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H. Lundbeck A/S is a Danish international pharmaceutical company engaged in the research and development, production, marketing, and sale of drugs for the treatment of disorders in the central nervous system , including depression, schizophrenia, Alzheimer's disease, Parkinson's disease, Huntington's disease, epilepsy and insomnia.Headquartered in Copenhagen, Denmark Lundbeck has international production facilities in Denmark, Mexico, Italy and France and affiliates or sales offices in 57 countries. Lundbeck employs around 5.500 people globally , and the company’s products are registered in more than 100 countries world wide.In 2013, the company's revenue was DKK 15.2 billion .Lundbeck is listed on the Copenhagen Stock Exchange .Lundbeck is a full member of the European Federation of Pharmaceutical Industries and Associations and of the International Federation of Pharmaceutical Manufacturers and Associations Wikipedia.

This invention is directed to compounds, which are PDE10A enzyme inhibitors. The invention provides a pharmaceutical composition comprising a therapeutically effective amount of a compound of the invention and a pharmaceutically acceptable carrier. The present invention also provides processes for the preparation of the compounds of formula I. The present invention further provides a method of treating a subject suffering from a neurodegenerative disorder comprising administering to the subject a therapeutically effective amount of a compound of formula 1. The present invention also provides a method of treating a subject suffering from a drug addiction comprising administering to the subject a therapeutically effective amount of a compound of formula I. The present invention further provides a method of treating a subject suffering from a psychiatric disorder comprising administering to the subject a therapeutically effective amount of a compound of formula 1.

Pedersen J.T.,Lundbeck | Sigurdsson E.M.,New York University
Trends in Molecular Medicine | Year: 2015

Targeting pathological tau protein in Alzheimer's disease (AD) and related tauopathies has shown great potential in animal models. Given that tau lesions correlate better with the degree of dementia than do amyloid-β (Aβ) plaques, their clearance may be clinically more efficacious than removing Aβ when cognitive deficits become evident in AD. Several complementary mechanisms of antibody-mediated removal of tau aggregates are likely to act in concert and the importance of each one may depend on antibody properties, the disease, and its stage. Clinical trials of tau immunotherapy are already underway and several more are likely to be initiated in the near future. © 2015 Elsevier Ltd.

Wilkinson D.,Memory Assessment and Research Center | Windfeld K.,Lundbeck | Colding-Jorgensen E.,Lundbeck
The Lancet Neurology | Year: 2014

Background: In human beings, 5-HT6 receptors are almost exclusively expressed in the brain, particularly in areas relevant for cognition, such as the hippocampus and frontal cortex. We assessed the effect on cognitive performance of Lu AE58054 (idalopirdine), a selective 5-HT6 receptor antagonist, in donepezil-treated patients with moderate Alzheimer's disease. Methods: For this randomised, double-blind, placebo-controlled phase 2 trial (LADDER), we recruited patients from 48 outpatient clinical sites in seven countries. Patients were 50 years or older, had moderate Alzheimer's disease (a mini-mental state examination score of 12-19), and had been stably treated with donepezil 10 mg per day for 3 or more months. Using a computer-generated sequence, we randomly assigned patients (1:1, stratified by site) to receive either idalopirdine 90 mg per day (30 mg thrice daily) or placebo. The primary endpoint was change from baseline in the 11-item Alzheimer's Disease Assessment Scale-cognitive subscale (ADAS-cog) at week 24. We analysed all efficacy endpoints in the full-analysis set (modified intention-to-treat analysis). This trial is registered with ClinicalTrials.gov, number NCT01019421. Findings: Between Dec 8, 2009, and Dec 23, 2011, we randomly allocated 278 patients to treatment: 133 to placebo and 145 to idalopirdine. 132 patients in the placebo group and 140 in the experimental group were included in the final analysis. At week 24, the change from baseline in ADAS-cog total score was +1·38 (SD 0·53) in the placebo group and -0·77 (0·55) in the idalopirdine group (treatment difference of -2·16 points, 95% CI -3·62 to -0·69; p=0·0040). 25 patients (seven taking placebo and 18 taking idalopirdine) discontinued treatment because of adverse events, the difference between groups being mainly due to asymptomatic transient increases in transaminase concentrations in some idalopirdine-treated patients. The most common adverse events (occurring in >3% of patients) were increased γ-glutamyltransferase (14 [10%] patients in the idalopirdine group vs two [2%] in the placebo group), diarrhoea (six [4%] vs nine [7%]), urinary tract infection (three [2%] vs nine [7%]), fall (three [2%] vs eight [6%]), increased alanine aminotransferase (nine [6%] vs none), and benign prostatic hyperplasia (two [5%] vs none). Serious adverse events were reported by 14 (10%) patients in the idalopirdine group and 13 (10%) patients in the placebo group. One death occurred in each treatment group, neither were regarded as being related to treatment. Interpretation: Idalopirdine improved cognitive function in donepezil-treated patients with moderate Alzheimer's disease. Larger studies in a broader population of patients are ongoing to substantiate the effects reported here. Funding: H Lundbeck A/S. © 2014 Elsevier Ltd.

Agency: Cordis | Branch: H2020 | Program: MSCA-ITN-ETN | Phase: MSCA-ITN-2014-ETN | Award Amount: 3.89M | Year: 2015

The human visual brain can learn and adapt to change, which solves many of the problems posed by an ever-changing visual environment. However, to maintain a consistent overall representation of the visual world, the brain also has to retain previously acquired neuronal mechanisms. The key is to strike a balance between plasticity and stability. Increasing our knowledge about the stability and plasticity of the visual brain has tremendous potential for innovation in health care and high-tech industry: 1) rehabilitation, treatments and detection of disease can be developed and refined based on knowing how the brain changes as a result of visual loss or neural dysfunction; 2) it can inspire the development and implementation of artificial intelligence, such as adaptive automated vision systems. However, our present knowledge of the adaptive capacity of the human brain is incomplete and largely qualitative in nature. This limits translation into significant applications. To overcome this, NextGenVis Research Network for training the Next Generation of European Visual Neuroscientists will aim its research and training efforts on teaching young researchers in how to a) acquire new, quantitative knowledge on the adaptive properties of the visual brain in health and disease with a strong focus on the neurocomputational basis and b) apply this new knowledge to boost innovation in health care and technology. Our pan-European team of academic, health care and private sector partners is ideally suited to accomplish this as it bundles and focuses unique European expertise and resources in brain imaging, psychology, neurology, ophthalmology and computer science. Importantly, the positive impact of this network will extend beyond the current focus on vision and will last long after the funding period. It will continue to link together a team of highly skilled researchers who will inspire each other to excel in visual neuroscience and its applications.

Agency: Cordis | Branch: H2020 | Program: RIA | Phase: PHC-03-2015 | Award Amount: 6.00M | Year: 2016

COSYN integrates outstanding European academic and three large Pharma to exploit genomic findings for intellectual disability (ID), autism, and schizophrenia. We capitalise on comorbidity, from clinic to cells and synapses, and have access to large existing samples. We focus on rare genetic variants of strong effect in patients with clinical comorbidity. Our aims are: (1) Understand comorbidity by comparing symptom and syndrome overlap with novel neurobiological criteria; (2) Elucidate mechanisms of comorbidity using neurobiology for the major genomic clue of synaptic dysfunction to unravel the cellular mechanisms of comorbidity; (3) Generate novel neuronal cell models by using advanced technologies to make neurons from carefully selected patients, and use genome editing to create or correct genetic variants. Multiple advanced neuroscience platforms are in place to evaluate an extensive set of molecular and cellular parameters, and to identify alterations in synaptic biology characteristic of ID, autism, and schizophrenia. These cellular models will, with Pharma partners, be up-scaled to provide industry-standard cellular assays for compound screening; (4) Refine diagnostic tools, use novel genomic and cellular features to improve disease classification and discriminate specific patient subtypes; and (5) Case studies in precision medicine: with Pharma partners, identify patients with a genetic change whose consequences can be reproducibly ameliorated in vitro by an approved medication. Recommend to the patient and clinician a double-blinded, N-of-one crossover case study to evaluate the clinical utility of a medication precisely indicated for that person. COSYN is an integrated, state-of-art, bench-to-bedside programme focused on personalised therapeutics. COSYN is a crucial next step in decoding the genetic findings via intensive focus on the clinical and molecular comorbidities of ID, autism, and schizophrenia.

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