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Princeton, NJ, United States

Bristol-Myers Squibb, often referred to as BMS, is an American pharmaceutical company, headquartered in New York City.Bristol-Myers Squibb manufactures prescription pharmaceuticals in several therapeutic areas, including cancer, HIV/AIDS, cardiovascular disease, diabetes, hepatitis, rheumatoid arthritis and psychiatric disorders. Its mission is to "discover, develop and deliver innovative medicines that help patients prevail over serious diseases."BMS' primary R&D sites are located in Lawrence Township and Wallingford, Connecticut , with other sites in Hopewell and New Brunswick, New Jersey, and in Braine-l'Alleud, Belgium, Tokyo, and Bangalore, India. Wikipedia.


Ptaszynska A.,Bristol Myers Squibb
Postgraduate medicine | Year: 2013

People with diabetes are more likely to develop a cardiovascular (CV) disease compared with those without diabetes. Although effective glycemic control has been the focus of the management of type 2 diabetes mellitus (T2DM), it is also important to control other CV risk factors to improve outcomes in these patients. Dapagliflozin, a sodium-glucose co-transporter 2 inhibitor, lowers glucose levels in patients with T2DM by increasing urinary glucose excretion. Dapagliflozin therapy has been shown to impact a number of CV risk factors. Dapagliflozin improved glycemia with a low intrinsic propensity to cause hypoglycemia. Caloric loss associated with dapagliflozin-induced glucosuria also led to body weight reduction. Small changes from baseline in mean lipid parameters and reductions in serum uric acid levels were observed in patients taking dapagliflozin. Blood pressure reductions were also noted, consistent with modest drug-induced diuresis and weight loss. Furthermore, a lower rate of cardiac events was seen in patients taking dapagliflozin compared with those taking comparators in a meta-analysis of clinical trials on dapagliflozin. Overall, dapagliflozin has shown beneficial effects on CV risk factors in patients with T2DM. Further studies are underway to evaluate the effect of dapagliflozin on CV outcomes.


Hoos A.,Bristol Myers Squibb
Annals of Oncology | Year: 2012

The effect of cancer immunotherapies is on the immune system and not directly on the tumour. The kinetics of immunotherapy are characterised by a cellular immune response followed by potential changes in tumour burden or patient survival. To adequately investigate immunotherapies in clinical trials, a new development paradigm including reconsideration of established end points addressing this biology is needed. Over the last 7 years, several initiatives across the cancer immunotherapy community were facilitated by the Cancer Research Institute Cancer Immunotherapy Consortium. They systematically evolved an immunotherapy-focused clinical development paradigm and proposed to redefine trial end points. On that basis, analysis of several large datasets generated throughout the immunotherapy community supports three novel end point proposals. First, results from T-cell immune response assays are highly variable and often nonreproducible. Harmonisation of assays can minimise this variability and support the investigation of the cellular immune response as a biomarker and testing it for clinical surrogacy. Secondly, immunotherapy induces novel patterns of the antitumour response not captured by World Health Organisation criteria or Response Evaluation Criteria in Solid Tumours. New immune-related response criteria were defined which more comprehensively capture all response patterns. Thirdly, survival curves in randomised immunotherapy trials can show a delayed separation, which can impact study results. Altered statistical models are needed to describe the hazard ratios as a function of time, and differentiate them before and after separation of curves to improve planning of phase III trials. Taken together, these recommendations may improve our tools for cancer immunotherapy investigations. © The Author 2012. Published by Oxford University Press on behalf of the European Society for Medical Oncology. All rights reserved.


Zhao Q.,Bristol Myers Squibb
Journal of Leukocyte Biology | Year: 2010

A cardinal feature of inflammation is the tissue recruitment of leukocytes, a process that is mediated predominantly by chemokines via their receptors on migrating cells. CCR2 and CCR5, two CC chemokine receptors, are important players in the trafficking of monocytes/macrophages and in the functions of other cell types relevant to disease pathogenesis. This review provides a brief overview of the biological actions of CCR2 and CCR5 and a comprehensive summary of published data that demonstrate the involvement of both receptors in the pathogenesis of immunologic diseases (RA, CD, and transplant rejection) and cardiovascular diseases (atherosclerosis and AIH). In light of the potential for functional redundancy of chemokine receptors in mediating leukocyte trafficking and the consequent concern over insufficient efficacy offered by pharmacologically inhibiting one receptor, this review presents evidence supporting dual targeting of CCR2 and CCR5 as a more efficacious strategy than targeting either receptor alone. It also examines potential safety issues associated with such dual targeting. © Society for Leukocyte Biology.


Sinz M.W.,Bristol Myers Squibb
Drug Metabolism Reviews | Year: 2013

The increased capacity to rapidly eliminate drugs can have a profound effect on the efficacious exposure of coadministered drugs, especially in today's medical world of polypharmacy. There are numerous drug-drug interactions (DDIs) related to a loss of therapeutic efficacy and many of these are caused by pregnane X receptor (PXR)-mediated transcriptional activation of drug-metabolizing enzymes or drug transporters. Evaluation of PXR activation and subsequent induction of proteins involved in drug elimination and distribution have become routine in drug discovery and drug development. The assays used to evaluate PXR directly are high throughput and provide useful information on the ability of a drug's potential to precipitate a DDI. In addition, they may serve as useful tools to support structure-activity or structure-liability relationships to eliminate or minimize the potential of new drug candidates to cause induction and, ultimately, a DDI. © 2013 Informa Healthcare USA, Inc.


Rapisarda A.,Frederick National Laboratory for Cancer Research | Melillo G.,Bristol Myers Squibb
Nature Reviews Clinical Oncology | Year: 2012

Cancer cells rely on angiogenesis to fulfil their need for oxygen and nutrients; hence, agents targeting angiogenic pathways and mediators have been investigated as potential cancer drugs. Although this strategy has demonstrated delayed tumour progression-leading to progression-free survival and overall survival benefits compared with standard therapy-in some patients, the results are more modest than predicted. A significant number of patients either do not respond to antiangiogenic agents or fairly rapidly develop resistance to them, which raises questions about how resistance develops and how it can be overcome. Furthermore, whether cancers, once they develop resistance, become more invasive or lead to metastatic disease remains unclear. Several mechanisms of resistance have been recently proposed and emerging evidence indicates that, under certain experimental conditions, antiangiogenic agents increase intratumour hypoxia by promoting vessel pruning and inhibiting neoangiogenesis. Indeed, several studies have highlighted the possibility that inhibitors of VEGF (and its receptors) can promote an invasive metastatic switch, in part by creating an increasingly hypoxic tumour microenvironment. As a potential remedy, a number of therapeutic approaches have been investigated that target the hypoxic tumour compartment to improve the clinical outcome of antiangiogenic therapy. © 2012 Macmillan Publishers Limited. All rights reserved.

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