In Vivo Gene Therapy For Heart Failure
- Technology Benefits
- A novel approach to increase the function of a failing heart The use of adenovirus vectors enable easy application of gene therapy in clinical settings The strategy can be used in combination with recommended treatments
- Detailed Technology Description
- Scientists at UCSD and San Diego VA Healthcare System have discovered methods and compositions for increasing function of the failing heart by a one-time intracoronary infusion of an adenovirus vector encoding human AC VI. Salutary effects on the failing heart include increased contractile performance, reduced heart block, normalization of action potential duration, regression of adverse LV remodeling and reduced mortality. These effects have been demonstrated in preclinical animal models. This technology can therefore be used in the treatment of heart disease, especially congestive heart failure.
- Supplementary Information
- Patent Number: US6306830B1
Application Number: US19988097A
Inventor: Hammond, H. Kirk | Insel, Paul A. | Ping, Peipei | Post, Steven R. | Gao, Meihua
Priority Date: 5 Sep 1996
Priority Number: US6306830B1
Application Date: 16 Jan 1998
Publication Date: 23 Oct 2001
IPC Current: C12N000988 | A61K004800
US Class: 514044A | 514044 | 4240932 | 4352351 | 4353201
Assignee Applicant: The Regents of the University of California
Title: Gene therapy for congestive heart failure
Usefulness: Gene therapy for congestive heart failure
Summary: USE (I) can be used to form a filtered adenovirus particle preparation. (I) is used to enhance cardiac function in mammals.
Novelty: Vectors containing transgene(s) encoding beta-adrenergic signalling proteins useful for gene therapy of congestive heart failure
- Industry
- Biomedical
- Sub Category
- DNA/Gene Engineering
- Application No.
- 6306830
- Others
-
Additional Technologies by these Inventors
Tech ID/UC Case
22727/1998-B28-0
Related Cases
1998-B28-0
- *Abstract
-
Congestive heart failure (CHF) is defined as abnormal heart function resulting in inadequate cardiac output for metabolic needs. It has been reported that 3-4 million adults in the United States have CHF and the incidence is increasing. Annually in US hospitals, CHF is the most frequent non-elective admission and the discharge diagnosis for 500,000 patients. Once symptoms of heart failure are moderately severe, the prognosis is worse than most cancers in that 50% of such patients are dead within 4 years. Present treatments for CHF include pharmacological therapies, coronary revascularization procedures (e.g. coronary artery bypass surgery and angioplasty), and implantable cardiac defibrillators and biventricular pacemakers. However, even with optimal therapy, approximately half of the patients with severe CHF die within 4 years. Cardiac transplantation provides a better solution, but is available for only 1 patient per 1000 with CHF.
Adenylyl cyclase has long been recognized as a pivotal effector molecule in cardiac myocytes and other cells. It has been demonstrated that the amount of adenylyl cyclase type VI (AC VI ) sets a limit on the ability of cardiac myocytes to generate cAMP and that cardiac-directed expression of AC VI increases cardiac contractile function in transgenic mice. When AC VI is expressed in the background of G q -associated cardiomyopathy, cardiac function and survival are improved. It has also been shown that global left ventricular ( LV ) function and responsiveness can be changed by gene transfer of AC VI in a manner that can be applied clinically through intracoronary delivery.
- *IP Issue Date
- Oct 23, 2001
- *Principal Investigator
-
Name: Mei Hua Gao
Department:
Name: H. Kirk Hammond
Department:
Name: Paul Insel
Department:
Name: Peipei Ping
Department:
Name: Steven Post
Department:
- Country/Region
- USA
