Methods for Prevention and Treatment of Polyomavirus Infection or Reactivation

Available for licensing and commercial development are methods of using two MAP kinase kinase (MEK) inhibitors, PD98059 and U0126, in the prevention and treatment of polyomavirus infection. Decrease in viral protein expression upon treatment with the MEK inhibitors has been demonstrated for two polyomavirus species, JC virus (JCV) and BK virus (BKV). It is believed that these MEK inhibitors may also be effective against other polyomavirus species in which TGF-beta expression is elevated.

Methods for Prevention and Treatment of Polyomavirus Infection or Reactivation (E-179-2007)

Available for licensing and commercial development are methods of using Tranilast [N-(3',4'-dimethoxycinnamoyl)anthranilic acid] in the prevention and treatment of human polyomavirus infection. Treatment with Tranilast decreases viral protein expression for two human polyomavirus species, JC virus (JCV) and BK virus (BKV). Furthermore, the increase in JCV/BKV protein production observed upon the addition of TGF-beta could also be effectively abolished by Tranilast co-treatment.

Hydrocarbon Stapled Peptides that Inhibit the Linear Ubiquitin Chain Assembly Complex (LUBAC) for the Therapy of the Activated B Cell-like (ABC) Subtype of Diffuse Large B Bell Lymphoma (A Type of Non-Hodgkin’s Lymphoma)

Diffuse large B-cell lymphoma (DLBCL) is the most common type of non-Hodgkin’s lymphoma and consists of three subtypes: activated B-cell (ABC), germinal center B-cell (GBC), and primary mediastinal B-cell (PMB). Despite advances in the front-line therapy for DLBCL, approximately one-third of patients will relapse. Substantially worse outcomes have been reported for patients diagnosed with ABC DLBCL and treated with standard chemoimmunotherapy, suggesting the need for novel strategies that improve treatment outcomes.

Licensing Availability: Methods of Diagnosing and Treating CHAPLE, A Newly Identified Orphan Disease

This technology is directed towards a potential treatment for a new disease, CHAPLE (Complement Hyperactivation, Angiopathic thrombosis, and Protein-Losing Enteropathy), identified by NIAID researchers. CHAPLE is associated with GI symptoms and vascular thrombosis and is caused by loss-of-function variants in the gene encoding the complement regulatory protein CD55. The disease is caused by enhanced activation of the complement pathway and complement-mediated induction of intestinal lymphangiectasia and protein-losing enteropathy.
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