Office of Technology Management
University Center Tower (UCT)
7000 Fannin Street, Suite 720  
Houston, Texas 77030
Phone: (+1) 713-500-3369    
Fax: (+1) 713-500-0331
Email: otm@uth.tmc.edu

Latest Technologies

Formulation of HDACi Loaded ß-Cyclodextrin-poly (ß-amino ester) Nanoparticles

Researchers have developed a novel formulation strategy to encapsulate molecules, including but not limited to histone deacetylase inhibitor (HDACi) drugs in nanoparticle networks composed of beta-cyclodextrin-poly(beta-amino esters). Advantages of this system include high loading capacity, increased in vivo tolerability, sustained release, and improved drug distribution and activity in the treatment of solid tumors. Technology OverviewA beta-cyclodextrin-based, cross-linked polymer is employed in the formulation as a novel excipient instead of conventional diblock copolymers like PLGA an...

Monoclonal antibodies against human endotrophin for therapeutic and diagonostic use.

BackgroundStudies have shown that endotrophin, the carboxy-terminal cleavage product of the COL6α3 chain, has potent effects on transformed mammary ductal epithelial cells in rodents. It is abundantly expressed in adipose tissue and is a chemoattractant for macrophages, exerts effects on endothelial cells and enhances the progression through epithelial-mesenchymal transition (EMT) in tumor cells. In a recombinant form, human endotrophin exerts similar effects on human macrophages and endothelial cells as in its rodent counterpart. It enhances EMT in human breast cancer cells and upon ove...

HER3 specific monoclonal antibodies for diagnosis and therapeutic use

BackgroundHER-3 is a receptor in the tyrosine kinase family that is a key oncogenic protein in breast cancer as well as other cancers. HER-3 is centrally involved in signaling leading to tumor growth and has been implicated in resistance to cancer treatments, making it an attractive target for cancer therapies.  Several drugs, including some in clinical use, directly target HER-2, the oncogenic signaling partner of HER-3. However, these treatments often activate compensatory HER-3 signaling, which circumvents the activity of the drug and frequently leads to treatment failure. Drugs that t...

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