This technology includes a new class of synthetic peptides that activate Lipoprotein Lipase (LPL), a key plasma enzyme that lowers triglycerides. Mutations in apoC-II is a genetic cause of severe hypertriglyceridemia, which can lead to cardiovascular disease and pancreatitis.

This technology includes a small molecule drug (VDAC inhibitor, also known as VBIT4) that may be useful for inhibiting lupus disease. To test lupus animal model, VBIT4 was continuously administered for 5 weeks to mice and there was no mortality or clinical symptoms in these animals. Additionally, VBIT4 treatment blocked the development of skin lesions and alopecia of the ears and face, and suppressed the thickening of the epidermis that accompanies leukocyte infiltration.

This technology includes a novel concept and design for a lipoprotein targeting protease inhibitor for the treatment of Alpha-1-antitrypsin (A1AT) deficiency. A1AT deficiency occurs in about 1 in 2500 individuals in the United States and Europe, and people with this condition develop severe liver disease and emphysema/chronic obstructive pulmonary disease (COPD). Current treatment involves intravenous infusion of purified human A1AT protein, which is very expensive and only modestly effective.

This technology includes a novel capsid protein for recombinant adeno-associated virus (AAV)-mediated gene transfer evaluation. We have identified a "fossilized" endogenous AAV sequence element (referred to as mAAV-EVE) within the germline of an ancient lineage of Australian marsupials and have cloned and sequenced mAAV-EVE orthologs from at least fifteen lineage-specific taxa.

This technology includes efficient lentiviral gene delivery system for both guide RNA and Cas9 endonuclease as a method to cure sickle cell disease. Gene correction is an ideal gene therapy strategy for hereditary disease, including sickle cell disease.

This technology includes in vitro-generated trophectoderm (TE) cells, which are ideal for modeling diseases of the placenta, drug screening, and cell-based therapies. The TE lineage which gives rise to placental cells during early human development. Derivation of definitive placental cells from human pluripotent stem cells in culture remains controversial and so far, placental cells can only be derived directly from primary placental tissue, which largely limits their access and study in the laboratory.

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.