Therapeutics

Displaying 1 - 10 of 33


Vascular Restoration Therapy with Cell-Penetrating CRADD Protein

Vascular inflammation caused by metabolic, autoimmune, and microbial insults mediates cardiovascular diseases that include hypertension and atherosclerosis (heart attacks, strokes), systemic lupus, and giant cell arteritis. An estimated 35 million Americans have hypercholesterolemia, contributing to 500,000 deaths underlying heart attacks and strokes. In these diseases, metabolic, autoimmune, and microbial insults continually challenge blood and vascular cells by triggering signaling to the nucleus mediated by BCL10. Genetic ablation of BCL10 rescues animals from atherosclerosis, aortic aneurysms, and fatty liver and insulin resistance due to overnutrition. Intracellular therapy with CP-CRADD is designed to extinguish BCL10-mediated noxious signals to avert vascular inflammation and its life-threatening complications including ruptured aneurysms in aorta and brain.


Licensing Contact

Janis Elsner

615.343.2430
Therapeutics

Prevention of Cytokine Induced Apoptosis In Intestinal Epithelial Cells By A Probiotic Bacterium

The present invention provides therapeutic and prophylactic compositions for use in treating and preventing disorders involved epithelial cell apoptosis, such as gastrointestinal disorders (e.g., inflammatory bowel disease, Crohn's disease or ulcerative colitis) in a subject, such as a human patient.


Licensing Contact

Janis Elsner

615.343.2430

Inventors

Brent Polk, Fang Yan
Therapeutics
Protein/Peptide
Gastrointestinal

Fused in Sarcoma (FUS) Nuclear Translocation Inhibitors for Preventing Fibrosis

The research team has found that one of the key regulators of collagen production in fibrotic diseases is the FUS ribonucleoprotein. This protein is upregulated in fibrotic diseases leading to additional collagen formation and deposition. In order to combat FUS upregulation, a new approach to blocking nuclear translocation has been developed using an FUS targeting peptide approach.


Licensing Contact

Janis Elsner

615.343.2430
Therapeutics

Cell-Permeable Socs Proteins That Inhibit Cytokine-Induced Signaling

Scientists at Vanderbilt have developed a unique polypeptide using cell-penetrating SOCS polypeptides or SOCS sequences designed to inhibits cytokine signaling and thus prevent or treat inflammation or an inflammatory related disease such as diabetes. This strategy has been validated in NOD mice models for either induced or naturally occurring diabetes and have been efficacious.


Licensing Contact

Janis Elsner

615.343.2430
Therapeutics

Small Molecule Theraputics That Target the Muscarinic Acetylcholine Receptor 1 For The Treatment of Alzheimer's Disease

The Vanderbilt Center for Neuroscience Drug Discovery (VCNDD) has a mission to promote the translation of advances in basic science towards novel therapeutics. They have recruited faculty and staff with experience at over 10 different pharmaceutical companies to ensure a diverse set of approaches, techniques and philosophies to advancing compounds. Together they aim to de-risk drug discovery programs.


Licensing Contact

Tom Utley

615.343.3852
Therapeutics
Neuroscience/Neurology

Long-Lasting and Self-Sustaining Cell Therapy System

Researchers at Vanderbilt have created a novel drug delivery system using two distinct T-cell populations that interact to promote engraftment and persistence in pre-clinical models, increasing the efficacy of T-cell therapies. Furthermore, "booster" treatments can be administered months after the first dose to produce an expansion of antigen specific T cells. These advantages result in longer-term therapeutic efficacy and could reduce the number of treatments required. This system also represents a viable self-renewing platform for the delivery of biologic drugs in patients who would otherwise require frequent administration.


Licensing Contact

Clarissa Muere

615.343.2430

Natural product for seizure relief and long term disease modification in Dravet Syndrome

Dravet syndrome is a lifelong form of epilepsy beginning in early childhood. Children with Dravet syndrome suffer aggressive seizures, impaired cognition, and an increased risk of premature death. Dravet syndrome does not respond to conventional anti-epileptic drugs, and current treatment regimens fail to fully elevate seizures. No disease modifying treatments exist. Researchers at Vanderbilt University have discovered a novel application of a known natural product in treating Dravet syndrome. This natural product could be beneficial to children suffering from Dravet syndrome in both reducing seizures and treating the underlying disease cause.


Licensing Contact

Tom Utley

615.343.3852

Inventors

Jingqiong Kang
Therapeutics
Neuroscience/Neurology

New Clostridium Difficile Recombinant Toxin for Safe Vaccine Development

A structural biology approach has identified a conserved region common to multiple Clostridium toxins. Specific mutations of the protein sequence in this region prevent the toxins from entering into intestinal cells, thereby preventing widespread tissue damage. These recombinant Clostridium toxins may be used to create a multivalent vaccine to protect against multiple species of Clostridium. Furthermore, the recombinant toxin may be used as a safer alternative to the native toxins in vaccine manufacturing. This discovery stems from a collaboration between the laboratories of Dr. Borden Lacy of Vanderbilt University and Dr. Roman Melnyk of the Hospital for Sick Children.


Licensing Contact

Jody Hankins

615.322.5907

Systems-Biology Infrastructure to Identify Drug Repurposing Opportunities as Antiviral & Anticancer Therapeutics

Vanderbilt researchers have developed an in-silico screening method to reveal new indications for existing drugs with known protein targets using a novel infrastructure. The infrastructure integrates multiple factors across system-biology models to create a drug discovery pipeline.


Licensing Contact

Janis Elsner

615.343.2430

Targeting microRNAs as a Treatment for Vascular Disease

Vanderbilt researchers have identified a highly expressed microRNA crucial in angiotensin induced hypertension; and developed a therapeutic strategy that focuses on local or systemic administration of antisense microRNA to inhibit microRNA expression as treatment for vascular diseases. Promising data in animal models reveals that the inhibition of such microRNA not only prevents fibrosis but also reverses previously established aortic stiffening.


Licensing Contact

Jody Hankins

615.322.5907