Projects

Project title:  Mast cells as effectors in hemorrhage and acute cardiovascular diseases. (2024-2026)

Funding: ERA.Net COFUND

Promotor: Ilze Bot

co-promotor: Guido De Meyer, Florent Ginhoux

Project: Development of a pancreatic cancer drug-nanocarrier system selectively targeting tumour cells and tumour stroma to overcome treatment failure (2023-2027)

Funding: ERA.Net COFUND

Funding: FWO TBM

Beneficaries: Didier Ebo, Vito Sabato, Jessy Elst, Margo Hagendorens

Abstract: Elastin is responsible for the elasticity of the vessel wall, but due to repetitive stretches and relaxations as we age, it will fracture, leading to arterial stiffness and the release of soluble elastin-derived peptides (EDPs). Some of these EDPs are biologically active by interacting with the elastin receptor complex (ERC) and can play a role in the development of cardiovascular disease (CVD). Existing literature points towards a decline in autophagy by EDPs. Autophagy is a protective mechanism, that recycles damaged cell products into building blocks that are used to maintain cellular health. Lower autophagy levels can contribute to CVD. If EDPs can reduce autophagy, this might be an important mechanism by which they exert their detrimental effects. Therefore, we would like to investigate whether EDPs can reduce autophagy and how this affects arterial stiffness and CVD. This will answer three research questions: (1) Can EDPs affect cellular function and lead to autophagy deficiency in vascular cells? (2) What is the role of ERC signalling in the progression of arterial stiffness and is autophagy deficiency responsible for the observed effects? (3) Can ERC signalling enhance atherogenesis and is autophagy deficiency responsible for the observed effects? Overall, this research plan aims to better understand the role of EDPs in autophagy decline, vascular ageing and arterial stiffness in order to prevent or slow down this process and to improve quality of life.

Funding: FWO junior research project (2023-2026)

Promoter: Roth Lynn

Abstract: Morphological studies indicate that the vast majority of dying cells in advanced human atherosclerotic plaques undergo necrosis. Although the role of necrosis in atherosclerosis remains ill-defined, a growing body of evidence suggests that necrotic death stimulates atherogenesis and plaque instability through induction of inflammation and enlargement of a central necrotic core. For a long time, necrosis in advanced plaques has been considered as a merely accidental and uncontrolled form of cell death, but recent data indicate that it can also occur in a regulated fashion through induction of necroptosis. However, it should be noted that other examples of regulated necrosis such as ferroptosis are emerging. Moreover, gasdermins have recently been identified as essential effector molecules in different types of programmed necrosis by forming pores in the plasma membrane. Because regulated necrosis is considered an important pharmacological target to stabilize plaques, the following objectives are defined: (1) identification of ferroptosis and gasdermin E-mediated necrosis in both human and mouse plaques, (2) inhibition of both processes via genetic or pharmacological approaches, and (3) characterization of autophagy as a natural defense mechanism against necrosis in atherosclerosis. This project may lead to the discovery of novel anti-atherosclerosis therapies, and will allow a significant advance in the fundamental understanding of regulated necrosis in atherosclerosis.

Funding: FWO senior research project (2023-2026)

• Promoter: Martinet Wim
• Co-promoter: De Meyer Guido

Project: Innovative cell death diagnostics allowing stratifying critically ill patients for novel ferroptosis or pyroptosis intervention strategies​

Funding: BOF-IMPULS (2023-2026)

Promoter: Vanden Berghe Tom

Co-promoter: Jorens Philippe

Co-promoter: Koljenovic Senada

Project: Protease‐guided tumor targeting tools to revolutionize cancer diagnosis and treatment. OncoProTools will deliver a training program that truly captures the MSCA values to 10 Doctoral Candidates. They will benefit from an international, interdisciplinary an intersectoral network and will be provided with all capabilities to become leaders of tomorrow's R&I in patient-centered oncotherapy and diagnostics.

Funding: HORIZON MSCA Doctoral Network (2022-2026)

Coordinator: Prof. Pieter Van der Veken (UAMC, UAntwerp)

Beneficiaries: University of Antwerp, University of Copenhagen, HZDR, JG-University of Mainz, University of Lisboa, CSIC and the companies CROmed and CellPly. 

https://www.uantwerpen.be/en/projects/protease-guided-tumor-targeting-tools/

Project: Upon gastrointestinal and reproductive homeostasis, there is an intimate crosstalk between mucins (MUCs) and the microbiome at the mucosal surface to maintain barrier integrity but a disbalance between both actors could dictate disease development, such as inflammatory bowel diseases (IBD) and aerobic vaginitis (AV). Indeed, thinning of the epithelium and aberrant MUC1 and MUC13 expression have been associated with barrier dysfunction in IBD. Also MUC1 seems to be increasingly expressed upon vaginal infection. Such defective mucus layer will thus allow microbiota to come in close contact with these mucins and co-elicit inflammation and mucosal damage. Nevertheless, which microbes interact with MUC1 and MUC13 in response to inflammation and dysbiosis and mediate barrier dysfunction in IBD and AV remains poorly understood. Therefore, we will first characterize microbiome diversity and function in IBD and AV using shotgun metagenomic sequencing. In parallel, we will also unravel the MUC1 and MUC13 mRNA isoform landscape using targeted isoform sequencing. Combining both sequencing data will allow to identify microbial-mucin isoform associations in IBD and AV. Finally, we will investigate the mechanism(s) by which abundant microbial species in IBD and AV interact with the aberrantly expressed MUC1 and MUC13 isoforms resulting in barrier dysfunction. To do so, bacterial mutant approaches and human epithelial organoid cultures established from IBD and AV samples will be used.

Funding: Research Fund Flanders

Researchers: Annemieke Smet (PI), Hannah Ceuleers (co-PI), Sarah Lebeer (co-PI) 

Project: Despite exercise being our oldest and most efficacious medicine, animal and human data suggest that excessive exercise may contribute to pathological cardiac remodelling in some, resulting in increased susceptibility for atrial and ventricular arrhythmias and sudden cardiac death. One hallmark of this pathological remodelling is the development of myocardial fibrosis (MF). In two specific types of MF in athletes (i.e. insertion point MF and right ventricular fibrosis in the context of arrhythmogenic cardiomyopathy), exercise contributes as a causal factor. We hypothesise that exercise also contributes to the development of MF in the left ventricle after (silent) myocarditis, which could explain its higher incidence in athletes. We will verify this hypothesis in a murine coxsackie B virus-induced myocarditis and exercise model. MF will be evaluated by standard histology, as well as by whole mount 3D microscopic imaging. Further, innovative serial multiplex immunohistochemistry (IHC) will be used for detailed cellular and molecular phenotyping, providing unrivalled insights into (patho)physiological remodelling during myocaditis. In addition, the modulating effect of NSAIDs will be evaluated. In parallel, clinical studies are conducted to gain insight into the aetiology and evolution of MF in athletes. Ultimately, our results will contribute to the development of guidelines on safe sport participation and NSAIDs use in the setting of viral syndromes.

Funding: Research Fund Flanders (FWO)

Researchers: Hein Heidbuchel (PI), Pieter-Jan Guns (co-PI), Tanja Roskam (KULeuven)

Project: The success of transplantation is hampered by a shortage in suitable organ grafts and the adverse effects of ischemia reperfusion injury (IRI). Inflammation and cell death in the transplanted organ, caused by the activation of the innate immune system as part of the IRI process, leads to primary graft dysfunction (PGD). Transplant recipients that suffer from severe PGD have an increased risk for early and late morbidity and mortality. The organ perfusion strategy was developed to increase the number of available grafts. During the ex situ phase between organ retrieval and transplantation, machine perfusion offers a unique window of opportunity for organ graft modulation to target IRI due to ferroptosis. Ferroptosis is an iron-dependent type of cell death in which oxidative stress initiates excessive lipid peroxidation of cellular membranes leading to cell death. Our in-house developed and patented third generation ferroptosis inhibitors show superior protection in preclinical models of organ injury and are therefore good drug candidates to block injury during transplantation. In this project, we will firstly verify the efficacy of the lead ferroptosis inhibitor in protecting against ferroptosis using genetic organ injury models along experimental IRI or transplantation models in rodents. We will focus on liver, kidney and lungs as vital organs. Secondly, we will analyse the efficacy of adding our lead ferroptosis inhibitor to perfusate during normothermic machine perfusion preceding ex situ reperfusion in pigs. In parallel, we will evaluate the potential of ferroptosis inhibitors to recondition human organ grafts. This research plan is a first step to implement ferroptosis inhibitory strategies in the clinical practice of transplantation, which is a stepping-stone for building a spin-off case in ferroptosis therapeutics.

Funding: FWO-SBO

Researchers:

Principal investigator: Tom Vanden Berghe

Co-principal investigators: Koen Augustyns (UAntwerpen), Arne Neyrinck, Jacques Pirenne (KULeuven)

Project: OneHealth Drugs against parasitic vector borne diseases in Europe and beyond (CA21111).

Funding: Horizon Europe

Beneficiaries: Guy Caljon (LMPH), Yann Sterckx (LMB)

Project: The success of transplantation is hampered by a shortage in suitable organ grafts and the adverse effects of ischemia reperfusion injury (IRI). Inflammation and cell death in the transplanted organ, caused by the activation of the innate immune system as part of the IRI process, leads to primary graft dysfunction (PGD). Transplant recipients that suffer from severe PGD have an increased risk for early and late morbidity and mortality. The organ perfusion strategy was developed to increase the number of available grafts. During the ex situ phase between organ retrieval and transplantation, machine perfusion offers a unique window of opportunity for organ graft modulation to target IRI due to ferroptosis. Ferroptosis is an iron-dependent type of cell death in which oxidative stress initiates excessive lipid peroxidation of cellular membranes leading to cell death. Our in-house developed and patented third generation ferroptosis inhibitors show superior protection in preclinical models of organ injury and are therefore good drug candidates to block injury during transplantation. In this project, we will firstly verify the efficacy of the lead ferroptosis inhibitor in protecting against ferroptosis using genetic organ injury models along experimental IRI or transplantation models in rodents. We will focus on liver, kidney and lungs as vital organs. Secondly, we will analyse the efficacy of adding our lead ferroptosis inhibitor to perfusate during normothermic machine perfusion preceding ex situ reperfusion in pigs. In parallel, we will evaluate the potential of ferroptosis inhibitors to recondition human organ grafts. This research plan is a first step to implement ferroptosis inhibitory strategies in the clinical practice of transplantation, which is a stepping-stone for building a spin-off case in ferroptosis therapeutics.

Funding: FWO-SBO

Researchers:

Principal investigator: Peter Vandenabeele (VIB-UGent)

Co-principal investigators: Mohamed Lamkanfi (UGent), Jonathan Maelfait (UGent), Mathieu Bertrand (UGent), Koen Augustyns (UAntwerpen), Tom Vanden Berghe (UAntwerpen), Wouter Coppieters (ULiège), Emmanuel Dejardin (ULiège), Michel Moutschen (ULiège), Raffaella Gozzelino (ULisbon), Matthias Heikenwälder (German Cancer Research Center), Denis Lafontaine (ULB). 

Project: Atrial fibrillation (AF) is the most common arrhythmia and a common cause of stroke, heart failure, and death. AF is induced by structural remodeling of the atria, also called atrial myopathy. Current therapy is limited to antiarrhythmic drugs and ablations, but these do not cure the disease. Since atrial myopathy is incompletely understood, we aim to define the molecular, cellular, and structural changes in atrial myopathy. To this end, we will use single-cell RNA sequencing and high-resolution microscopy on a pig model and on human atrial tissues. To integrate these diverse data sets and test their relationships in atrial myopathy that predisposes the tissue to AF, mathematical modelling approaches will be employed. Collectively, these versatile models will create a highly anticipated foundation for various applications, stretching from disease modeling to testing novel strategies for development of curative therapies for an ever-growing group of patients with AF.

Funding: iBOF

Researchers:

Principal investigator: Hein Heidbüchel

Co-principal investigators: Gilles De Keulenaer, Vincent Segers (UAntwerpen), Roderick Llewelyn, Peter Haemers (KULeuven), Nele Vandersickel (UGent)

Project: Autophagy is crucial in the (patho)physiology, including inflammation, infection and cancer. Autophagy functions as a survival mechanism by maintaining viability during periods of stress, and by removing damaged organelles and toxic metabolites, such as protein aggregates or intracellular pathogens. The Atlantis research consortium (AuTophagy in InfLAmmatioN and inflammaTory dISorders) brings together a team of expert investigators from the complementary fields of autophagy, (cancer) cell death signaling, inflammation signaling, angiogenesis and atherosclerosis, and drug screening and medicinal chemistry. We will study in an integrated way the impact of autophagy and its pharmacological modulation in various vascular diseases with a focus on the endothelium and its functional interaction with immune cells in sepsis, tumor-driven (lymph)angiogenesis, and atherosclerosis.

Funding: BOF

Researchers:

Principal investigator: Peter Vandenabeele (VIB-UGent)

Co-principal investigators: Claude Libert, Mathieu Bertrand (UGent), Guido De Meyer, Wim Martinet, Pieter Van der Veken (UAntwerpen), Patrizia Agostinis, Gabriele Berger( KU Leuven)

Project: Preliminary evidence shows that the enzyme dipeptidyl peptidase 9 (DPP9), which is present in macrophages, plays a role in controlling the inflammatory response and associated cell death. Inflammation is a normal response of tissues against infections, chemical insults and physical injuries. However, in some cases, it becomes chronic and causes harm. A better understanding of the inflammatory process provides new therapeutic opportunities. In this project, we will focus on the role of the intracellular protease DPP9 in macrophages derived from human white blood cells. The crystal structure of DPP9 was recently solved, and can now be used to design DPP9 inhibitors. We will develop selective and potent DPP9 inhibitors and substrates. We will also engineer the human THP-1 cell line to eliminate DPP9. Using the DPP9 inhibitors and engineered cell lines, we will determine under which conditions DPP9 plays a key role in macrophage function. Finally, the molecular binding partners of DPP9 will be identified. We will look for natural substrates as well as non-substrate interaction partners of DPP9 in macrophages. The interactions will be characterized at the molecular level. Our fundamental biochemical findings and novel chemical tools will significantly advance the development of future therapies for diseases where DPP9 plays a role.

Funding: Research Fund Flanders (FWO)

Researchers:

Principal investigator: Ingrid De Meester

Co-principal investigators: Pieter Van der Veken

Project: Despite a global distribution of Leishmaniasis and 1.5 to 2 million new cases annually, no effective human vaccines are available and treatment failure with current drugs is on the rise. Mast cells (MCs) are immune sentinels in the skin that are amongst the first to contact the Leishmania parasite following a sand fly bite. These cells play major roles in orchestrating early inflammatory responses, regulating vascular permeability and influencing immunity development in lymph nodes. Despite seminal work in mosquito-transmitted viral diseases, MCs remain underexplored as target cell during parasitic infections. Combining the strengths in immunology, parasitology, transcriptomics and biostatistics, the role of MCs will be assessed in natural Leishmania infection. Combining digital transcriptomic data from large human cohorts and experimental mouse infections, will enable detailed cross-species and multi-tissue insights into MC responses across the whole clinical spectrum of leishmaniasis. Using human MCs derived from progenitors in donor blood, a battery of cellular activation markers and specific silencing of MC gene expression using an in-house, cutting-edge method will enable unprecedented mechanistic insights in the interaction with infectious agents, i.e. Leishmania spp. parasites. This may provide new biomarkers for clinical follow-up as well as novel therapeutic targets that will be explored in the appropriate animal models of leishmaniasis initiated by a sand fly bite.

Funding: Research Fund Flanders (FWO)

Researchers:

Principal investigator: Guy Caljon

Co-principal investigators: Didier Ebo

Project: Autophagy is a normal physiological process that removes unnecessary or dysfunctional cellular components from the cytoplasm. Defective autophagy is currently emerging as a hallmark feature of many diseases, including Charcot-Marie-Tooth (CMT) neuropathy. In this framework, basic research and drug development have a strong need for reliable, drug-like autophagy inducers. We carried out a phenotypic high-throughput screen on compounds that were preselected based on drug likeness parameters. In total, 3 distinct chemical families were identified that previously have not been associated with autophagy induction. After thorough validation, potency and gross mode-of-action studies, the most promising chemical family was prioritized. Structure-activity relationships will be constructed for this chemical family. In addition, chemical optimization will be pursued to obtain novel representatives with further improved potency and a maximally favorable physicochemical profile. Efforts will be done for target finding. All novel compounds will be thoroughly investigated in a cell model for CMT neuropathy associated with mutations in the small heat shock proteins HSPB1 and HSPB8. To fully characterize this translational potential, in vivo evaluation in an established mouse model will be carried out for one maximally optimized compound.

Funding: Research Fund Flanders (FWO)

Researchers:

Principal investigator: Vincent Timmerman

Co-principal investigators: Pieter Van der Veken

Project: Autophagy is a ubiquitous process that removes unnecessary or dysfunctional cellular components from the cytoplasm. Defective autophagy is currently emerging as a hallmark of many diseases. In this framework, there is strong interest in pharmacological agents that stimulate autophagy (so-called 'autophagy inducers'), as a potential treatment for these diseases. The unequivocal validation of autophagy induction as a therapeutic strategy, however, is far from established. Many obstacles persist, including the lack of druglike, selective autophagy inducers and readily translatable preclinical results that are obtained with such compounds. In addition, the availability of reliable biomarkers for autophagy and additional fundamental safety data for the approach, would strongly contribute to its validation. This proposal addresses existing limitations in the state-of-the art in the domain. We have recently carried out a phenotypic High-Throughput Screen (HTS) on a curated compound library. Members in this library were preselected from different providers based on in silico druglikeness scores. One compound family that was identified in the screen and maximally validated prior to this application, will be further optimized chemically for autophagy induction potency and biopharmaceutical properties. The biopharmaceutical profile of the best new representative will be thoroughly characterized in vivo, both involving PET-based pharmacokinetics and phenotypic pharmacodynamics. The compound will subsequently be investigated in two mouse models of diseases characterized by defective autophagy: atherosclerosis and Charcot-Marie-Tooth periferal neuropathy. In addition, we propose to investigate whether autophagy induction is intrinsically sufficiently safe as a therapeutic strategy. Existing hypotheses that autophagy induction could accelerate tumorigenesis and/or tumor growth will be investigated in vivo. In the same framework, metabolomics will be relied on to monitor eventual cellular stress fingerprints that result from chronic or long-term autophagy stimulation. Finally, metabolomics will also be relied on to identify cellular biomarkers of autophagy induction. The latter will be validated in plasma samples of animals that were systemically treated with autophagy inducers. Combined, we expect the knowledge and tools that are generated by this proposal to have strong impact on the field of autophagy research and ongoing endeavors to validate autophagy induction as a therapeutic strategy.

Funding: BOF-GOA

Researchers:

Principal investigator: Pieter Van der Veken

Co-principal investigators: Wim Martinet, Vincent Timmerman, Sigrid Stroobants, Alexander van Nuijs ( (UAntwerpen),

Project: Anthracyclines are the mainstay of chemotherapeutic treatment in a wide range of malignancies, including breast cancer. Cardiotoxicity is a well-known and feared adverse effect of anthracyclin therapy and due to the growing population of cancer survivors, cardiovascular disease in these patients is expected to escalate. Unless we can identify high-risk patients for anthracycline therapy, today's breast cancer patients may become tomorrow 's heart failure patients. However, there is an important inte individual susceptibility for the development of cardiotoxicity and at present, it is not possible to predict which patients will develop cardiotoxicity. It was recently shown that genetic variants in titin, an import anchoring protein in the cardiomyocytes, can cause a predisposition to dilated cardiomyopathies and are also more prevalent in chemotherapy-induced cardiotoxicity. In this research project we investigate if mutations in titin increase the susceptibility for cardiotoxicity to anthracyclines, in order to identify high -risk patients. If this can be confirmed, the impact on both the individual patient (morbidity, mortality) and on society will be huge. The development of an hiPSC-CM model harbouring different TTNtv will allow us to test different possible therapeutic and preventive measures for this high risk population.

Funding: Research Fund Flanders (FWO)

Researchers:

Principal investigator: Emeline Van Craenenbroeck

Co-principal investigators: Maaike Alaert

Project: Sustainable Plant Protection Transition: a global health approach

Funding: H2020 MSCA Sustainable Security, 2020-2025

Coordinator: Prof. Violette Geissen (Wageningen University, The Netherlands)

Beneficiaries: 28 beneficiaries among which UAntwerp (Benjamin Vervaet, Patrick D'Haese, Pathophysiology)

Project: Mucine isoform-microbiome interactions determing the severity of a COVID-19 infection: useful for patient stratification?

Funding: FWO Covid-19 call 2

PIs: Benedicte De Winter (LEMP), Annemieke Smet (LEMP), Kevin Ariën (ITM); Aline Verstraeten (GENCOR), Surbhi Malhotra, Koen Vercauteren

Project: SPRINGBOARD for excellence in advanced development of antibacterials

Funding: H2020 Widespread, 2020-2023

Coordinator: Prof. RAIVIS ZALUBOVSKIS (Latvian Institute for Organic Synthesis, Riga, Latvia)

Beneficiaries: UAntwerp (Paul Cos, Koen Augustyns), University of Firenze, University of Copenhagen, University of Helsinki

Project: Advancing a portfolio of novel compounds with the potential to treat TB to address AMR. Progress new assets (one pre New Molecular Entity (preNME) and one first-time-in-human (FTIH) for tuberculosis that act synergistically with bedaquiline, cytochrome bc or cytochrome bd inhibitors

Funding: IMI (European Union and EFPIA)

More info: https://www.studio98.nl/Projects/tmp/respiritb/V4/index.html

Principal investigators for University of Antwerp:

LMPH: Prof. Paul Cos, Dr. Davie Cappoen, Prof. Yann Sterckx, Prof Peter Delputte 

UAMC: Prof. Koen Augustyns, Prof. Pieter Van der Veken, Prof. Hans De Winter

ORSY: Prof. Bert Maes

Other principal investigators: Janssen Pharmaceutica, Leiden University Medical Center, Sorbonne University, Medical University of Vienna, University of Copehnagen, Mitologics (SME), FFUND (SME) 

Project: Advancing a portfolio of novel compounds with the potential to treat NTM to address AMRProgress novel assets (One first-time-in-human (FTIH)) for non-tuberculosis mycobacteria (NTM) that may act synergistically with bedaquiline and cytochrome bc drugs

Funding: IMI (European Union and EFPIA)

More info: https://www.studio98.nl/Projects/tmp/respiritb/V4/index.html

Principal investigators for University of Antwerp:

UAMC: Prof. Koen Augustyns, Prof. Pieter Van der Veken, Prof. Hans De Winter

ORSY: Prof. Bert Maes

Other principal investigators: Janssen Pharmaceutica, Leiden University Medical Center, Sorbonne University, Medical University of Vienna, University of Copehnagen, Mitologics (SME), FFUND (SME) 

Project: INSPIRE aims to extend the SP toolbox by exploring novel technologies and by turning these into new products or services for improved assessment of drug-induced CV toxicity.For more details, please visit: https://www.uantwerpen.be/en/projects/inspire-safety-pharmacology/research/

Funding: H2020 MSCA European Training Network, 2020-2023

Coordinator: Prof. Pieter-Jan Guns (PHYSPHAR, UAntwerp)

Beneficiaries:UAntwerp (coordinator), Maastricht University, University of Nottingham, INRIA (the French National Institute for Computer Science and Applied Mathematics),Weismann Institute of Science (Israel), Ncardia, UCB; Notocord, TSE Systems, Boehringer-Ingelheim

The Mosquito Xtal3 is a state-of-the-art crystallization robot that has become an indispensable workhorse in any structural biology laboratory. The Mosquito Xtal3 allows fast, robust and high-throughput crystallization of biological macromolecules, which is a basic requirement for structure determination through macromolecular X-ray crystallography.

PIs: Prof. dr. I. De Meester (FAR/LMB); Prof. dr. ir. Y. Sterckx (FAR/LMB); Prof. dr. X. Van Ostade (BMW/PPES); Prof. dr. H. De Winter (FAR/UAMC); dr. D. Cappoen (BMW/LMPH)

In case of interest: please contact yann.sterckx@uantwerpen.be

Project: ADME studies of lead ferroptosis inhibitor which blocks organ injury and neurodegeneration in mice

Funding: IOF

PIs: Tom Vanden Berghe, Koen Augustyns, Alexander van Nuijs

Cell Death Platform to measure cell death along any other biochemical parameter that is crucial to determine the mode of cell death such as caspase activation, reactive oxygen species, calcium, mitochondrial membrane potential, lysosomal leakage and lipid peroxidation:

In case of interest: contact Tom Vanden Berghe (tom.vandenberghe@uantwerpen.be)

Project: From laboratory to patients: Moving new compounds through Phase I for the development of novel visceral leishmaniasis (VL) combination treatments

Funding:H2020-SC1-BHC-2018-2020: Better Health and care, economic growth and sustainable health systems.

Participants:

1 (Coordinator) Drugs for Neglected Diseases initiative DNDi Switzerland

2 Accelera ACC Italy

3 Diomune DIO Spain

4 GalChimia GAL Spain

5 GlaxoSmithKline GSK Spain

6 The Institute of Endemic Diseases IEND Sudan

7 Swiss Tropical and Public Health Institute SwissTPH Switzerland

8 University of Antwerp UA Belgium (LMPH: Prof. Louis Maes, Prof. Guy Caljon)

9 University of Dundee UNIVDUN United Kingdom

10 University of Gondar UOG Ethiopia

Project: We hypothesize that the endothelium-derived NRG-1 – ErbB4 system is activated in atrial tissue of patients with atrial fibrillation.If successful, this project could open new avenues for treatment of atrial fibrillation by addressing atrial tissue remodeling.

Funding: BOF (University Research Fund)

PI: Hein Heidbuchel (Cardiology)

co-PI: Gilles De Keulenaer, Guido De Meyer (both Physiopharmacology)

Project: Drug delivery systems and in vivo efficacy of the serine protease inhibitor UAMC-00050 in a preclinical model for Irritable Bowel Syndrome

Funding: IOF

Principal investigator: Benedicte De Winter (LEMP)

co-PIs: Koen Augustyns (UAMC), Filip Kiekens

Project: We propose a multi-disciplinary approach to identify novel potent and selective agonists of the ErbB4 receptor, to test these in validated rodent models of chronic heart failure, and to define specific patient populations in the heterogeneous field of cardiovascular diseases that could benefit from ErbB4 agonists.

Funding: FWO (Flanders-Belgium),  SNSF (Switserland), RFBR (Russian Foundation for Basic Research)

Principal investigator: Prof. Gilles De Keulenaer (Physiopharmacology lab, University of Antwerp, Belgium)

Co-principal investigators: Prof. Vincent Segers (Physiopharmacology lab, University of Antwerp, Belgium), Prof. Marijke Brink (University of Basel, Switserland),  Prof. Yuri Belenkov (University of Sechenov, Moscow, Russia)

Project: Physical and functional interactions between biomolecules play pivotal roles in all aspects of human health and disease.  Biomedically important enzymes, such as proteases and kinases, despite regulating nearly every biological function, remain a relatively underdeveloped drug target group.  This new biomolecular interactions platform will aid with the search for new  enzyme-based drug targets for diseases such as cancer, metabolic disorders and neurodegenerative disorders.

Funding: FWO-Medium Scale Research Infrastructure 

PI: I. De Meester

co-PIs: A. Lambeir, H. De Winter, P. Van der Veken, S. Maudsley, S. Dewilde, X. Van Ostade, W. Vanden Berghe, P. Delputte, F. Kooy, K. De Wael

Project: Metabolomics is the study of the unique chemical fingerprints that specific cellular processes leave behind. The metabolome is the collection of all metabolites in a biological cell, tissue, organ or organism, which are the end products of cellular processes.  Metabolomics can be used to investigate diseases, drug responses and pollutants in our environment.

Funding: FWO-Medium Scale Research Infrastructure 

PI: A. Covaci

co-PIs: L. Maes, K. Augustyns, G. De Meyer, N. Hermans, G. Baggerman, F. Lemière, K. Laukens, L. Bervoets, I. De Meester, A. Van Nuijs.

Project: The research program on MOlecular mechanisms of cellular DEath and Life decisions in Inflammation, Degeneration and Infection (MODEL-IDI) aims at performing fundamental research on the biology of cell death modalities, cell survival regulation and their consequences on the onset/progression of diseases

Funding: FWO Excellence of Science (FWO-EOS)

Principal investigator: Peter Vandenabeele (VIB-UGhent)

Co-principal investigators: Mathieu Bertrand (VIB-UGhent), Tom Vanden Berghe (VIB-UGhent), Koen Augustyns (UAntwerp), Wim Martinet (UAntwerp), Emmanuel Dejardin, Isabelle Manfroid (Université de Liège), Alessandra Cardozo (Université Libre de Bruxelles), Mathias Heikenwälder (Deutsches Krebsforschungszentrum - Heidelberg), Raffaella Gozzelino (Universidade Nova de Lisboa)  

Project: The European network for Integrated Training in Dry Eye Disease Drug Development (IT-DED3) aims to deliver multidisciplinary and entrepreneurial researchers trained to develop new therapies for patients suffering from dry eye diseases (DED). For more details, please visit: www.itded3.eu

Funding: H2020 MSCA European Training Network

Coordinator: Prof. Koen Augustyns (UAMC, UAntwerp)

Beneficiaries: Prof. Paul Cos (LMPH, UAntwerp), Prof. Christophe Baudoin (Vision Institute, Paris), Dr. Philipp Steven (University Hospital Cologne), Prof. Margarita Calonge (University of Valladolid, Spain), Prof. Osvalds Pucovics (Latvian Institute of Organic Synthesis), Prof. Arto Urtti (University of Eastern Finland), Dr. Ana Matias (iBET)

https://www.uantwerpen.be/en/projects/dry-eye-disease-drug-development/

Project: This project represents a formal research agreement between UA and on the other hand the Hercules Foundation. UA provides the Hercules Foundation research results mentioned in the title of the project under the conditions as stipulated in this contract.

Funding: Hercules Foundation

Researchers:

Principal investigator: De Meyer Guido (Physiopharmacology)

Co-principal investigators: Claeys Marc (Cardiovascular Diseases), De Keulenaer Gilles (Physiopharmacology), D'Haese Patrick (Pathophysiology), Loeys Bart (Medical Genetics), Vrints Christiaan (Translational Pathophysiological Research (TPR) - Cardiovascular Diseases)

Project: This project represents a formal research agreement between UA and on the other hand the Hercules Foundation. UA provides the Hercules Foundation research results mentioned in the title of the project under the conditions as stipulated in this contract.

Funding: Hercules foundation

Researchers:

Principal investigator: Maes Louis (LMPH)

Co-principal investigators: De Meyer Guido (Physiopharmacology), Delputte Peter (LMPH), Kumar-Singh Samir (Laboratory of Cell Biology & Histology), Lambeir Anne-Marie (Medical Biochemistry), De Meester Ingrid (Medical Biochemistry), Dewilde Sylvia, Lebeer Sarah, Leroy Jo, Van Cruchten Steven, Wenseleers Wim