Technology Partnership of Nagoya University, Inc.
World Class Research Contributing to Society
Available Technologies
PHARMA & DRUGS
(for more information, click title to open PDF file)
A-59 Novel Biomarkers and Agents to Screen Molecular-Targeted Therapeutics for Peritoneal Metastasis from Gastric Cancer
NU Researchers identified Synaptotagmin VIII (SYT8) as a candidate biomarker specific to peritoneal metastasis.
A-60 Novel Biomarkers and Agents to Screen Molecular-Targeted Therapeutics for Hepatic Metastasis from Gastric Cancer
Nagoya University researchers conducted transcriptome analysis using a next-generation sequencing platform and identified major facilitator superfamily domain containing 4 (MFSD4) as a candidate biomarker for hepatic metastasis of GC.
A-61 Antibody that Inhibits Wnt Signal Activation Pathway
Although it is known that ADAM family proteases cause the severe bleeding from haemorrhagic snake venom, the detailed mechanism of the haemorrhage is unclear. Researchers at Nagoya University have found that the target of ADAM proteases is a Wnt/β-catenin signal receptor, LRP5/6 which controls cell differentiation and proliferation.
A-65 Method for Preparing Genetically-Modified T Cells Which Express Chimeric Antigen Receptor
The research team at Nagoya University has improved the large-scale T cell culture method and achieved the highest introduction efficiency in a non-viral system; over 50%, by mixing and co-culturing Genetically-modified T Cells with activated T Cells that were separately prepared.
A-66 Novel Artificial T cell Activating Adapter Molecules to Improve TCR-T Therapy
To improve the effect of TCR-T without modifying TCR affinity, researchers at Nagoya University have developed two artificial T cell activating adapter molecules (ATAMs), CD3ζ/CD28 and CD3ζ/4-1BB, for cancer immunotherapy.
A-67 A new animal model and therapeutic agent for synaptic dysfunction, FTLD and ALS
Researchers at Nagoya University have identified a potential therapeutic agent by developing a novel knockout mouse that presents the symptoms mimicking FTLD patients.
A-68 Novel Drug for the Treatment of Juvenile Myelomonocytic Leukemia
Nagoya University researchers have successfully identified a drug for the treatment of JMML using integrated molecular profiling.
A-69 Noble therapeutics targeting a neuromuscular disease, Spinal and bulbar muscular atrophy
Researchers in Nagoya University have successfully identified the therapeutics of SBMA targeting the spatiotemporal dysregulation of signaling pathways in SBMA.
A-70 Novel biomarker to predict immunotherapy effect on cancer patients
Nagoya University researchers have successfully elucidated functional molecular mechanism of the ISLR, immunoglobulin superfamily containing leucin e-rich repeat, to develop highly sensitive biomarker as a checkpoint protein for Immunotherapies.
A-71 A Novel mouse model for the study of narcolepsy and orexin system function
To create a model with closer fidelity to human narcolepsy, researchers used the Tet-off system in which expression of diphtheria toxin A (DTA) in orexin neurons is controlled by the presence or absence of doxycycline (DOX). By changing DOX-containing diet to normal diet, all narcolepsy symptoms were reproduced in this model mice, that is robust cataplexy as well as disrupted sleep architecture and weight gain.
A-72 Transgenic Archaerhodopsin-3 mice as Type 2 Narcolepsy model mice
Researchers created a transgenic mice line to control the activity of the orexin neurons in the hypothalamus by exposure to light. This mice express a light-sensitive proton pump called archarhodopsin-3 exclusively in orexin neurons. Archarhodopsin-3 enables block neural activity by sensing green light. When green light was applied into the hypothalamus, activity of orexin neurons was suppressed, and as a result, mice started sleep. In addition, transgenic mice that express a large amount of the archarhodopsin-3 protein in orexin neurons showed abnormality of circadian rhythm, metabolic and sleep disturbances without illumination of green light onto the hypothalamus. This mice showed an increase in REM sleep which is seen in patients with narcolepsy, but no cataplexy-like symptoms characteristic of narcolepsy type. It is noteworthy that no loss of orexin neurons was observed in this mouse. Since there is no loss of orexin neurons in this model mice, it can be said that it succeeded in making a model mouse of type 2 narcolepsy.