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This technology includes inhibitors of the Eya phosphatase which can be utilized as anticancer therapy. The Eya proteins are essential co-activators of the Six1 transcription factor, a gene that is abnormally re-expressed in a large percentage of breast cancers. This over-expression plays a causal role in the initiation and metastatic development of breast cancers. The Eya family of proteins was also found to contain a unique haloacid dehalogenase phosphatase domain with protein Tyr phosphatase activity which can potentially play a role in Six1- mediated breast tumorigenesis.

This technology includes a series of imidazo[1,2-a]pyridines that potently inhibit FLT3, which can be utilized as an anticancer agent. These molecules retain potent binding and activity against FLT3 tyrosine kinase domain and gatekeeper mutations. This chemotype exhibits superior anti-leukemic activity against clinically-relevant FLT3-mutant acute myeloid leukemia (AML) in vitro and in vivo. Tyrosine kinase domain mutations are a common cause of acquired resistance to FLT3 inhibitors used to treat FLT3-mutant AML.

This technology includes a series of imidazo[1,2-a]pyridines that potently inhibit FLT3, which can be utilized as an anticancer agent. These molecules retain potent binding and activity against FLT3 tyrosine kinase domain and gatekeeper mutations. This chemotype exhibits superior anti-leukemic activity against clinically-relevant FLT3-mutant acute myeloid leukemia (AML) in vitro and in vivo. Tyrosine kinase domain mutations are a common cause of acquired resistance to FLT3 inhibitors used to treat FLT3-mutant AML.

This technology includes a method of analyzing the potency of membrane transporter protein-based drugs acting on intracellular antioxidant and redox response pathways (and associated apoptosis pathways), wherein the drug delivery and activity is lipid associated. The present invention is a cell-based bioassay for measuring the bioactivity of drug substance and formulated drug product by determining the drug's dose-dependent inhibitory effects on 4 hydroxynonenal (4-HNE)-induced antioxidant response element (ARE) activity.

This technology includes small molecule inhibitors of O-linked N-acetyl glucosamine (OGlcNAc) transferase (OGT) as molecular probes to better understand OGT function in cell homeostasis, and to eventually be used as therapeutic agents against cancer and to reduce viral replication. OGT is a ubiquitous enzyme catalyzing the transfer of N-acetylglucosamine to the serine or threonine residues of nuclear and cytoplasmic proteins. This cellular process is tightly regulated and is sensitive to levels of cellular stress and of nutrients levels.

This technology includes a codon optimized expression vector for the high expression and production of RLIP-76 which can be used to provide protection from radiation. RLIP-76 is a multifunctional membrane protein that transports glutathione conjugates of electrophilic compounds outside the cell. The sequence was generated with codon bias alterations, reduction of secondary structure, lowering of GC content, and removal of cryptic elements that could affect expression in E.coli.

This technology includes a newly designed chemical molecule that is both an antifungal agent, by inhibiting CYP51, and an anti-inflammatory agent, by inhibiting 5-lipoxygenase, for the treatment of dandruff. Both of these properties would be useful for antifungal treatments, and both of these attributes are required to combat dandruff. However, typical therapies involve treating the infection and inflammation separately.

This technology includes a precise measurement assay of cellular FMRP levels in patients, which can assist in the diagnosis and assess the severity of Fragile X syndrome (FXS). FXS is an X-linked disorder that produces intellectual disability, cognitive impairment, epilepsy, depression and anxiety. FXS is caused by mutations in the Fragile X Mental Retardation-1 (FMR1) gene that result in the absence or a loss of function of its protein product, FMRP.

This technology includes a group of eight AMPK activating compounds to be further developed for the treatment of Niemann Pick Type C (NPC) disease. Through the recent molecular biology and pharmacological experiments, we have identified the cyclodextrin which directly binds to beta-subunits of AMP-activated protein kinase (AMP), resulting in subsequently activations of AMPK and AMPK linked autophagy, and restoration of autophagy function that is impaired in the NPC cells.

This technology includes newly identified best-in-class inhibitors of the p53-S100B interaction that plays a role in malignant melanoma. S100B contributes to cancer cell proliferation (particularly malignant melanoma) by binding to p53 and inhibiting its tumor suppressor function. A high-throughput screen was used to find p53-S100B inhibitors, leading to the identification of a putative inhibitor, which was then subjected to medicinal chemistry optimization. Structure-based design was then used to develop compounds with significantly improved potency.