Guilford, CT, United States

Time filter

Source Type

News Article | December 10, 2016

— Stroke Pipeline Market Companies Involved in Therapeutics Development are AB Science SA, Acticor Biotech, ActiveSite Pharmaceuticals Inc, Addex Therapeutics Ltd, advanceCor GmbH, Affibody AB, Amarantus Bioscience Holdings Inc, Anavex Life Sciences Corp, Angion Biomedica Corp, Antoxis Ltd, APT Therapeutics, Inc., ArmaGen Inc, Asterias Biotherapeutics, Inc., AstraZeneca Plc, Athersys Inc, Bayer AG, Bioasis Technologies Inc, Biogen Inc, Boehringer Ingelheim GmbH, Cardax Inc, Cellular Biomedicine Group Inc, CHA Bio & Diostech Co Ltd, ContraVir Pharmaceuticals Inc, CSPC Pharmaceutical Group Limited, D-Pharm Ltd, Daiichi Sankyo Company Ltd, DiaMedica Inc, Diffusion Pharmaceuticals Inc, F. Hoffmann-La Roche Ltd, Fina Biotech, Genervon Biopharmaceuticals LLC, Glialogix Inc, Glucox Biotech AB, Green Cross Corp, Huons Co Ltd, International Stem Cell Corp, Jeil Pharmaceutical Co Ltd, JN-International Medical Corp, Laboratoires Pierre Fabre SA, LegoChem Biosciences Inc, Les Laboratoires Servier SAS, Living Cell Technologies Ltd, Lumosa Therapeutics Co Ltd, M et P Pharma AG, Magnus Life Ltd, Mapreg SAS, Mast Therapeutics Inc, Medestea Research & Production SpA, Mitochon Pharmaceuticals Inc, Mitsubishi Tanabe Pharma Corp, Neuralstem Inc, Neuren Pharmaceuticals Ltd, Neurofx Inc, Neuronax SAS, Neurotec Pharma SL, NeuroVive Pharmaceutical AB, New Haven Pharmaceuticals, Inc., New World Laboratories Inc, NoNO Inc, NuvOx Pharma LLC, Omeros Corp, Panacea Pharmaceuticals Inc, PharmatrophiX, Inc., Pharmaxis Ltd, Pharmicell Co Ltd, Phoenix Biotechnology Inc, Phylogica Ltd, PhytoHealth Corp, Pluristem Therapeutics Inc, Primary Peptides, Inc., Q Therapeutics Inc, QR Pharma Inc, ReCyte Therapeutics Inc, Regenera Pharma Ltd, RegeneRx Biopharmaceuticals Inc, Remedy Pharmaceuticals Inc, ReNeuron Group Plc, SanBio Inc, Saneron CCEL Therapeutics Inc, Shin Poong PharmCo Ltd, Simcere Pharmaceutical Group, Stemedica Cell Technologies Inc, SynZyme Technologies LLC, Targazyme Inc, The International Biotechnology Center (IBC) Generium, TikoMed AB, vasopharm GmbH, Verseon Corp, Vicore Pharma AB, Virogenomics BioDevelopment Inc, WhanIn Pharmaceutical Co Ltd and Zocere Inc. This research provides comprehensive information on the therapeutics under development for Stroke (Cardiovascular), 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 The Stroke (Cardiovascular) pipeline guide also reviews of key players involved in therapeutic development for Stroke 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, IND/CTA Filed, Preclinical and Discovery stages are 1, 10, 21, 14, 1, 89 and 11 respectively. Similarly, the Universities portfolio in Phase III, Preclinical and Discovery stages comprises 1, 35 and 4 molecules, respectively. Stroke (Cardiovascular) 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 • The pipeline guide provides a snapshot of the global therapeutic landscape of Stroke (Cardiovascular). • The pipeline guide reviews pipeline therapeutics for Stroke (Cardiovascular) 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 Stroke (Cardiovascular) therapeutics and enlists all their major and minor projects. • The pipeline guide evaluates Stroke (Cardiovascular) 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 Stroke (Cardiovascular) • 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 Stroke (Cardiovascular). • 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 Stroke (Cardiovascular) 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

Pucci M.J.,New Haven Pharmaceuticals | Bush K.,Indiana University Bloomington
Clinical Microbiology Reviews | Year: 2013

New antimicrobial agents are always needed to counteract the resistant pathogens that continue to be selected by current therapeutic regimens. This review provides a survey of known antimicrobial agents that were currently in clinical development in the fall of 2012 and spring of 2013. Data were collected from published literature primarily from 2010 to 2012, meeting abstracts (2011 to 2012), government websites, and company websites when appropriate. Compared to what was reported in previous surveys, a surprising number of new agents are currently in company pipelines, particularly in phase 3 clinical development. Familiar antibacterial classes of the quinolones, tetracyclines, oxazolidinones, glycopeptides, and cephalosporins are represented by entities with enhanced antimicrobial or pharmacological properties. More importantly, compounds of novel chemical structures targeting bacterial pathways not previously exploited are under development. Some of the most promising compounds include novel β-lactamase inhibitor combinations that target many multidrug-resistant Gram-negative bacteria, a critical medical need. Although new antimicrobial agents will continue to be needed to address increasing antibiotic resistance, there are novel agents in development to tackle at least some of the more worrisome pathogens in the current nosocomial setting. © 2013, American Society for Microbiology. All Rights Reserved.

Patrick J.,New Haven Pharmaceuticals | Dillaha L.,New Haven Pharmaceuticals | Armas D.,Celerion | Sessa W.C.,Yale University
Postgraduate Medicine | Year: 2015

Aims. Low-dose acetylsalicylic acid (ASA; aspirin) for secondary prevention reduces cardiovascular disease mortality risk. ASA acetylates cyclooxygenase in the portal circulation and is rapidly (halflife, 20 min) hydrolyzed. Certain patients with cardiovascular disease may exhibit high on-therapy platelet reactivity as a result of high platelet turnover, a process whereby platelets are produced and are active beyond the duration of antiplatelet coverage provided by once-daily immediaterelease (IR) ASA. A once-daily, extended-release (ER) ASA formulation using ER microcapsule technology was developed to release ASA over the 24-h dosing interval and reduce maximal plasma concentrations to spare peripheral endogenous endothelial prostacyclin production. Methods. Healthy adults (n = 50) were randomized in a crossover study to receive two different ER-ASA single doses (up to 325 mg) and two different IR-ASA single doses (up to 81 mg) in four periods, each separated by ‡14 days. Pharmacodynamics was assessed by measuring serum thromboxane B2 (TXB2), urine 11-dehydro-TXB2, and arachidonic acid-induced platelet aggregation. Pharmacokinetics was determined for ASA and salicylic acid (SA). Results: Both formulations produced dose-dependent inhibition on all pharmacodynamic parameters. Marked inhibition of TXB2 and 11-dehydro-TXB2 was maintained over the 24-h dosing interval after a dose of ‡81 mg ER-ASA or ‡40 mg IR-ASA. The dose required to achieve 50% of maximum TXB2 inhibition with ER-ASA was 49.9 mg versus 29.6 mg for IR-ASA, for a similar maximum pharmacodynamic effect (98.9% TXB2 inhibition). This suggests that an approximately twofold greater ER-ASA dose (162.5 mg) is necessary to obtain the same response as that of IR-ASA 81 mg. Peak ASA concentrations were lower and Tmax was longer with ER-ASA versus IR-ASA. Administration of IR-ASA resulted in a dosenormalized mean Cmax of ASA that was approximately sixfold higher than that for ER-ASA and a Cmax of SA approximately two- to threefold higher than that for ER-ASA. Conclusion. Both ASA formulations showed dose-dependent antiplatelet activity. Compared with the IR-ASA, ER-ASA released active drug more slowly, resulting in prolonged absorption and lower systemic drug concentrations, which is expected for an ER (24-h) formulation. © 2015 Informa UK Ltd.

Podos S.D.,New Haven Pharmaceuticals | Thanassi J.A.,New Haven Pharmaceuticals | Leggio M.,New Haven Pharmaceuticals | Pucci M.J.,New Haven Pharmaceuticals
Antimicrobial Agents and Chemotherapy | Year: 2012

Many bacterial infections involve slow or nondividing bacterial growth states and localized high cell densities. Antibiotics with demonstrated bactericidal activity rarely remain bactericidal at therapeutic concentrations under these conditions. The isothiazoloquinolone (ITQ) ACH-702 is a potent, bactericidal compound with activity against many antibiotic-resistant pathogens, including methicillin-resistant Staphylococcus aureus (MRSA). We evaluated its bactericidal activity under conditions where bacterial cells were not dividing and/or had slowed their growth. Against S. aureus cultures in stationary phase, ACH-702 showed concentration-dependent bactericidal activity and achieved a 3-log-unit reduction in viable cell counts within 6 h of treatment at >16x MIC values; in comparison, the bactericidal quinolone moxifloxacin and the additional comparator compounds vancomycin, linezolid, and rifampin at 16x to 32x MICs showed little or no bactericidal activity against stationaryphase cells. ACH-702 at 32x MIC retained bactericidal activity against stationary-phase S. aureus across a range of inoculum densities. ACH-702 did not kill cold-arrested cells yet remained bactericidal against cells arrested by protein synthesis inhibitors, suggesting that its bactericidal activity against nondividing cells requires active metabolism but not de novo protein synthesis. ACH-702 also showed a degree of bactericidal activity at 16x MIC against S. epidermidis biofilm cells that was superior to that of moxifloxacin, rifampin, and vancomycin. The bactericidal activity of ACH-702 against stationary-phase staphylococci and biofilms suggests potential clinical utility in infections containing cells in these physiological states. Copyright © 2012, American Society for Microbiology. All Rights Reserved.

Marra A.,New Haven Pharmaceuticals
Future Microbiology | Year: 2011

Evaluation of: Kumarasamy KK, Toleman MA, Walsh TR et al.: Emergence of a new antibiotic resistance mechanism in India, Pakistan, and the UK: a molecular, biological, and epidemiological study. Lancet Infect. Dis. 10(9), 597-602 (2010). Are bacteria always going to outsmart us? With the emergence of the metallo-β-lactamase blaNDM-1 gene, it certainly seems so. Whereas at one time bacterial clones resided in hospitals or long-term care facilities, it is now apparent that they have the capability of thriving in the community and quickly spreading across countries and continents with few impediments, thanks to accessible, rapid global travel. Thus, under conditions favoring the organism (promiscuous or inappropriate antibiotic use and poor infection control procedures), what was at one time a local problem can rapidly become a worldwide health crisis. Given that the discovery and development of a new antibiotic can take a decade or more, multiply resistant pathogens can have ample time to wreak havoc before a successful novel agent comes to market. At one time a single drug, penicillin, was enough to raise expectations that new antibiotics were unnecessary; we have since seen that bacteria can generate stable resistance to every antibiotic in rapid fashion, with no detrimental effects on their pathogenicity. © 2011 Future Medicine Ltd.

Bush K.,Indiana University | Pucci M.J.,New Haven Pharmaceuticals
Biochemical Pharmacology | Year: 2011

Antibiotic resistance issues necessitate the continued discovery and development of new antibacterial agents. Efforts are ongoing in two approaches to find new compounds that are effective against antibiotic-resistant pathogens. These efforts involve modification of existing classes including fluoroquinolones, tetracyclines, aminoglycosides, and β-lactams and identification of inhibitors against previously unexploited antibacterial targets. Examples of both approaches are described here with emphasis on compounds in late pre-clinical or clinical stages of development. © 2011 Elsevier Inc. All rights reserved.

Podos S.D.,New Haven Pharmaceuticals | Thanassi J.A.,New Haven Pharmaceuticals | Pucci M.J.,New Haven Pharmaceuticals
Antimicrobial Agents and Chemotherapy | Year: 2012

We report the use of a known pyridochromanone inhibitor with antibacterial activity to assess the validity of NAD+-dependent DNA ligase (LigA) as an antibacterial target in Staphylococcus aureus. Potent inhibition of purified LigA was demonstrated in a DNA ligation assay (inhibition constant [Ki]=4.0 nM) and in a DNA-independent enzyme adenylation assay using full-length LigA (50% inhibitory concentration [IC50]=28 nM) or its isolated adenylation domain (IC50=36 nM). Antistaphylococcal activity was confirmed against methicillin-susceptible and -resistant S. aureus (MSSA and MRSA) strains (MIC = 1.0 μg/ml). Analysis of spontaneous resistance potential revealed a high frequency of emergence (4 × 10-7) of high-level resistant mutants (MIC>64) with associated ligA lesions. There were no observable effects on growth rate in these mutants. Of 22 sequenced clones, 3 encoded point substitutions within the catalytic adenylation domain and 19 in the downstream oligonucleotide-binding (OB) fold and helix-hairpin-helix (HhH) domains. In vitro characterization of the enzymatic properties of four selected mutants revealed distinct signatures underlying their resistance to inhibition. The infrequent adenylation domain mutations altered the kinetics of adenylation and probably elicited resistance directly. In contrast, the highly represented OB fold domain mutations demonstrated a generalized resistance mechanism in which covalent LigA activation proceeds normally and yet the parameters of downstream ligation steps are altered. A resulting decrease in substrate Km and a consequent increase in substrate occupancy render LigA resistant to competitive inhibition. We conclude that the observed tolerance of staphylococcal cells to such hypomorphic mutations probably invalidates LigA as a viable target for antistaphylococcal chemotherapy. Copyright © 2012, American Society for Microbiology. All Rights Reserved.

Marra A.,New Haven Pharmaceuticals
Methods in Molecular Biology | Year: 2014

One of the foremost challenges of drug discovery in any therapeutic area is that of solidifying the correlation between in vitro activity and clinical efficacy. Between these is the confirmation that affecting a particular target in vivo will lead to a therapeutic benefit. In antibacterial drug discovery, there is a key advantage from the start, since the targets are bacteria-therefore, it is simple to ascertain in vitro whether a drug has the desired effect, i.e., bacterial cell inhibition or killing, and to understand the mechanism by which that occurs. The downstream criteria, whether a compound reaches the infection site and achieves appropriately high levels to affect bacterial viability, can be evaluated in animal models of infection. In this way animal models of infection can be a highly valuable and predictive bridge between in vitro drug discovery and early clinical evaluation. The Gram-positive pathogen Staphylococcus aureus causes a wide variety of infections in humans (Archer, Clin Infect Dis 26:1179-1181, 1998) and has been said to be able to infect every tissue type. Fortunately, over the years a great deal of effort has been expended toward developing infection models in rodents using this organism, with good success. This chapter will describe the advantages, methods, and outcome measurements of the rodent models most used in drug discovery for S. aureus. Mouse models will be the focus of this chapter, as they are the most economical and thus most commonly used, but a rat infection model is included as well. © 2014 Springer Science+Business Media, LLC.

News Article | October 4, 2012

New Haven Pharmaceuticals, Inc. (NHP) develops proprietary, controlled release specialty pharmaceuticals based on approved or GRAS active pharmaceutical ingredients for use in new therapeutic indications. NHP’s novel product pipeline is built on three licenses from Yale University and Micropump Aspirin, the world’s only 24-hour controlled-release aspirin, licensed from Flamel Technologies.

Loading New Haven Pharmaceuticals collaborators
Loading New Haven Pharmaceuticals collaborators