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This technology includes the use of LZK and DLK inhibitors to be used for the treatment of head and neck squamous cell carcinoma (HNSCC) or lung squamous cell carcinoma (LSCC). Specifically, we demonstrate that inhibitors that can be repurposed to target LZK suppresses LZK kinase-dependent stabilization of MYC and activation of the PI3K/AKT pathway. In vivo preclinical cell line xenograft mouse model demonstrates that targeting LZK will suppress tumor growth. We also demonstrate that several additional compounds potently inhibit LZK and could serve as new therapeutic modalities.

This technology includes Spodoptera frugiperda (Sf9) cells which were developed to produce recombinant adeno-associated virus. The cells maintain a copy of the vector genome and for production, require infection with a single baculovirus that expresses either structural and nonstructural proteins to produce rAAV, or the non-structural (Rep) proteins to produce ceDNA.

The technology described involves the use of a compound called prazole as an anti-viral agent specifically targeting HIV-1. It was found that prazole binds to a protein called Tsg101, which is crucial for the virus's life cycle. This binding disrupts the normal interaction of Tsg101 with another protein, ubiquitin, thereby inhibiting the release of HIV-1 particles from infected cells. Additionally, the interference caused by prazole leads to the degradation of the viral protein Gag within host cells.

This technology includes a novel vaccine for forming autoantibodies against apoC-III, a plasma enzyme that inhibits lipolysis. The vaccine can possibly be used to treat patients with high triglycerides and are at risk for pancreatitis and cardiovascular disease. This disclosure describes an ApoC3 immunogen that includes an antigenicApoC3 peptide linked to a bacteriophage virus-like-particle (VLP) immunogenic carrier.

This technology includes monoclonal antibodies (mAb) that specifically and with high affinity bind the final complement components C3dg and C3d (subsequently referred to as C3d), which can be used to kill tumor cells that carry C3d on their cell surface. We show that tumor cells of patients treated with the therapeutic anti-CD20 mAb ofatumumab carry C3d on the cell surface and can bind and be killed by addition of anti-C3 mAbs. In contrast, further addition of more ofatumumab has only minimal effects.

This technology includes an IgA antibody, specifically designed to target the receptor binding domain of SARS-CoV-2, the virus causing COVID-19. Administered intranasally, this antibody has potential neutralizing activity, aiming to prevent COVID-19. IgA, an antibody class present in mucosal areas, plays a crucial role in immune defense at the initial site of viral infection. The primary application of this technology is envisioned as a therapeutic nasal spray, intended to prevent SARS-CoV-2 infection, particularly in high-risk populations.

This technology includes a mouse model of TRIOBP human deafness which can be used for research and treatment development for deafness. This model contains mutations altering the TRIOP-5 isoform.

This technology includes a mouse model containing a hypothetical, previously undescribed, gene that we have proven is expressed in hair cells of the inner ear and few other tissues in the body. The hair-cell limited expression of Cre is a genetic tool for creating conditional mutations affecting hair cells almost exclusively. Hair cells are the sensory receptors of both the auditory system and the vestibular system in the ears of all vertebrates.

This technology includes antibodies for TMC1 protein as a treatment for hearing loss. TMC1 is one of the common genes causing hereditary hearing loss. Our laboratory used synthetic peptides corresponding to the TMC1 protein to immunize rabbits. The resulting antisera were shown to bind to TMC1 protein expressed in heterologous expression systems. TMC1 protein is required for the transduction of sound into electrical impulses in inner ear sensory cells.