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This technology includes EPHX1/EPHX2 null mice and showed that disruption of both EPHX1 and EPHX2 almost completely abolished hydrolysis of several EETs which can be used in the treatment of cardiovascular diseases. EPHX 1 is significantly involved in EET hydrolysis, and we believe the combined use of EPHX1 and EPHX2 inhibitors would provide a better alternative to currently available therapeutic options or the EPHX2-based therapies currently in trials for the treatment of cardiovascular diseases.

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 the use of atorvastatin, a medication to manage hypercholesterolemia, as a method to protect patients receiving cisplatin from hearing loss. Cisplatin chemotherapy is indicated in various cancer types in adults and children and is known to cause hearing loss. A patient on atorvastatin during chemotherapy is 46% less likely to acquire a significant cisplatin-induced hearing loss relative to a non-statin user. Atorvastatin is an FDA-approved medication routinely prescribed and well-tolerated clinically.

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 the development of selective P2Y14R antagonists for the treatment of asthma, sterile inflammation of the kidney, diabetes, and neurodegeneration. The P2Y14 receptor (P2Y14R) is a target for the treatment of inflammatory diseases, including pulmonary and renal conditions. Selective P2Y14R antagonists have demonstrated efficacy in animal models of asthma, pain, diabetes, and acute kidney injury. However, the prototypical antagonist is not optimal for in vivo administration, as it displays a low oral bioavailability.

This technology includes the creation and use of A3 adenosine receptor (A3AR)-selective agonists for treating chemotherapy-induced peripheral neuropathy, chronic neuropathic pain, rheumatoid arthritis, psoriasis, and other conditions. A3 receptors for adenosine are found in most cells and endogenous activation of the A3 receptors can result in apoptosis, thereby relieving the inflammation or targeting a tumor. A3AR agonists have been a promising strategy for the treatment of various diseases.

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.