37 innovations from Bar-Ilan University, available for licensing, co-investment, or spin-out through BIRAD.
Cohen Cyrille
We have developed an improved T-cell receptor targeting the NYESO1 antigen to generate a T-cell based therapy for cancer.
Cohen Yigal
We discovered a new gene in basil Pb2 which controls resistance against downy mildew.
Cohen Cyrille
In this project we have generated novel targeting chimeric receptors based on the extra cellular domain of two members of the SIGLEC family: SIGLEC7 and SIGLEC9. These targeting moieties were fused to different signalling domains and expressed in primary human T-cells. We identified for each SIGLEC receptor the optimal molecules and went on and performed multiple functional assays. We observed enhanced cytokines secretion and recognition of multiple tumors (ovarian cancer, cervical cancer, lung cancer) mediated by SIGLEC chimeras. We also demonstrate that these receptors can upregulate the activation marker 41BB as well as display significant anti-tumor cytotoxicity, upon co-culture with tumor cells. Overall, we propose that engineering T-cells with a SIGLEC-based chimeric receptors bears important implications for the improvement of T cell-based immunotherapy.
Cohen Cyrille
The invention involves the computational design and development of novel constant regions for human T-cell receptors (TCRs), termed "Structurally Enhanced TCR" (SET). By introducing a set of strategic mutations into the TCR constant domains, the SET design improves receptor stability, enhances surface expression, increases functional avidity, and ensures preferential pairing of the α and β chains, minimizing mispairing with endogenous TCRs. This innovation offers a universal platform to optimize T-cell therapies for cancer and infectious diseases without requiring additional gene editing.
Barda-Saad Mira
The focus of this patent application is the development of a novel therapeutic approach for controlling and improving NK cell killing of cancer cells or viruses in vivo by suppressing the key negative regulators of NK cell cytotoxicity. Natural-killer (NK) cells represent a powerful weapon of immune defense against viral infections and tumor growth, via cytotoxicity of target cells. Specifically, NK cells are particularly efficient in removing metastatic cells and tumor grafts. We recently revealed that NK cell response is inhibited by two main mechanisms: (1) dephosphorylation of signaling molecule by the protein tyrosine phosphatase SHP-1, and (2) ubiquitylation mediated degradation of signaling molecule by the E3 ubiquitin ligases c-Cbl and Cbl-b. These molecular events block NK cell activation; however, their suppression increases NK cell cytotoxicity of cancer cells. NK cell-based immunotherapies represent a promising strategy to combat cancer, yet, no clinical trial has demonstrated a significant benefit in malignancies. Our novel approach for improving NK cell killing of cancer cells is composed of an in vivo NK-targeted drug-delivery system that strike the molecular mechanisms that inhibits NK cell activation, i.e. SHP-1 and the Cbls, using specific siRNA. To specifically target the NK cells, the siRNA will be coupled to nanoparticles coated with specific antibodies to NK cells.
Margel Shlomo
Synthesis and Characterization of New Durable Anti-biofilm and Antiviral Silane-Phosphonium Thin Coatings for Medical and Agricultural Applications
Popovtzer Rachala
The human microbiome is emerging as a central player in health and disease. In particular, a strong connection has been shown between the human gut microbiome population and the etiology of a variety of diseases, ranging from gastrointestinal diseases to cancer, cardiovascular disease, and brain disorders. A fundamental phenomenon of bacterial communication is quorum sensing, in which signal molecules, termed autoinducers (AI), regulate bacterial colony density and coordinate pathogenic behaviors. AI molecules are emerging as important factors, and key indicators, in various diseases. However, despite their importance, there has not yet been developed a sensitive and reliable sensor that can detect AI communication molecules in real-time, for early diagnosis and monitoring of disease. The present project aims to develop an innovative biochip technology, combining advanced synthetic biology together with cutting-edge electronic systems, for quantitative, sensitive, and real-time detection of AI signals for diagnosis of gastrointestinal diseases. Our technology consists of a nano biochip, incorporating a variety of synthetic bacteria each engineered to sense a specific disease-associated AI molecule and generate a quantifiable electric signal in response, which will be measured, and wirelessly transmitted, by the electronic component. The nano biochip will accurately associate a specific electric response with a specific AI type. The ability of the nano-biochip system to identify the specific AI signals will be investigated in bacterial conditioned media and in ex vivo samples from gastrointestinal disease patients at different stages of the disease. This novel technology has the potential to serve as a next-generation tool for non-invasive early diagnosis, staging, and monitoring of gastrointestinal diseases. The nanobiochip’s unique features will also advance the potential for real-time detection of gastrointestinal disorders within the human body.
Okun Eitan
Down Syndrome (DS), which results from a trisomy of chromosome 21 (Hsa21), is the most prevalent genetic cause of intellectual disability worldwide1-3. Some genes on the human chromosome 21 are highly correlated to Alzheimer's disease (AD) pathogenesis, including the amyloid precursor protein (APP), which is overexpressed in individuals with DS, causing early-onset AD (EOAD)-related neuropathology4-6. Furthermore, an alarming association was found between pregnancy with a DS-affected fetus and a 5-fold increased risk of mothers developing late-onset AD (LOAD) later in life, compared with pregnancies with fetuses affected by other forms of intellectual disability7,8. We suggest that fetomaternal transfer of APP and its proteolytic fragments occurs during pregnancy with a DS fetus and that these fetal factors infiltrate the maternal central nervous system, contributing to Aβ-seeding in the maternal brain, adversely affecting their cognitive abilities. By modeling DS-like pregnancies in mice, by mating of wild-type (WT) female mice for 4 consecutive pregnancies with mouse strains that overexpress the human amyloid precursor protein (hAPP) during early embryonic stages, we have observed fetal DNA, mRNA, proteins, and cells in the mothers' brains and periphery tissues following pregnancies, resulting in maternal cognitive decline. To delay the observed cognitive decline resulting from the transfer of neurotoxic peptides, we have generated a novel vaccine specific for the human neurotoxic N-terminal epitope of APP, the N-APP (APP108-113) fragment, which we observed to reside in the periphery of Aβ plaques in the brain of EOAD mouse brains and present in the brains of mothers to hAPP-expressing mouse fetuses. Vaccinating WT female mice with the N-APP vaccination prior to their exposure to hAPP-expressing fetuses improved short-term memory abilities in several behavioral assays and may therefore be helpful as a preventative treatment for maternal cognitive decline following DS pregnancies. In addition, vaccinating 5xFAD mice, which model EOAD, with the N-APP vaccine, improved cognitive measures in various cognitive tasks.
Popovtzer Rachala
The next generation FDG-PET, based on radioactive
Efroni Sol
גילוי מוקדם של סרטן בעזרת כימות רפרטואר תאי טי
Gruzman Aric-lev
Inhibitors of leucocyte rolling and recruiting as an anti-inflammatory novel drug candidates
Nudelman Abraham
Indoline derivatives possessing antioxidant and anti-inflammatory properties for the treatment of hronic inflammatory diseases
