Leuven, Belgium
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Patent
Remynd Nv | Date: 2015-03-17

The present invention relates to a compound of formula (I) or (II) or a stereoisomer, enantiomer, racemic, or tautomer thereof, (I) (II) wherein R^(1), R^(2), R^(3), L^(1), L^(2), L^(3), L^(4), L^(5 )and n, have the same meaning as that defined in the claims and the description. The present invention also relates to compositions, in particular pharmaceuticals, comprising such compounds, and to uses of such compounds and compositions for the prevention and/or treatment of metabolic disorders and/or neurodegenerative diseases, and/or protein misfolding disorders.


Patent
reMYND NV | Date: 2017-01-25

The present invention relates to a compound of formula (I) or (II) or a stereoisomer, enantiomer, racemic, or tautomer thereof, (I) (II) wherein R1,R2,R3,L1,L2,L3,L4,L5 and n, have the same meaning as that defined in the claims and the description. The present invention also relates to compositions, in particular pharmaceuticals, comprising such compounds, and to uses of such compounds and compositions for the prevention and/or treatment of metabolic disorders and/or neurodegenerative diseases, and/or protein misfolding disorders.


Patent
reMYND NV | Date: 2017-01-25

The present invention relates to a compound of formula (I) or a stereoisomer, enantiomer, racemic, or tautomer thereof, Formula (I), wherein R1, R3, R4, L1, L2, L3, L4, and n, have the same meaning as that defined in the claims and the description. The present invention also relates to compositions, in particular pharmaceuticals, comprising such compounds, and to uses of such compounds and compositions for the prevention and/or treatment of metabolic disorders and/or neurodegenerative diseases, and/or protein misfolding disorders.


Grant
Agency: European Commission | Branch: FP7 | Program: MC-ITN | Phase: FP7-PEOPLE-2011-ITN | Award Amount: 3.95M | Year: 2012

Brain disorders impose an increasing economical and social burden in the member states of the European Union (EU). For most neurodegenerative diseases and many neuropsychiatric disorders no efficient treatment is available and no cure exists. In the next coming years the number of particularly elderly people suffering from brain disorders will tremendously increase. Predictions from the turn of the century about the exponential increase of dementia patients turned out to be correct and Alzheimers disease alone is underway to become the most expensive and most pressing health problem in the EU. The complexity of these diseases requires a more integrative view of the multiple interactions between genes and environment, synaptic processes and neuronal cicuitry. This is, however, not only achieved by training more young scientists in the relevant disciplines. The plastic properties of the brain can only be exploited by scientists that are trained to deal with this complexity and that are familiar with state of the art technology as well as with the principles at different levels of analysis. In consequence it is advisable for a training network to study more than one disease and to train scientists with a wide range of skills and background knowledge. The NPlast consortium consists of four partners from the private and seven partners from the public sector and will provide a research training program for fifteen young scientists. The program covers a broad spectrum of disorders and interventions ranging from synaptopathies and trafficking deficiencies to Alzheimers disease, and from altering gene expression programs to manipulations of the extracellular matrix of the brain to preserve or restore synaptic function. The key objective of the NPlast training network is to investigate neuroplastic principles that can preserve or restore function and that can be used to rejuvenitate the brain in the elderly as well as to treat neuropsychiatric conditions in adults.


Grant
Agency: European Commission | Branch: FP7 | Program: CP-FP | Phase: HEALTH.2012.2.2.2-1 | Award Amount: 8.22M | Year: 2013

In spite of valuable approaches applied to get a broad understanding of genetic, epidemiologic and molecular and system-level biological principles of human aging, cognitive decline remains as one of the greatest health challenges of the old age, with nearly 50% of adults over 85 afflicted of Alzheimers disease. Furthermore, drug development has not performed as expected in clinical trials, at least in part because of an insufficient mechanistic understanding at the systemic level in human. AgedBrainSYSBIO is a timely and straightforward project based on the integration of available transcriptomics, proteomics and metabolomics data, addition of relevant novel sets of data, their modeling and experimental testing in both human, mouse and drosophila. The concept is to identify subsets of pathways with two unique druggable hallmarks: (i) the validation of interactions occurring locally in subregions of neurons and (ii) a human and/or primate accelerated evolutionary signature, using six interacting approaches: (1) the identification of interacting protein networks from recent Late-Onset Alzheimer Disease- Genome Wide Association Studies (LOAD-GWAS) data, (2) the experimental validation of interconnected networks working in subregion of a neuron (such as dendrites and dendritic spines), (3) the inclusion of these experimentally validated networks in larger networks obtained from available databases to extend possible protein interactions, (4) the identification of human and/or primate positive selection either in coding or in regulatory gene sequences,(5) the manipulation of these human and/or primate accelerated evolutionary interacting proteins in human neurons derived from induced Pluripotent Stem Cells (iPSCs) and modeling prediction challenged in drosophila and novel mouse transgenic models. This work will finally allow (6) the validation of new druggable targets and markers as a proof-of-concept towards the prevention and cure of aging cognitive defects.


Grant
Agency: European Commission | Branch: H2020 | Program: RIA | Phase: NMP-12-2015 | Award Amount: 7.78M | Year: 2016

Alzheimers disease (AD) is the leading cause of dementia and loss of autonomy in the elderly, implying a progressive cognitive decline and limitation of social activities. Progressive aging of EU population will increase the magnitude of this problem in the next decades. Currently, there is not an effective method for the early diagnosis of AD. Therefore, there is an urgent need to develop new effective early diagnostic and therapeutic strategies to help in delaying the appearance of the most adverse symptoms of this disease. To defeat this challenge, PANA project bases its approach on the importance of tau oligomers in the early pathophysiological processes of AD. The effective strategy will be based on two fundamental pillars; on one hand, efforts will be focused on multimodal PET/MRI imaging which is gaining relevance as the best solution for diagnostic purposes due to the complementary advantages of both technologies, combining the high structural characterization of tissue provided by MRI with the enhanced sensitivity of PET imaging. On the other hand, the challenging development of a theragnostic nanostructures will be focused on tau oligomers detection, which would have to deliver theragnostic agents into the brain to provide in situ diagnostic and therapeutic effects. Therefore, PANA project focuses on developing theranostic nanostructures that specifically recognize very-early molecular markers of AD, and can be detected by means of non-invasive imaging methodologies (MRI and/or PET, which are already common techniques accessible in most hospitals) and eventually provide a therapeutic action if needed. To achieve this goal, we propose a unique consortium which combines neuroscientists, nanotechnologists, molecular imaging experts, clinicians and Small/Medium/Large Enterprises in an effort to use smart nanoparticles engineered with multifunctional biomaterial to provide new very-early diagnostic tools for AD, a vital medical/social problem in EU.


The present invention relates to a compound of formula (IA), wherein G^(1 )is lower alkyl; lower alkyl substituted by one or more halogens; cycloalkyl; tetrahydropyran-4-yl; phenethyl; phenethyl substituted by one or more halogens; phenoxymethyl; phenoxymethyl substituted by one or more halogens; benzyloxyethyl; benzyloxy-ethyl substituted by one or more halogens; or is NR^(2)R^(3); R^(2 )is hydrogen or lower alkyl; R^(3 )is lower alkyl; tetrahydropyran-4-yl; CH_(2)-cycloalkyl; or cycloalkyl optionally substituted by lower alkyl substituted by one or more halogens; or R^(2 )and R^(3 )form together with the N-atom to which they are attached a heterocycloalkyl group with 4 or 5 carbon atoms, which is optionally substituted by one or more substituents selected from halogen; or lower alkyl substituted by one or more halogens; X is CH_(2) or (CH_(2))_(2); Ar is phenyl or pyridinyl; R^(4 )is halogen; lower alkyl; lower alkyl substituted by one or more halogens; or lower alkoxy; n is 1 or 2; or to a pharmaceutically active salt thereof, to a stereoisomeric form, including an individual diastereoisomer or enantiomer of the compound of formula (IA) as well as to a racemic or non-racemic mixture thereof. The present invention also relates to the use of a compound of formula (IA) for treating certain neurodegenerative disorders characterized by cytotoxic TAU misfolding and/or aggregation.


The present invention relates to a compound of formula (IA), wherein G^(1 )is lower alkyl; lower alkyl substituted by one or more halogens; cycloalkyl; tetrahydropyran-4-yl; phenethyl; phenethyl substituted by one or more halogens; phenoxymethyl; phenoxymethyl substituted by one or more halogens; benzyloxyethyl; benzyloxy-ethyl substituted by one or more halogens; or is NR^(2)R^(3); R^(2 )is hydrogen or lower alkyl; R^(3 )is lower alkyl; tetrahydropyran-4-yl; CH_(2)-cycloalkyl; or cycloalkyl optionally substituted by lower alkyl substituted by one or more halogens; or R^(2 )and R^(3 )form together with the N-atom to which they are attached a heterocycloalkyl group with 4 or 5 carbon atoms, which is optionally substituted by one or more substituents selected from halogen; or lower alkyl substituted by one or more halogens; X is CH_(2) or (CH_(2))_(2); Ar is phenyl or pyridinyl; R^(4 )is halogen; lower alkyl; lower alkyl substituted by one or more halogens; or lower alkoxy; n is 1 or 2; or to a pharmaceutically active salt thereof, to a stereoisomeric form, including an individual diastereoisomer or enantiomer of the compound of formula (IA) as well as to a racemic or non-racemic mixture thereof. The present invention also relates to the use of a compound of formula (IA) for treating certain neurodegenerative disorders characterized by cytotoxic TAU misfolding and/or aggregation.


Patent
Remynd Nv | Date: 2015-03-17

The present invention relates to a compound of formula (I) or a stereoisomer, enantiomer, racemic, or tautomer thereof, Formula (I), wherein R^(1), R^(3), R^(4), L^(1), L^(2), L^(3), L^(4), and n, have the same meaning as that defined in the claims and the description. The present invention also relates to compositions, in particular pharmaceuticals, comprising such compounds, and to uses of such compounds and compositions for the prevention and/or treatment of metabolic disorders and/or neurodegenerative diseases, and/or protein misfolding disorders.


The present invention relates to a compound of formula (IA) The present invention also relates to the use of the compound of formula IA for treating certain neurodegenerative disorders characterized by cytotoxic TAU misfolding and/or aggregation.

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