This technology is a method for treating c-Myc overexpressing cancers, graft-versus-host disease, and autoimmune diseases through administration of casein kinase-1 epsilon (CK-1) and phosphoinostidine 3-kinase (PI3K) dual inhibitors alone or in combination with proteasome inhibitors.
c-Myc is a regulatory gene frequently overexpressed in cancer and is also relevant for various immunological disorders. Although c-Myc is an attractive therapeutic target due to its involvement in many essential cellular functions, direct inhibition of this molecule poses risk of toxicity in patients. Therefore, targeting of upstream signals that regulate c-Myc expression is a promising approach. However, there are currently no effective strategies available for silencing c-Myc expression.
This technology is a method for treating c-Myc overexpressing cancers, autoimmune diseases, and graft-versus-host disease that can arise following organ transplant. Treatment with dual CK-1/PI3K inhibitors combined with proteasome inhibitors effectively leads to reduced c-Myc translation and inhibition of certain downstream functions of c-Myc. As a result, this combination therapy provides a safe, versatile method for treating autoimmune diseases, immunological complications resulting from organ transplant rejection, and various cancers.
This technology has been validated using select compounds in a phase 1 dose-escalation study for lymphocytic leukemia and lymphoma.
IR CU16047
Licensing Contact: Jerry Kokoshka