University of Utah Research Foundation

Navigen, Inc.

Dean Li

Mark T Keating

Lise Sorensen Brunhart

Brent D Wilson

Christopher C Gibson

Christopher Jones

Nyall London

Hariprasad Vankayalapati

Ashok Bajji

Kirill Ostanin

Mark Shenderovich

Christopher L Cioffi

Kyle Won Park

Neil Moss

Kye Won Park

Disclosed herein are compounds and methods for inhibiting Arf6. Pharmaceutical compositions and methods for treating a subject with an inhibitor of Arf6 are also disclosed herein.

Arf6 inhibitors and methods of synthesis and use thereof

The invention provides methods, compositions, and devices for promoting adhesion or migration of endothelial cell.

Tropoelastin for promoting endothelial cell adhesion or migration

Methods are provided of treating and preventing stroke diseases, such as cerebral cavernous malformation, by the administration of tempol and/or cholecalciferol.

Methods of treating and preventing vascular instability diseases

The invention provides methods, compositions, and devices for promoting adhesion or migration of endothelial cells.

Compounds, compositions and methods for inhibiting vascular permeability and pathologic angiogenesis are described herein. Methods for producing and screening compounds and compositions capable of inhibiting vascular permeability and pathologic angiogenesis are also described herein. Pharmaceutical compositions are included in the compositions described herein. The compositions described herein are useful in, for example, methods of inhibiting vascular permeability and pathologic angiogenesis, including methods of inhibiting vascular permeability and pathologic angiogenesis induced by specific angiogenic, permeability and inflammatory factors, such as, for example VEGF, bFGF and thrombin. Methods for treating specific diseases and conditions are also provided herein.

Compositions and methods for inhibiting vascular permeability

The present invention provides methods and compositions for modulating proliferation, differentiation, migration, and adhesion of cardiovascular cell types.

Methods for inhibiting angiogenesis

Compositions and methods for treating ocular pathologic angiogenesis and vascular permeability

Promoting angiogenesis with netrin1 polypeptides

Elastin, the main component of arterial extracellular matrix, was thought to have a purely structural role. Consistent with this view, elastin hemizygous mice maintain arterial extensibility by increasing the number of elastic lamellae during development. However, mice lacking elastin die of obstructive arterial pathology. This pathology results from subendothelial proliferation and reorganization of smooth muscle, cellular changes similar to those observed in atherosclerosis. Thus, elastin is a molecular determinant of arterial morphogenesis and likely plays a central role in vascular disease. Mice which are heterozygous and null for the elastin gene have been developed. These mice are extremely useful for screening for drugs useful for treating persons with atherosclerosis, hypertension, SVAS or other vascular diseases.

Mice which are +/&#x2212; or &#x2212;/&#x2212; for the elastin gene as models for vascular disease

The present invention provides screening methods that use organisms or cells that lack function in one or both elastin genes. These methods are useful in identifying drugs for the prevention and treatment of obstructive vascular diseases, such as atherosclerosis, vascular restenosis and transplant arteriopathy. Further, the invention provides pharmaceutical compositions containing elastin-based compositions that are particularly potent regulators of proliferation, differentiation, and migration of smooth muscle cells in vitro and in vivo. These pharmaceutical compositions and related methods are useful in the prevention and treatment of disorders characterized by diminished capacity to regulate smooth muscle cell function.

Elastin-based compositions

Transgenic mice are genetically engineered for a deficiency in endoglin production. These mice may have a homozygous or hemizygous disruption of the endogenous endoglin gene. Homozygous mice exhibit a lack of endoglin production. The failure to produce endoglin results in arrested development of the vascular system of the mouse and no survival beyond E11.5. These mice and cells derived therefrom provide useful reagents for understanding the development and pathology of the mammalian vascular system.

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Salt Lake City, UT, United States of America

Dean Li