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This technology uses lung-targeting lipid nanoparticles to deliver IL-10 mRNA directly to the lungs, reducing inflammation and injury in conditions like acute lung injury and ARDS, while minimizing side effects and improving treatment effectiveness. Background:
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are severe, life-threatening conditions characterized by widespread inflammation and damage to the lung tissue, leading to respiratory failure and high mortality rates. Despite decades of research, there are currently no FDA-approved pharmacologic therapies specifically targeting the underlying inflammation and tissue injury in ALI and ARDS. The clinical management of these conditions is largely supportive, relying on mechanical ventilation and general critical care measures, which do not address the root causes of lung dysfunction. The urgent need for effective, targeted therapies is underscored by the high morbidity and mortality associated with these syndromes, as well as the lack of options for directly modulating the inflammatory processes that drive disease progression. Current approaches to delivering anti-inflammatory therapies, such as systemic administration of interleukin-10 (IL-10) protein, are hampered by several significant limitations. Systemic IL-10 therapy suffers from poor pharmacokinetics, including rapid clearance and a short half-life, which necessitate frequent dosing and limit sustained therapeutic effects. Additionally, the lack of lung specificity means that high systemic doses are required to achieve therapeutic concentrations in lung tissue, increasing the risk of off-target toxicity and adverse effects. Conventional lipid nanoparticle (LNP) systems, such as those used in mRNA vaccine delivery, do not preferentially accumulate in the lungs, further reducing the efficiency of lung-targeted therapy. These challenges highlight the need for novel delivery systems capable of selectively targeting lung tissue, sustaining therapeutic protein expression in situ, and minimizing systemic exposure to improve both efficacy and safety in the treatment of ALI and ARDS.Technology Overview:  
This technology is a lung-targeting lipid nanoparticle (sLNP) system engineered for the precise delivery of anti-inflammatory agents to lung tissue, to treat acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). The sLNPs are constructed from sulfonium lipids, which confer unique properties enabling selective accumulation in the lungs and robust, uniform expression of protein across all lung lobes. This approach sustains therapeutic protein expression directly within lung tissue while minimizing systemic exposure, thereby reducing potential side effects. What differentiates this technology is its lung specificity and the use of sulfonium lipid chemistry, which sets it apart from conventional amine-based lipid nanoparticles commonly used. Traditional LNPs lack organ selectivity, often requiring higher systemic doses that can increase toxicity and limit therapeutic efficacy, especially for lung diseases. In contrast, the sLNP platform enables targeted delivery and sustained local expression of therapeutics, overcoming the pharmacokinetic limitations and short half-life associated with systemic therapies. This targeted approach not only enhances therapeutic outcomes for ALI and ARDS but also opens avenues for treating other pulmonary inflammatory conditions and advancing pulmonary drug delivery. The technology’s novel combination of materials and delivery strategy positions it as a promising solution for unmet clinical needs in respiratory medicine. https://suny.technologypublisher.com/files/sites/adobestock_874720379.jpegAdvantages:  
•    Selective delivery of IL-10 mRNA specifically to lung tissue, enhancing treatment precision for acute lung injury (ALI) and acute respiratory distress syndrome (ARDS).
•    Robust and uniform expression of therapeutic IL-10 protein across all lung lobes, ensuring effective local anti-inflammatory and tissue-protective effects.
•    Sustained in situ IL-10 protein expression, overcoming limitations of short half-life and poor pharmacokinetics associated with systemic IL-10 therapy.
•    Reduced systemic exposure and associated side effects, improving safety compared to non-targeted delivery methods.
•    Use of sulfonium lipid nanoparticles (sLNPs) enables selective lung accumulation, differentiating it from conventional amine-based lipid nanoparticles.
•    Potential applicability to a broad range of pulmonary inflammatory diseases beyond ALI and ARDS.
•    Significant reduction of lung injury demonstrated in preclinical models, indicating strong therapeutic potential. Applications:  
•    ALI/ARDS therapeutic development
•    Pulmonary anti-inflammatory drug delivery
•    Lung-targeted mRNA therapeutics Intellectual Property Summary:
Patent application 63/922,741 filed 11/21/2025Stage of Development: 4
TRL 4. The technology is at an early preclinical stage of development, demonstrating proofofconcept and feasibility of lungtargeted delivery using sulfoniumbased LNPs in laboratory and initial in vivo models.Licensing Status:
This technology is available for licensing.
 

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