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Grant
Agency: Cordis | Branch: FP7 | Program: CP-IP | Phase: NMP-2008-4.0-1 | Award Amount: 6.64M | Year: 2009

NANOFOL proposes to develop a new diagnostic/therapy approach using folate based nanobiodevices (FBN) able to provide a new type of cost efficient treatment for chronic inflammatory diseases such as Atherosclerosis and Rheumatoid Arthritis with low side effects that will constitute a more advantageous solution than current therapies. NANOFOL will achieve all that by fulfilling the following objectives: Design , development and production of nanobiodevices (FBN) targeting directly effector cells Proof of concept in vitro and in vivo of a folate based nanodevice targeting activated macrophages in chronic inflammation not affecting bystander cells Proof of concept in vitro and in vivo of a nanodevice containing a bispecific antibody (against folate receptor and another macrophage marker) targeting activated macrophages in chronic inflammation not affecting bystander cells Proof of concept of FBN delivery therapeutic agents (by small interfering ribonucleic acid molecules (siRNA) or lipophylic molecules) targeting inflammatory signaling pathways In vitro and in vivo testing of cellular toxicity caused by the novel nanobiodevices in cells other than activated macrophages Design of models that will enable to minimize animal experimentation. Development of a strategy to assess potential risks in order to ensure nanobiodevice safe delivery. NANOFOL has adopted a specific risk strategy to attain objectives in a step by step approach allowing improving gradually the concept (specificity, stability, side effects efficacy) from the lower to the higher risky solutions ensuring reduced experimental animal testing and high human safety. The NANOFOL project will combine expertise in nanotechnologies, biology, chemistry, materials science, biotechnology, engineering, risk analysis, medical and pharmaceutical sciences.


Grant
Agency: Cordis | Branch: FP7 | Program: CP-TP | Phase: NMP.2013.4.0-3 | Award Amount: 6.15M | Year: 2014

Early detection of an incipient wound infection is a challenge for the attending physician , since its early diagnosis allows the timely initiation of treatment, thus reducing the severity of the disease . Currently, however, wound infection is not diagnosed until becoming already evident. As a consequence, the treatment of the patient is further complicated and more likely to have a negative outcome4. Often wounds are treated with antibiotics before even the infection appears, leading to overdoses and development of bacterial resistance to antibiotics. Considering that optimal efficiency is reached when a material serves multiple functions without compromise, consortium partners have discovered the means to convert wound dressings into a diagnostic tool capable to inform both patient and therapist about the wound status, thus directing towards the following therapeutic step. The proposed functional materials include a real time diagnostic reaction that positively influences the wound healing due to the timely intervention to treat infection or proteolytic stasis in the wound The novel InFact technology will be translated into a low-cost, real-time diagnostic tool as a constituent part of a wound dressing material, i.e. the triple-P materials concept: - Protective - by a decoy substrate for destructive proteases - Predictive providing a cumulative wound status signal to predict the infection transition - Proactive - changing the dressing according to a signal, rather than on a schedule base, will provide therapeutic response in time, and not too late. More specifically, the functional materials (e.g. absorbent fibres and hydrocolloid pads) will incorporate immobilized substrates for three enzymes: myeloperoxidase, lysozyme and elastase. Upon infection, these enzymatic activities are highly elevated in wound fluids, and can be detected by the color change of the functional materials, visible via a window in the dressing.


Grant
Agency: Cordis | Branch: FP7 | Program: CP-FP | Phase: HEALTH.2011.2.3.1-5 | Award Amount: 3.93M | Year: 2012

Biofilms are bacterial communities encased in a self-produced hydrated polymeric matrix. An important characteristic of microbial biofilms is their innate resistance to the immune system and susceptibility to antibiotics. This resistance has made microbial biofilms a common cause of medical infections, and difficult-to-treat infections caused by colonized foreign bodies. The NOVO project aims at developing novel approaches to prevent and/or degrade biofilms on catheters elongating their usage in humans up to 10 days. Two complementary approaches for biofilm prophylaxis will be developed: A. Ultrasonic coating of Inorganic antibiofouling agents (process developed by partner BIU) based on a single step sonochemical process to: a) Produce metal fluorides or metal oxides (e.g. MgF2, ZnO) nanoparticles (NPs) and simultaneously b) Impregnate them as antibacterial factors on the catheters. c) Co-coating with bio-inert polymer layers (containing highly hydrophilic antifouling polyethylene glycol, zwitterionic moieties or sugar-groups) grafted onto NPs of adjusted size to the size of MgF2/ZnO NPs or directly onto MgF2/ZnO NPs; to form a hydrogel layer for the protection of the MgF2/ZnO antibiofouling activity. B. Bio/organic antibiofouling activation: 1) Novel coating for catheters based on radical catalyzed polymers to yield anti-bacterial activity. An enzymatic reaction will be applied on the phenolic compounds to generate phenolic radicals to be further polymerized on the catheter surface as an antibiofilm agent. 2) Develop and engineer Cellobiose Dehydrogenases (CDH) that actively oxidizes and degrades biofilms polysaccharides concomitantly producing stoichiometrically H2O2 as antibacterial agent. The enzymes will be coated on the catheters via a lubricant or by the Ultrasonic (US) process after their immobilization. Some novel CDH representatives already show very low activity on glucose which should be removed by further genetic engineering.


Grant
Agency: Cordis | Branch: H2020 | Program: RIA | Phase: NMP-06-2015 | Award Amount: 4.99M | Year: 2016

FOLSMART will bring to phase I clinical trials novel folate-based nanodevices (FBN) for the treatment of rheumatoid arthritis (RA). These nanodevices for folic acid (FA)-mediated targeting of activated macrophages showed improved clinical scores in a mouse model of RA when compared to methotrexate (MTX), a first-line drug therapy for the treatment of RA. In this way, FBN will be benchmarked against this drug. MTX has significant associated toxicity and second line biological therapies poses a great economic burden to hospital/public health systems. In parallel, nanodevices encapsulating Sulfasalazine (SSZ), will be tested. SSZ is a second line indication for the treatment of RA, unresponsive to MTX or MTXintolerant patients. Furthermore, FOLSMART propose the optimization of mechanisms for the release of the drugs, through pH and temperature sensitive nanodevices. An exploitation and business plans will be elaborated. In parallel, initial economic evaluation of all proposed treatments will be performed to validate these claims. Specific technological objectives of FOLSMART will be: Good Manufacturing Practice (GMP) production of the FBN based therapies which have been positively bench-marked in the previous FP7 European project NANOFOL in comparison with the use of MTX in a RA mouse model: -Liposomal MTX and SSZ with FA-neck domain peptide as targeting agent -Nanoparticles from HSA-FA/MTX conjugates and SSZ -Optimization of mechanisms of drug release and application to other fields Pre-clinical development on RA models -Toxicology and pharmacokinetics, to determine tolerability and efficacy benefit in two animal models rat and dog, under Good Laboratory Practice (GLP) standards -Genotoxicity and Carcinogenicity Phase I clinical trials of the best therapies bench marketed against MTX -Nanodevices with MTX and SSZ will offer improved tolerance and greater efficacy meaning that patients who do not do well on MTX will have cost-effective alternatives


Grant
Agency: Cordis | Branch: FP7 | Program: CP-FP | Phase: HEALTH.2012.2.4.5-1 | Award Amount: 7.41M | Year: 2012

The visual pathway is a component of the central nervous system (CNS) and therefore is not regenerative. Acute optic nerve injury, ischemic optic neuropathy and glaucoma are conditions that initially lead to partial blindness and eventually could lead to total blindness. Extensive neuron and retinal ganglion cells (RGC) death is evidenced in these pathologies. Semaphorin 3A (Sema3A) is a cell secreted protein that participates in the axonal guidance pathways. Partner TAU was the first to show that Sema-3A is also capable of inducing neuronal cell death. Elevated levels of Sema3A were than found in glaucoma. TAU further showed the viscous role of Sema3a that is mediating the vast RCG apoptosis following optic nerve injury. Importantly, marked inhibition of RGC loss was achieved when axotomized eyes were co-treated by intravitreous injection of antibodies against the Sema3A providing the proof of concept for the therapeutic approach to inhibit the Sema3A pathway following optic nerve injury. This concept was recently validated by partner SIC who developed a small molecule weight inhibitor of Sema3A and showed that this inhibitor promotes neural regeneration of damaged axons. Acute or chronic assault to neural cells create an immediate death of part of the population and a signal for further death of the remaining cells close to the damaged area. The project goal is to develop a therapeutic approach to stop further death of neural cells by providing prolonged inhibition of the apopototic pathway of Sema-3A using antibody targeted to this protein or a low MW inhibitor of sema3A. The Sema3A inhibitors would be constantly released from a novel intraocular biodegradable implant. The clinical efficacy of this approach will be evaluated in two common devastating pathologies: optic nerve injury and glaucoma.


Grant
Agency: Cordis | Branch: FP7 | Program: MC-ITN | Phase: FP7-PEOPLE-2012-ITN | Award Amount: 3.76M | Year: 2012

The ITN TIMCC brings together eight expert teams from different disciplines within Immunology, Genetics and Oncology, to provide substantive and methodological training in the analysis of the role of the Tumor Infiltrating Myeloid Cell Compartment (TIMCC) of the innate immune system. Leukocytes recruited to (pre)malignant tissues are mainly myeloid cells. They can either prevent or functionally contribute to cancer development. However, the mechanisms underlying pro- versus anti-tumor programming of neoplastic tissues by these immune cells remain obscure. The ITN TIMCC aims to improve anti-tumor therapy by defining general and tumor type specific molecular and cellular immunological pathways (e.g signal transduction and downstream effector pathways) in tumor development and during therapeutic intervention based on an extensive analysis of the infiltrating myeloid cell compartment in human tumor biopsies using a large variety of techniques and functional analysis of the corresponding models of a variety of human tumors, affecting different organs, in a unique cohort of genetically modified mice treated with different types of anti-tumor therapy. The program will train the appointed researchers in a variety of methodology and technology from genomic technologies and bioinformatics via genetically modified mice to the design and application of therapeutic strategies to understand and manipulate the many interactions of the myeloid cell compartment with developing tumors. By defining underlying molecular and cellular pathways new targets will be identified to be explored by the participating SMEs. The program will deliver young researchers equipped with a broad knowledge in immunology, genetics and oncology and insight in the complexity of translational medicine therefore better prepared to meet new challenges in the field.


Patent
Synovo GmbH | Date: 2012-08-15

A method of treating cancer in which a compound that inhibits the expression, production or release of IL-10 by immune cells is combined with a compound that stimulates the production of IL-12 when given in combination with, or in the presence of TNFa. Said method is effective when provided in addition to standard therapies, notably chemotherapy using cytotoxic drugs and other forms of immune therapy including therapeutic vaccines.


Patent
Synovo GmbH | Date: 2010-07-30

The invention features novel macrocyclic compounds, methods of making the compounds, pharmaceutical compositions including the compounds, and methods of treatment using the compounds.


Patent
Synovo Gmbh | Date: 2011-10-10

The invention provides novel compounds and compositions and methods for making and using the compounds and compositions.


Patent
Synovo GmbH | Date: 2014-03-28

Compounds of the substituted pyrazole class as treatments for cancer are reported. A method of treating cancer in which a compound that inhibits the activity of receptor kinases. Said method is effective and can be provided in addition to standard therapies, notably chemotherapy using cytotoxic drugs and other forms of immune therapy including therapeutic vaccines.

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