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Johns Hopkins, Scripps Research Institute, Competitive Technologies License Biotechnologies

Licensing institution: Johns Hopkins University
Primary inventors: Katharine Whartenby, assistant professor, oncology, JHU; Donald Small, professor, oncology, JHU
Licensee: Xanthus Pharmaceuticals, Cambridge, Mass.
Technology: Xanthus has taken an exclusive worldwide license to a patent estate for treating immune-related disorders by inhibiting the FLT3 tyrosine kinase. In addition, Xanthus and JHU have initiated a research project to assess novel compounds for FLT3 inhibitory activity and the downstream pathways relevant to a range of automimmune diseases.

Licensing institution: Scripps Research Institute
Primary inventor: Joel Gottesfeld, professor, molecular biology, Scripps Research Institute
Licensee: Repligen, Waltham, Mass.
Technology: Repligen has taken an exclusive worldwide license to IP covering compounds that may have utility in Friedreich’s ataxia, an inherited neurodegenerative disease in which low levels of the protein frataxin result in progressive damage to the nervous system and loss of muscle function.

Licensing institution: Competitive Technologies
Primary inventor: Harley Rotbart, professor, pediatrics and microbiology, University of Colorado Health Sciences Center
Licensee: Focus Diagnostics, Cypress, Calif.
Technology: Focus Diagnostics will be producing enterovirus assay kits under a recently expanded license granted to it for use of patented technology for the rapid assay of human enteroviruses. The technology was developed by Harley Rothbart at UC, a Competitive Technologies client.

The Scan

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A genome-wide association study meta-analysis of attention-deficit hyperactivity disorder appearing in Nature Genetics links 76 genes to risk of having the disorder.

MicroRNA Cotargeting Linked to Lupus

A mouse-based study appearing in BMC Biology implicates two microRNAs with overlapping target sites in lupus.

Enzyme Involved in Lipid Metabolism Linked to Mutational Signatures

In Nature Genetics, a Wellcome Sanger Institute-led team found that APOBEC1 may contribute to the development of the SBS2 and SBS13 mutational signatures in the small intestine.