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This technology is an advanced CAR T-cell therapy for triple-negative breast cancer that uses engineered T-cells to recognize and kill cancer cells regardless of HLA status and includes a built-in IL-15 signal to boost T-cell survival and effectiveness. Background:
Triple-Negative Breast Cancer (TNBC) is a particularly aggressive subtype of breast cancer characterized by the absence of estrogen, progesterone, and HER2 receptors, making it unresponsive to many of the targeted therapies available for other breast cancer types. This leaves chemotherapy as the primary systemic treatment, which often results in high relapse rates and poor long-term survival, especially among high-risk populations such as U.S. servicewomen and veterans. The emergence of immunotherapies, particularly Chimeric Antigen Receptor (CAR) T-cell therapies, has revolutionized the treatment of certain blood cancers, offering the promise of highly specific and durable anti-tumor responses. However, translating this success to solid tumors like TNBC has proven challenging, underscoring a critical need for innovative approaches that can overcome the unique barriers posed by these malignancies. Current CAR T-cell therapies for solid tumors face two major obstacles: immune evasion by tumor cells and rapid T-cell exhaustion within the tumor microenvironment. Many solid tumors, including TNBC, downregulate Human Leukocyte Antigen Class I (HLA-I) molecules on their surface, which are essential for recognition by conventional CAR T-cells. This allows tumor cells to escape immune detection and destruction. Additionally, the tumor microenvironment in TNBC is highly immunosuppressive, leading to rapid functional exhaustion and loss of persistence of infused CAR T-cells. Attempts to overcome these issues, such as systemic cytokine support, have been hampered by severe toxicities and limited efficacy, while alternative targeting strategies often lack the specificity or durability needed for effective tumor control. As a result, there remains a significant unmet need for CAR T-cell therapies that can both recognize tumor cells independently of HLA-I status and maintain robust, sustained activity within the hostile tumor microenvironment.Technology Overview:  
This technology is an advanced CAR T-cell therapy specifically engineered for the treatment of Triple-Negative Breast Cancer (TNBC). It features a dual-action design: first, the CAR T-cells are equipped a receptor, enabling them to recognize and attack cancer cells by detecting stress-induced ligands on their surface, independent of the tumor’s HLA-I status. Second, the CAR T-cells are further enhanced by the expression of a membrane-bound superagonist, which delivers a continuous, localized survival and proliferative signal. This modification boosts the persistence and cytolytic activity of the T-cells within the immunosuppressive tumor microenvironment, preventing exhaustion and loss of function. What differentiates this solution is its comprehensive approach to overcoming two of the most significant barriers in solid tumor immunotherapy: immune evasion and T-cell exhaustion. The therapy bypasses the need for HLA-I-mediated recognition, directly addressing a common escape mechanism in TNBC. The addition of the superagonist ensures sustained T-cell activity without the systemic toxicity associated with external cytokine administration. Preclinical data demonstrate superior tumor control, enhanced T-cell persistence, and reduced exhaustion in both in vitro and in vivo models. This modular platform not only offers a promising new treatment for TNBC but also sets the stage for adaptation to other hard-to-treat cancers, marking a significant advancement in the field of cellular immunotherapy. https://suny.technologypublisher.com/files/sites/adobestock_1642156830.jpegAdvantages:  
•    Enables HLA-independent recognition and killing of Triple-Negative Breast Cancer (TNBC) cells by targeting stress-induced ligands, overcoming tumor immune evasion.
•    Improves cytolytic activity and anti-tumor efficacy without the need for systemic cytokine administration, minimizing associated toxicities.
•    Demonstrates superior tumor control and prolonged survival in preclinical humanized mouse models of TNBC.
•    Reduces expression of exhaustion markers (e.g., PD-1) on tumor-infiltrating CAR T-cells, maintaining sustained immune response.
•    Offers a modular platform adaptable to other CAR T-cell therapies and solid tumors beyond TNBC. Applications:  
•    Triple-Negative Breast Cancer therapy
•    Solid tumor CAR T-cell treatment
•    Personalized immunotherapy for veterans
•    Next-generation cell therapy platform Intellectual Property Summary:
Patent application 63/922,634 filed on 11/21/2025Stage of Development:  
TRL 3. Based on current progress, the technology is at a preclinical development stage, demonstrating proof of concept and initial validation of the dual enhanced CAR T cell design in early in vitro and in vivo models.Licensing Status:
This technology is available for licensing.

This technology uses drugs that stabilize β-catenin to boost protective immune cells in the lungs, reducing damage from pulmonary hemorrhage and inflammatory lung diseases by activating a novel immunomodulatory pathway. Background:
Pulmonary hemorrhage and other inflammatory lung diseases represent significant clinical challenges due to their high morbidity and mortality rates. These conditions are characterized by excessive inflammation and immune dysregulation within the lung tissue, leading to tissue damage, impaired gas exchange, and life-threatening complications. Current therapeutic strategies primarily focus on symptomatic management, such as corticosteroids and supportive care, but these approaches often fail to address the underlying immune mechanisms driving disease progression. As a result, there is a pressing need for innovative therapies that can modulate the immune response more precisely, reduce inflammation, and promote tissue repair, thereby improving outcomes for patients affected by these severe pulmonary conditions. Despite ongoing research, existing treatments for inflammatory lung diseases and pulmonary hemorrhage remain inadequate. Corticosteroids and broad-spectrum immunosuppressants, while effective at dampening inflammation, carry significant risks of systemic side effects and increased susceptibility to infections. Moreover, these therapies do not selectively target the specific immune pathways implicated in lung injury, leading to suboptimal efficacy and frequent relapses. Attempts to modulate regulatory T cell (Treg) populations have been limited by challenges in achieving tissue specificity and sustained functional enhancement. Consequently, there is a critical gap in the development of targeted immunomodulatory therapies that can provide durable protection against lung inflammation and hemorrhage without compromising overall immune competence.Technology Overview:  
This technology utilizes β-catenin agonists to pharmacologically stabilize β-catenin, offering a novel therapeutic approach for protecting against pulmonary hemorrhage and other inflammatory lung diseases. The treatment works by inducing a specialized phenotype in tissue-resident regulatory T cells (Tregs) within the lung. In preclinical studies using a mouse model of lung injury, administration of β-catenin agonists led to increased lung Treg populations and significantly reduced lung damage, as evidenced by pathology and histological analysis. This method demonstrates the potential for a targeted, immune-based intervention in the management of inflammatory lung conditions, with applications for clinicians, pharmaceutical developers, and researchers in immunology and pulmonary medicine. What differentiates this technology is its ability to pharmacologically mimic the protective effects seen in genetic models of β-catenin stabilization, offering a practical and scalable therapeutic strategy. Unlike conventional anti-inflammatory treatments that broadly suppress immune responses, this approach specifically enhances a beneficial immunoregulatory pathway thereby promoting tissue protection without compromising overall immune function. The elucidation of this pathway provides a unique target for drug development, setting the technology apart from existing therapies by focusing on the modulation of tissue-resident Tregs and their role in lung repair. This targeted mechanism not only addresses a critical unmet need in pulmonary hemorrhage treatment but also opens avenues for broader applications in inflammatory disease management. https://suny.technologypublisher.com/files/sites/adobestock_282277137.jpegAdvantages:  
•    Provides pharmacological protection against pulmonary hemorrhage and inflammatory lung diseases.
•    Induces a specialized tissue-resident regulatory T cell (Treg) phenotype to modulate immune response.
•    Recapitulates protective effects observed in genetic β-catenin stabilization models without genetic modification.
•    Demonstrated efficacy in preclinical mouse models with significant reduction of lung damage.
•    Potentially applicable to broader inflammatory disease management beyond pulmonary conditions.
•    Offers a new therapeutic approach for clinicians and pharmaceutical developers targeting lung inflammation. Applications:  
•    Pulmonary hemorrhage therapeutic development
•    Inflammatory lung disease treatment
•    Immunomodulatory drug discovery
•    Acute lung injury intervention Intellectual Property Summary:
Patent application 63/922,548 filed on 11/21/2025Stage of Development:  
TRL 3. The technology is currently at a preclinical development stage, with proof of concept demonstrated through pharmacologic β-catenin stabilization and validation in relevant in vitro and in vivo lung injury modelsLicensing Status:
This technology is available for licensing.
 

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