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This technology includes genetic manipulation of natural killer (NK) cells to express thrombopoietin receptor (c-MPL) growth factor receptor as strategy to augment NK cell proliferation and anti-tumor immunity. Many investigational adoptive immunotherapy regimens utilizing NK cells require the administration of IL-2 or IL-15 cytokines to support the survival and function of the cells in patients, however administration of these cytokines causes a number of serious dose-dependent toxicities.

This technology includes anti-PSMA antibody labeled with 177Lu, which has shown to be an effective treatment for prostate cancer. Several small molecules targeting PSMA were also evaluated in prostate cancer patients labeled with betta emitters such as 177Lu. The most common one is 177Lu-PSMA-617 which is under clinical evaluation in many countries. Usual treatment in patients in most clinical trials was composed of up to 3 cycles of 177Lu-PSMA-617.

This technology includes synthesis of S-2-((S)-3-(4-chlorophenyl)-N'-((4-chlorophenyl) sulfonyl)-4-phenyl-4,5-dihydro-1 H-pyrazole-1-carboximidamido)- 3-(methyld3) butanamide-d5, octadeuterated JD5037 for possible use in clinical Absorption, Distribution, Metabolism, and Excretion (ADME) studies for drug discovery studies.

This technology includes a method to identify potentially therapeutic microRNAs in cancer, particularly squamous cell carcinoma of the head and neck (HNSCC). This approach first utilizes a large and publicly available expression dataset, which is then validated by a smaller independent dataset to determine deregulated microRNAs expression. These results are then intersected with in vitro functional anti-proliferative screening data to select for microRNAs that play a functional tumor suppressive role and likely serve as therapeutic targets.

This technology includes AAVS1 and C13 “safe harbor” transcription activator-life effector nucleases (TALENs) for drug screening or gene therapy applications. TALENs are engineered sequence-specific DNA endonucleases that can significantly enhance genome-editing efficiency by >100-1000 folds. “Safe harbor” such as AAVS1 safe harbor and C13 safe harbor is genome locus that allows robust and persistent transgene expression with no or minimal interference of endogenous gene expression and cell properties.

This technology includes apoE-apoCII chimeric peptides that possess the ability to lower the triglyceride level both in vitro and in vivo. These peptides can be used for treating hypertriglyceridemia and alleviating other diseases and conditions associated with increased triglycerides.

This technology includes a new method to prepare very long chain fatty acids (VLCFA), which does not use the previously reported toxic mercury amalgam, for use as nutritional supplements, and as therapeutics for various diseases. The key coupling step involves an organocopper mediated coupling of the Grignard regent derived from the bromo alkyl tetraene with a bromoalkyl containing a protected alcohol. After the coupling the alcohol Is deprotected and oxidized to prepare the very long fatty acid. The synthetic approach is flexible and can be used to prepare the other VLCFA compounds.

This technology includes a new class of synthetic peptides that activate Lipoprotein Lipase (LPL), a key plasma enzyme that lowers triglycerides, by displacing apoC-111, a potent inhibitor of LPL. ApoC-11 is a known activator of LPL, whereas ApoC-111 inhibits LPL and raises triglycerides either directly by blocking lipolysis and or by preventing hepatic uptake of lipoproteins. Both apoC-II and apoC-III have to bind to the surface of a lipoprotein particle to mediate their effects.

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.