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A novel approach to the development of new and effective cancer treatment options.  Background:
The Mixed Lineage Leukemia 1 (MLL1) protein is a member of the SET1 family of proteins. Mutations of the MLL1 core complex leads to excessive di- and trimethylation of H3K4 which alters gene regulation. This has been linked to certain types of leukemia, solid tumors, and psychotropic disorders such as schizophrenia and bipolar disorders. The minimal complex required for di- and trimethylation of H3K4 includes MLL1 or SETd1a, WDR5, RbBP5, Ash2L and DPY-30. The protein WDR5 bridges the catalytic SET domain of SET1 family proteins and the regulatory components of RbBP5 and Ash2L. Currently, there are no approaches for inhibiting the formation of SET1 family core complexes for the treatment of leukemia and other disorders.Technology Overview:  
This technology from Upstate Medical University provides peptide-based inhibitors of the SET1 family core complexes. These peptides can be used to inhibit the growth of cancer cells. These peptide inhibitors can inhibit the enzymatic activity of complexes of MLL1 and SETd1A. The peptide inhibitors may act by inhibiting the formation of, or by disrupting, MLL1 and SETd1A complexes. The peptide inhibitors may also enhance the activity of MLL3, which is a known tumor suppressor. The administration of a compound based on this approach can be used alone or combined with chemotherapy, radiation therapy, surgical removal of tumors, or combinations thereof, and/or with a diagnostic technique. https://suny.technologypublisher.com/files/sites/adobestock_2229417291.jpeg Advantages:  
This technology provides a new approach for the development of compounds that could treat various forms of cancer. It may also be used for the development of treatments for psychotropic disorders.  Applications:  
The primary application for this technology is cancer treatment. It may also be used for the treatment of psychotropic disorders such as schizophrenia and bipolar disorders.
 Intellectual Property Summary:
This technology is covered by the patent US 10392423 B2, “Peptide-Based Inhibitors of MLL / SET1 Family Core Complexes.”
https://patents.google.com/patent/US10392423B2/ Stage of Development:
TRL 3 - Experimental proof of concept
Licensing Status This technology is available for licensing. Licensing Potential
This technology will be of value to any company or institution involved in treating cancer. This includes:
•    Pharmaceutical companies
•    Hospitals 
•    Research centers

Targeted gene silencing technology promotes corneal wound healing. Background: Ocular scarring after surgery, trauma, or infection leads to vision loss and blindness. Blindness due to corneal scarring can currently only be resolved by transplantation, necessitating new approaches in regenerative wound healing in the eye.Technology Overview:  A self-deliverable siRNA has been developed by Upstate Medical University researchers to specifically target a gene that modulates scarring in order to promote corneal wound healing. The approach has been validated ex vivo and in vivo, with treatment after corneal wounding resulting in faster wound closure, limited scarring, suppression of fibrotic markers, and restoration of corneal thickness. https://suny.technologypublisher.com/files/sites/110-2089.jpghttps://www.pexels.com/photo/human-eye-2609925/Advantages:  

• Targeted siRNA therapy circumvents the need for immunologically compatible corneal donors.
• In vivo studies demonstrate this therapy promotes 41.5% reduction in scarring

• Effective treatment for corneal scarring resulting from mechanical injuries, burns, infections or surgery.
• Model useful to study pathogenesis of fibrotic healing.

Mouse model stably overexpressing Ant-1 for muscle atrophy therapy development. Background: Muscle disorders are commonly manifested in mitochondria-induced diseases, which are clinically referred to as mitochondrial myopathies. In classic mitochondrial myopathies, caused by mutations in mitochondrial DNA or in nuclear genes encoding mitochondrial function, biochemical and histological biomarkers indicative of bioenergetic defects can be readily detected. In contrast, the role of mitochondria in other progressive muscle diseases, including sarcopenia is less clear.Technology Overview:  Overexpression of the muscle/heart isoform of adenine nucleotide translocase, Ant1 is associated with the clinically well-defined progressive muscle disorder Facioscapulohumeral Dystrophy (FSHD). Upstate Medical University researchers have generated a transmissible transgenic mouse line that stably overexpresses Ant1, resulting in manifestation of severe muscle disorders in the transgenic animals.Thus, this invention provides a unique animal model for studying the pathogenic mechanism of FSHD and other mitochondria-induced diseases including sarcopenia of aging (aging-dependent muscle wasting), as well as a tool for the development of therapeutic drugs in the treatment of these diseases  https://suny.technologypublisher.com/files/sites/110-2097.jpghttps://www.pexels.com/photo/white-baby-mouse-159483/Advantages:  

• Ant1-transgenic mice progressively lose muscle, making them relevant for musculoskeletal disorders.
• Animal lifespan remains unaffected, enabling the detailed study of muscle wasting mechanism

• Research tool for mitochondrial disorders
• Drug screening for neuromuscular degenerative disorders
• Muscle degeneration research

 A new class of antifungal drugs to treat resistant fungal infections.   Background: Fungal Infections are a major cause of human disease. Annually, over 150 million severe cases of fungal infections occur worldwide, resulting in approximately 1.7 million deaths per year.The four classes of antifungal drugs to treat life-threatening infections have limitations, including toxicity, drug-drug interactions, inconvenient dosing, and increasing incidence of resistance. There is an urgent need to discover and develop the next generation of antifungal drugs.  Technology Overview:  This technology developed by researchers at SUNY Upstate Medical University consists of a new molecular target, Ess1 for inhibition as a potential treatment for fungal infections, including those resistant to currently used antifungal drugs. The novel molecular target of this method is a highly conserved fungal enzyme essential for growth and virulence of various fungal species, including Saccharomyces cerevisiae, Candida albicans, and Cryptococcus neoformans. Thus, the technology promises broad-spectrum activity against various pathogenic fungi.   https://suny.technologypublisher.com/files/sites/110-21001.jpghttps://unsplash.com/photos/Wk902ZLaA7M Advantages:  

• Treatment of antimycotic-resistant infections. 
• Broad-spectrum activity.