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The National Cancer Institute is seeking parties interested in collaborative research to co-develop or license the in vitro and in vivo removal of targets using light energy.

Investigators at the National Cancer Institute have discovered fluoroquinolone derivatives as specific Tdp1 inhibitors that could potentiate the pharmacological action of Top1 inhibitors currently used in cancer treatment.

The National Cancer Institute seeks partners interested in collaborative research to co-develop PARP inhibitor and NO-donor hybrid prodrugs for the treatment of cancer.

Researchers at the National Cancer Institute found that the absence of CD47 enhances stem cell renewal in vitro and in vivo by increasing expression of four stem cell transcription factors.

To improve the therapeutic effectiveness of PE-based immunotoxins through multiple rounds of drug administration, NIH inventors have sought to identify and remove the human B cell epitopes within PE. Previous work demonstrated that the removal of the murine B cell and T cell epitopes from PE reduced the immunogenicity of PE and resulted in immunotoxins with improved therapeutic activity. The National Cancer Institute's Laboratory of Molecular Biology seeks interested parties to co-develop and commercialize immunotoxins using toxin domains lacking human B cell epitopes.

The Frederick National Laboratory for Cancer Research seeks parties interested in collaborative research to co-develop software for the automatic 3-D visualization of biological image volumes.

The present invention describes novel virus-like particles (VLPs) that are capable of binding to and replicating within a target mammalian cell, including human cells. The claimed VLPs are safer than viral delivery because they are incapable of re-infecting target cells. The National Cancer Institute's Protein Expression Laboratory seeks parties interested in licensing the novel delivery of RNA to mammalian cells using virus-like particles.

Pulmonary surfactant plays a critical role in preventing alveolar collapse by decreasing surface tension at the alveolar air-liquid interface. Surfactant deficiency contributes to the pathogenesis of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), common disorders that can afflict patients of all ages and carry a mortality rate greater than 25%. Excess surfactant leads to pulmonary alveolar proteinosis. NCI investigators created a G-protein coupled receptor GPR116 mutant mouse model and showed that GPR116 plays a previously unexpected, essential role in maintaining normal surfactant levels in the lung. The National Cancer Institute seeks partners interested in collaborative research to license surfactant modulating agents for the treatment of surfactant related lung disorders.

The National Cancer Institute seeks partners interested in licensing or co-development of assays for determining the levels of gamma-H2AX/H2AX to measure and quantify DNA damage.