Trophos is a biopharmaceutical company specialising in the discovery and development of novel therapeutics to treat both orphan neurodegenerative diseases and more prevalent disorders.Trophos was founded in 1999 in Marseille by three scientists, Christopher Henderson, Olivier Pourquie and Jean-Louis Kraus and two entrepreneurs, Antoine Beret and Michel Delaage. Trophos' lead compound is TRO19622 / olesoxime,.. Olesoxime is a mitochondrial targeted compound, which will be established as first of a new class of therapeutic agents aimed at bringing significant therapeutic benefit to patients suffering from devastating neurological diseases. Spinal Muscular Atrophy is an autosomal recessive genetic disease that affects the motor neurons of the voluntary muscles used for activities such as crawling, walking, head and neck control and swallowing. SMA affects approximately 20,000 people worldwide. One in every 6,000 babies is born with SMA. It is the number one genetic cause of death in children under the age of two. Results from an international, double-blind, placebo-controlled phase II study involving 165 type II and non-ambulatory type III SMA patients, completed in February 2014 to assess safety and efficacy of olesoxime were recently released. The data shows that patients treated with olesoxime were able to maintain motor function over the two-year period of the study and that typical health complications associated with SMA occurred less frequently than in patients treated with a placebo, leading to better well being.In January 2015, the firm was acquired by Hoffmann-La Roche. Wikipedia.


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Grant
Agency: Cordis | Branch: FP7 | Program: CP-FP | Phase: HEALTH-2007-2.2.1-7 | Award Amount: 10.33M | Year: 2009

Mitochondrial dysfunction is a major hallmark of various neurodegenerative disorders including Alzheimers disease, Parkinsons disease, Huntingtons diseases or Amyotrophic Lateral Sclerosis (ALS). However linking mitochondrial dysfunction to the pathogenesis of some of these diseases still needs to be elucidated. Furthermore, in pathologies where this link is already established, the question remains whether specific targets or mechanisms involved in mitochondrial dysfunction will be amenable to therapeutic intervention. MitoTarget is an ambitious project aimed at providing solid data to better understand and exploit the circumstantial evidence linking mitochondrial dysfunction with neuronal dysfunction culminating in neurodegenerative disease. A 36 months translational research program will bring together a unique partnership between basic scientists, a seasoned team of clinical investigators and a SME that has identified a first-in-class compound, TRO19622, that targets mitochondria and has powerful neuroprotective and neuroregenerative activities. In parallel, and orchestrated by the SME that is the coordinator of the project, MitoTarget will bring together a more comprehensive insight into the mechanisms leading to mitochondrial impairments and establish their clinical relevance in a severe orphan neurodegenerative disease, ALS. If successful, it is expected that from this proof of principle a new class of therapeutic agents targeting the underlying mitochondrial dysfunction in neurons or their supporting cells will emerge. Results of the project have the potential to create a new paradigm for the drug discovery for neurodegenerative diseases.


Grant
Agency: Cordis | Branch: FP7 | Program: CP-FP | Phase: HEALTH-2009-2.4.4-1 | Award Amount: 8.05M | Year: 2010

The Collaborative Project on Mendelian Forms of Parkinsons Disease (MEFOPA) will bring together the major groups in Europe with a track-record in basic and clinical research on rare Mendelian forms of Parkinsons disease (PD) in order to identify and validate relevant disease-related molecular pathways, drug-targets and biomarkers for disease susceptibility and progression.. Over the last years it has become increasingly clear that progress in the understanding of the molecular basis of PD, the second most common neurodegenerative disorder, and hence the chance to develop effective disease-modifying treatments, will most likely be brought about by focusing on the rare variants of the disease with known genetic defects. The groups forming the MEFOPA-consortium will therefore analyze the molecular pathways underlying inherited forms of PD with autosomal-dominant and autosomal-recessive inheritance in an integrative way, using cellular and animal models and cutting-edge technology. These two subprojects will provide targets for novel, disease-modifying treatment strategies. In a third subproject, a European registry and biobank for patients with rare Mendelian forms of PD will be established. Body fluids will be collected and systematically analyzed by unbiased proteomic techniques as well as by focussed analysis of candidate proteins, and ex vivo cellular models will be generated, in order to allow validation of disease-related alterations detected in the models analyzed in subprojects 1 and 2. Through this integrated, translational approach combining basic and clinical research groups, the project aims to achieve measurable progress in defining the relevant targets and readouts for disease-modifying therapies and will set the stage for rationally designed drug trials in carefully selected groups of patients and even presymptomatic mutation carriers.


Grant
Agency: Cordis | Branch: FP7 | Program: CP-FP | Phase: HEALTH.2010.2.4.2-2 | Award Amount: 8.19M | Year: 2011

Current interventional treatment of acute myocardial infarction (AMI) focused on re-establishing cardiac reperfusion has significantly improved clinical outcome by reducing infarct size and mortality due to cardiac ischemia.It is now recognized that events triggered at reperfusion also result in cell death and may account for as much as 50% of the infarct volume, this being termed ischemia-reperfusion injury (IRI). Mitochondrial permeability transition pore (mPTP) opening appears to be a responsible for IRI and a recent small clinical trial with cyclosporine A shows that it is a feasible target for the development of new therapies to treat it. Since total infarct size is a major determinant of a patients risk to develop heart failure, treating IRI is expected to further reduce morbidity, mortality and the need for regenerative medicine following cardiac ischemia. By harnessing a multi-disciplinary consortium of clinical and basic scientists along with four SMEs, MitoCare brings state-of-the art expertise together to 1) better understand IRI pathophysiology and factors directly or indirectly influencing patients recovery or response to treatment; 2) investigate the translational usefulness of preclinical models; and 3) compare selected treatments. These objectives will be reached through the following work plan: A) a medium-scale phase II clinical study will evaluate the efficacy of a novel complementary therapy to PCI, the new mPTP modulator TRO40303, while at the same time 1) perform extensive sampling from subjects in the study for analysis of standard and emerging biomarkers; 2) identify confounding factors influencing patients outcomes. B) Parallel investigations in preclinical in vitro and in vivo AMI models. C) Statistical analysis of data from clinical and preclinical studies, to identify better diagnostic and prognostic endpoints in man and assess predictive utility of preclinical models.


Grant
Agency: Cordis | Branch: FP7 | Program: CP-FP | Phase: HEALTH-2009-2.4.4-1 | Award Amount: 9.25M | Year: 2010

Leukodystrophies (LDs) are inherited rare neurodegenerative diseases of the white matter and its main component, the myelin, that are affecting predominantly children. Severity of the disease is related to the axonal dysfunction due to myelin deficiency or destruction. Despite the achievement of remarkable advances made in the past decade, there is no current curative therapy. The development of therapeutic approaches for myelin repair and neuroprotection constitutes the main objective of the LeukoTreat project. Indeed LDs constitute prototypic pathologies to tackle myelin formation/destruction issues as well as glial cells dysfunctions in neurodegeneration. The global aim is to promote the development of therapeutic strategies for the largest number of LD affected patients and further applications to more common white matter disorders and finally neurodegenerative diseases. For this purpose, the project will combine the expertise of (i) recognized European research teams in the field of White Matter diseases (COST Myelinet), (ii) high-technology SMEs, (iii) experts in medical ethics and (iv) LD patients and families associations. To develop efficient therapies, the LeukoTreat project is based on 5 complementary approaches consisting in: (i) collecting information on the epidemiology, the natural history, the genotype/phenotype correlation of LDs for at least 500 patients; (ii) validating/identifying biomarkers for therapeutic decisions/follow up to isolate new therapeutic targets; (iii) developing pharmacological strategies with the ultimate objective to launch at least 4 pharmacological clinical trials during 5 years following the project; (iv) developing innovative gene and cell therapies with the ultimate objective to launch at least 3 clinical trials during the next 5 years; (v) tackling ethical impacts of the proposed therapeutic challenges by integrating the participation of patients driven by a well-experienced research team strongly skilled in ethics


The object of the invention is the use as a drug of a compound fitting formula I


A method for providing neuroprotection to a patient in need of neuroprotection, comprising administering a neuroprotective-effective amount of a compound of formula I


The present invention relates to a novel galenic form of cholesterol derivative. More particularly the invention relates to liposomes comprising at least one cholesterol derivative and compositions comprising said liposomes.


Patent
Trophos | Date: 2012-08-22

A method for providing neuroprotection to a patient in need of neuroprotection, comprising administering a neuroprotective-effective amount of a compound of formula I in which X is an oxygen atom or an =NOH group, R is selected from the group consisting of A is a hydrogen atom or together with B a carbon-carbon bond, B is a hydrogen atom, a hydroxy group or together with A a carbon-carbon bond, C is a hydrogen atom or together with D a carbon-carbon bond, D is a hydrogen atom or together with C a carbon-carbon bond, E is a hydrogen atom or together with F a carbon-carbon bond, F is a hydrogen atom or together with E a carbon-carbon bond, or an addition salt with a pharmaceutically acceptable acid.


The present invention relates to a novel galenic form of cholesterol derivative. More particularly the invention relates to liposomes comprising at least one cholesterol derivative and compositions comprising said liposomes.


The object of the invention is the use as a drug of a compound fitting formula I wherein X represents an oxygen atom or a NOH group and R represents a group selected from

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