Anti-SST monoclonal antibody, clone ZD8

An 87-year-old woman with leg-type lymphoma underwent a staging F-18-FDG PET/CT, which demonstrated besides leg lymphomatous lesions a round, well-defined, preduodenal mass with moderate FDG uptake. This mass remained unchanged after chemotherapy treatment completion, despite a complete metabolic response of lymphomatous lesions. A biopsy revealed a gangliocytic paraganglioma. Subsequent F-18-FDOPA PET/CT and somatostatin receptor scintigraphy were positive and did not depict any other lesions.

Primary Objective We tested whether KPT-350, a novel selective inhibitor of nuclear export, could attenuate cortical network hyperexcitability, a major risk factor for developing post-traumatic epilepsy (PTE) following traumatic brain injury (TBI). Research Design All mice in this study underwent TBI and were subsequently treated with either KPT-350 or vehicle during the post-injury latent period. Half of the animal cohort was used for electrophysiology while the other half was used for immunohistochemical analysis. Methods and Procedures TBI was induced using the controlled cortical impact (CCI) model. Cortical network activity was recorded by evoking field potentials from deep layers of the cortex and analyzed using Matlab software. Immunohistochemistry coupled with fluorescence microscopy and Image J analysis detected changes in neuronal and glial markers. Main Outcomes and Results KPT-350 attenuated TBI-associated epileptiform activity and restored disrupted input-output responses in cortical brain slices. In vivo KPT-350 treatment reduced the loss of parvalbumin-(+) GABAergic interneurons after CCI but did not significantly change CCI-induced loss of somatostatin-(+) GABAergic interneurons, nor did it reduce reactivity of GFAP and Iba1 glial markers. Conclusion KPT-350 can prevent cortical hyperexcitability and reduce the loss of parvalbumin-(+) GABAergic inhibitory neurons, making it a potential therapeutic option for preventing PTE.