidy (#PS-041: “ Hepatitis B and D: emerging treatment options”). “ The results observed in these studies reinforce Vemlidy as an important treatment option for patients living with chronic HBV infection,” said Norbert Bischofberger, PhD, Executive Vice President of Research and Development and Chief Scientific Officer at Gilead. “ Additionally, the preclinical data presented at this EASL meeting illustrate our scientific approach to evaluating compounds with distinct mechanisms of action aimed at curing HBV infection.” Vemlidy has a boxed warning in its U.S. product label regarding the risk of post-treatment severe acute exacerbation of hepatitis B. See below for important safety information. The two randomized, double-blinded Phase 3 studies (Studies 108 and 110) from which the data are presented evaluated the use of Vemlidy given once-daily versus Gilead’s Viread given once-daily in treatment-naïve and treatment-experienced adults with HBeAg-negative and HBeAg-positive chronic HBV infection. Results demonstrate continued advantages of treatment with Vemlidy over Viread between Week 48 and Week 96. Virologic response rates at Week 96 were 90 percent (n=257/285) and 91 percent (n=127/140) in HBeAg-negative patients (Study 108) receiving Vemlidy and Viread, respectively. In HBeAg-positive patients (Study 110), virologic response rates at Week 96 were 73 percent (n=423/581) and 75 percent (n=218/292) in the Vemlidy and Viread groups, respectively. In both studies, a greater percentage of patients taking Vemlidy achieved normalization of ALT levels relative to patients taking Viread as measured by both central laboratory criteria, and by the American Association for the Study of Liver Diseases (AASLD) criteria. Patients receiving Vemlidy also demonstrated ongoing benefits at Week 96 in bone and renal safety parameters, including smaller declines from baseline in hip and spine bone mineral density (BMD) and smaller declines from baseline in estimated creatinine clearance compared with patients taking Viread in both studies. Similar rates of adverse events and low and similar rates of adverse events leading to discontinuation were observed in both treatment arms. Viral resistance analyses showed no resistance to Vemlidy or Viread at Week 96. A post-hoc analysis evaluated a subset of 541 patients from Studies 108 and 110 who completed 96 weeks of treatment with double-blind Vemlidy or Viread and were then switched to open-label treatment with Vemlidy. Among patients switched from Viread to Vemlidy at Week 96 (n=180), virologic suppression was maintained and the rates of ALT normalization by central laboratory criteria and AASLD criteria significantly increased during the subsequent 24 weeks of Vemlidy therapy. These patients also demonstrated further improvements in hip and spine BMD and had significant improvements in estimated creatinine clearance. Longer-term data are required to confirm the benefits of switching from Viread to Vemlidy for the treatment of chronic HBV. In addition, Gilead has several ongoing research programs with the goal of achieving functional cure for HBV-infected patients. Preclinical data with some of Gilead’s novel investigational compounds are being presented at the Congress. GS-5801 is an oral liver-targeted prodrug of a small molecule inhibitor of KDM5, a histone lysine demethylase. Results from in vitro preclinical studies (#SAT-160) demonstrated activity of GS-5801 in HBV-infected primary human hepatocytes with significant declines in viral proteins and HBV RNA. In addition, in vivo data (#THU-171) demonstrated the pharmacodynamic response of GS-5801 within the liver, in animal models. GS-5801 is currently being evaluated in Phase 1 trials in healthy subjects and in patients with chronic HBV infection. GS-9688, an oral selective toll-like receptor 8 (TLR8) agonist, demonstrated in vitro and in vivo pharmacodynamic effects consistent with selective TLR8 activation, including the production of antiviral cytokines (#SAT-168). Further, in an efficacy animal model of chronic HBV infection, GS-9688 treatment demonstrated a sustained antiviral response in chronically infected woodchucks (#SAT-165). GS-9688 is currently being evaluated in Phase 1 trials in healthy subjects and in patients with chronic HBV infection. Further information about the clinical studies described above can be found at http://anzctr.org.au/. GS-5801 and GS-9688 are investigational products and have not been determined to be safe or efficacious. Most common adverse reactions (incidence ≥5%; all grades) were headache, abdominal pain, fatigue, cough, nausea and back pain. Consult the full prescribing information for Vemlidy for more information on potentially significant drug interactions, including clinical comments. Gilead Sciences is a biopharmaceutical company that discovers, develops and commercializes innovative therapeutics in areas of unmet medical need. The company’s mission is to advance the care of patients suffering from life-threatening diseases. Gilead has operations in more than 30 countries worldwide, with headquarters in Foster City, California. This press release includes forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 that are subject to risks, uncertainties and other factors, including the risk that physicians may not see the benefits of prescribing Vemlidy for the treatment of HBV. In addition, Gilead may be unable to achieve a functional cure for HBV with any of its product candidates, including GS-5801 and GS-9688. These risks, uncertainties and other factors could cause actual results to differ materially from those referred to in the forward-looking statements. The reader is cautioned not to rely on these forward-looking statements. These and other risks are described in detail in Gilead’s Annual Report on Form 10-K for the quarter ended December 31, 2016, as filed with the U.S. Securities and Exchange Commission. All forward-looking statements are based on information currently available to Gilead, and Gilead assumes no obligation to update any such forward-looking statements. U.S. full Prescribing Information including BOXED WARNING for Vemlidy is available at www.gilead.com. Vemlidy and Viread are registered trademarks of Gilead Sciences, Inc., or its related companies. For more information on Gilead Sciences, please visit the company’s website at www.gilead.com, follow Gilead on Twitter (@GileadSciences) or call Gilead Public Affairs at 1-800-GILEAD-5 or 1-650-574-3000.


Dublin, May 01, 2017 (GLOBE NEWSWIRE) -- Research and Markets has announced the addition of the "Global Cancer Immunotherapy Market & Clinical Trials Outlook 2022" report to their offering. Global Cancer Immunotherapy Market & Clinical Trials Outlook 2022 report gives comprehensive insight on clinical and non-clinical developments in the field of cancer immunotherapy. As per report findings, cancer immunotherapy has emerged as the new growth frontier for the pharmaceutical companies involved in the clinical research and development of cancer drugs and therapeutics. Currently there are more than 2000 cancer immunotherapies based drugs/therapies are in clinical pipeline. Majority of these are in preclinical, Phase-I and Phase-II trials. There are 14 cancer vaccine, 44 Cancer monoclonal antibodies, 3 cancer cell therapies and 61 cancer Immunomodulators are commercially available in the market. Pharmaceutical companies are actively engaged in research and development of cancer immunotherapies because of large unmet medical necessities. Investigators are trying to come forth with innovative cancer immunotherapeutic products having high safety and efficacy profiles which are not offered by conventional therapeutics. Higher investments in research and development segment could significantly increase the drug discovery rates which will alleviate the medical condition of cancer patients. Simultaneously, technological advancements are being made due to which development of worthy candidates with high commercialization and pharmacological potential is expected to increase in coming years. Investigators are trying to decipher underlying principle of cancer progression and proliferation. Different cancer indications have different requirements for developing effective therapeutics due to which identification of these factors have become important. This knowledge would be used for developing innovative cancer immunotherapies for various malignancies. Cancer immunotherapeutics based on these discoveries would pave path for market introduction of highly effective therapeutics. Some progress has been made which could be noticed by observing plethora of cancer immunotherapeutics available for different cancer indications. Their clinical pipeline is also developing rapidly and various products are at different stages of clinical trials. They are expected to offer severe competition to presently available cancer therapeutics with modest pharmacological efficacy. Cancer immunotherapies have been used for limited number of malignancies as compared to other drug categories. Mostly hematological malignancies like follicular lymphoma, chronic lymphocytic leukemia and diffuse large B cell non-Hodgkin's lymphoma have remained the focal point. Other cancer indications like melanoma, NSCLC, prostate cancer and RCC have also got cancer immunotherapeutics. Most like, cancer therapeutics in clinical trials would be able to present positive data that will allow them to easily enter in global market. Cancer incidences are escalating rapidly and cancer immuno therapeutics seems to play an important role in offering better medical care to patients. Some of them have received FDA's accelerated approval and breakthrough therapy designation due to their superior pharmacological benefits. It is expected that similar progress would be shown by cancer immunotherapeutics under development for different malignancies. - Competitive Analysis Key Topics Covered: 1. Immunotherapy: Mending Cancer Regimens 1.1 Preface to Cancer Immunotherapy 1.2 Evolution of Cancer Immunotherapy 2. Categorization of Cancer Immunotherapy 2.1 Specific Cancer Immunotherapy 2.1.1 Cancer Vaccines 2.1.2 Monoclonal Antibodies 2.2 Non-Specific Cancer Immunotherapy 2.2.1 Adoptive Cell Transfer Immunotherapy 2.2.2 Immune Checkpoint Inhibitors 3. Fundamentals of Cancer Vaccines 3.1 Prologue of Cancer Vaccines 3.2 Cancer Vaccines in Immunotherapy 3.3 Commercial Aspects of Cancer Vaccines 4. New Era of Monoclonal Antibodies 4.1 Rudiments of Monoclonal Antibodies 4.2 Advents of Monoclonal Antibodies 4.3 Commercial Aspects of Monoclonal Antibodies 5. Trails of T-Cell Therapies 5.1 Adoptive Cell Transfer Technology 5.2 Strategies of Adoptive Cell Transfer 5.3 Commercial Aspects of Adoptive Cell Therapy 6. Aspects of Immune Checkpoint Inhibitors 6.1 Prelude to Immune Checkpoint Inhibitors 6.2 Implications of Immunecheck Point Inhibitors 6.3 Commercial Aspects of Immune Checkpoint Inhibitors 7. Immunomodulators in Cancer Immunotherapy 7.1 Perspective of Immunomodulators 7.2 Clinical Aspects of Immunomodulators 7.3 Commercial Aspects of Immunomodulators 8. Oncolytic Viral Immunotherapy 8.1 Concept to Oncolytic Viruses 8.2 Potential Approaches of Oncolytic Viruses 8.3 Commercial Aspects of Oncolytic Viruses 9. Cytokines in Cancer Immunotherapy 9.1 Fundamentals of Cytokines 9.2 Classification of Cytokines 9.3 Commercial Aspects of Cytokines 10. Interferons in Immunotherapy 10.1 Potentials of Interferons 10.2 Classification of Interferons 10.3 Clinical Applications of Interferons 11. Interleukins in Immunotherapy 11.1 Potentials of Interleukins 11.2 Clinical Applications of Interleukins 12. GM-CSF in Immunotherapy 12.1 Potentials of GM-CSF 12.2 Clinical Applications of GM-CSF 13. Global Economic Evaluations 13.1 Economic Aspects of Cancer Immunotherapy 13.2 Cancer Immunotherapy Cost by Product 14. Market Aspects of Cancer Immunotherapy 14.1 Current Market Trends 14.2 Cancer Immunotherapy Pipeline Overview 15. Global Cancer Immunotherapy Market Dynamics 15.1 Favorable Market Parameters 15.2 Commercialization Challenges 16. Marketed Cancer Cell Therapies Drugs 16.1 Sipuleucel-T (Provenge®) 16.2 T-Lymphocyte Cell Therapy(Immuncell-LC®) 17. Marketed Cancer Cytokines Drugs 17.1 Aldesleukin (Proleukin®) 17.2 Denileukin Diftitox (ONTAK®) 17.3 Interferon Alpha (Multiferon®) 17.4 Interferon Alpha-2a (Roferon-A®) 17.5 Interferon Alpha-2a (Veldona®) 17.6 Interferon Alpha-2a Biosimilar(Inferon/Inmutag) 17.7 Interferon Alpha-2b(Intron® A) 17.8 Interferon Alpha-2b Biosimilar(Bioferon) 17.9 Interferon Alpha-2b Biosimilar (Intalfa®) 17.10 Interferon Alpha-2b Biosimilar 17.11 Interferon-Alpha-n3 (Alferon N®) 17.12 Interferon-Beta-1b (Feron®) 17.13 Interferon-Gamma (Ogamma®) 17.14 Interleukin-2 Biosimilar (Ilcass) 17.15 Teceleukin (Imunace) 18. Marketed Cancer Vaccines 18.1 Bladder Cancer Vaccine (PACIS®) 18.2 Bladder Cancer Vaccine 18.3 BV NSCLC 001 18.4 Dendritic Cell Vaccine (CreaVax-HCC®, CreaVax-PC® & CreaVax-RCC®) 18.5 Human Papillomavirus Vaccine Quadrivalent (Gardasil®/Silgard®) 18.6 Human Papillomavirus Vaccine Recombinant Bivalent (Cervarix®) 18.7 Melanoma Vaccine (MVax®) 18.8 Melanoma Vaccine (Melacine®) 18.9 Racotumomab (Vaxira®) 18.10 Sipuleucel-T (Provenge®) 18.11 Tertomotide (LucaVax) 18.12 Vitespen (Oncophage®) 19. Marketed Cancer Monoclonal Antibodies 19.1 Bevacizumab 19.2 Trastuzumab Emtansine 19.3 Trastuzumab Subcutaneous 19.4 Brentuximab Vedotin 19.5 Catumaxomab 19.6 Ipilimumab 19.7 Nivolumab 19.8 Pembrolizumab 19.9 Pertuzumab 19.10 Rituximab 19.11 Trastuzumab 20. Global Cancer Immunotherapy Market Future Prospects 21. Competitive Landscape 21.1 Abbvie 21.2 Advaxis 21.3 Altor BioScience 21.4 Amgen 21.5 Biogen Idec 21.6 Biogenomics 21.7 Celldex Therapeutics 21.8 Dendreon Corporation 21.9 Eli Lilly 21.10 Expression Genetics 21.11 Galena Biopharma 21.12 Genmab 21.13 Gilead Sciences 21.14 GlaxoSmithKline 21.15 ImmunoCellular Therapeutics 21.16 ImmunoGen 21.17 Inovio Pharmaceuticals 21.18 IRX Therapeutics 21.19 Merck 21.20 NeoStem Oncology 21.21 NewLink Genetics 21.22 Northwest Biotherapeutics 21.23 Novartis 21.24 Peregrine Pharmaceuticals 21.25 Pfizer 21.26 Philogen 21.27 Regulon 21.28 Roche 21.29 Seattle Genetics 21.30 ZymoGenetics For more information about this report visit http://www.researchandmarkets.com/research/rl32xc/global_cancer


Patent
Gilead Sciences | Date: 2016-12-15

Compounds having the following formula (I) and methods of their use and preparation are disclosed:


Colby D.A.,Gilead Sciences | Tsai A.S.,Scripps Research Institute | Bergman R.G.,University of California at Berkeley | Ellman J.A.,Yale University
Accounts of Chemical Research | Year: 2012

Over the last several decades, researchers have achieved remarkable progress in the field of organometallic chemistry. The development of metalcatalyzed cross-coupling reactions represents a paradigm shift in chemical synthesis, and today synthetic chemists can readily access carbon-carbon and carbon-heteroatom bonds from a vast array of starting compounds. Although we cannot understate the importance of these methods, the required prefunctionalization to carry out these reactions adds cost and reduces the availability of the starting reagents. The use of C-H bond activation in lieu of prefunctionalization has presented a tantalizing alternative to classical cross-coupling reactions. Researchers have met the challenges of selectivity and reactivity associated with the development of C-H bond functionalization reactions with an explosion of creative advances in substrate and catalyst design. Literature reports on selectivity based on steric effects, acidity, and electronic and directing group effects are now numerous. Our group has developed an array of C-H bond functionalization reactions that take advantage of a chelating directing group, and this Account surveys our progress in this area. The use of chelation control in C-H bond functionalization offers several advantages with respect to substrate scope and application to total synthesis. The predictability and decreased dependence on the inherent stereoelectronics of the substrate generally result in selective and high yielding transformations with broad applicability. The nature of the chelating moiety can be chosen to serve as a functional handle in subsequent elaborations. Our work began with the use of Rh(I) catalysts in intramolecular aromatic C-H annulations, which we further developed to include enantioselective transformations. The application of this chemistry to the simple olefinic C-H bonds found in r, β-unsaturated imines allowed access to highly substituted olefins, pyridines, and piperidines. We observed complementary reactivity with Rh(III) catalysts and developed an oxidative coupling with unactivated alkenes. Further studies on the Rh(III) catalysts led us to develop methods for the coupling of C-H bonds to polarized p bonds such as those in imines and isocyanates. In several cases the methods that we have developed for chelation-controlled C-H bond functionalization have been applied to the total synthesis of complex molecules such as natural products, highlighting the utility of these methods in organic synthesis. © 2011 American Chemical Society.


Hocek M.,Gilead Sciences | Fojta M.,Academy of Sciences of the Czech Republic
Chemical Society Reviews | Year: 2011

Basic aspects of DNA electrochemistry with a strong focus on the use of modified nucleobases as redox probes for electrochemical bioanalysis are reviewed. Intrinsic electrochemical properties of nucleobases in combination with artificial redox-active nucleobase modifications are frequently applied in this field. Synthetic approaches (both chemical and enzymatic) to base-modified nucleic acids are briefly summarized and their applications in redox labelling are discussed. Finally, analytical applications including DNA hybridization, primer extension, PCR, SNP typing, DNA damage and DNA-protein interaction analysis are presented (critical review, 91 references). © The Royal Society of Chemistry 2011.


Patent
Gilead Sciences | Date: 2016-07-06

An intravenous pharmaceutical composition or kit comprising 4-(pyrimidin-2-ylmethyl)-7-(4-(trifluoromethoxy)phenyl)-3,4-dihydrobenzo[f][1,4]oxazepin-5(2H)-one (Compound I) and a beta-cyclodextrin derivative.

Loading Gilead Sciences collaborators
Loading Gilead Sciences collaborators