The General Hospital Corporation

Harvard College

Massachusetts General Hospital Corporation

Bristol-myers Squibb Compnay

Ionics, Inc.

Emory University

Edgar Haber

Gary R Matsueda

Guy L Reed

Mu-En Lee

Marschall S Runge

Shaw-Fang Yet

Mukesh Jain

Arthur L Goldstein

Ban A Khaw

Thomas Quertermous

Robert J Mandle

Michael N Margolies

Christoph Bode

Chengwei Shi

Kwan Hui

James D Burton

Meredith Mudgett-Hunter

Jer-Chia Tsai

James A Burton

Mitsuaki Isobe

Wen-Sen Lee

Winston Campbell Patterson

Paul H Ehrlich

Nicholas E S Sibinga

Charles J Homcy

The present invention relates to a treatment for myocardial infarction and blood clots within a patient, and more specifically to a therapy which enhances clot lysis comprising administering to a patient an antibody directed to &agr;2-antiplasmin crosslinked to fibrin (&agr;2AP-FX) which does not inhibit plasma &agr;2-antiplasmin (&agr;2AP). The invention also relates to a treatment for enhancing clot lysis comprising administering an antibody directed toward &agr;2-antiplasmin crosslinked to fibrin which does not inhibit plasma &agr;2AP together with a thrombolytic agent.

Antibodies that bind to &agr;2-antiplasmin crosslinked to fibrin which do not inhibit plasma &agr;2-antiplasmin

The invention provides an isolated DNA which regulates vascular smooth muscle cell-specific transcription of a polypeptide-encoding sequence to which it is operably linked

Smooth muscle cell LIM promoter

A mouse model for vein graft stenosis useful for identifying compounds which reduce or prevent such stenosis, consisting of a mouse engrafted with an autogenous vein which exhibits detectable stenosis within 30 days of transplantation. Also disclosed are therapeutic methods for inhibiting the development of vein graft stenosis.

Cellular basis of vascular-graft stenosis

A substantially pure DNA comprising a sequence encoding a smooth muscle cell LIM (SmLIM) polypeptide, methods of diagnosing vascular injury by detecting a decrease in SmLIM gene expression, and methods of inhibiting vascular smooth muscle cell proliferation.

Smooth muscle cell LIM protein

A substantially pure DNA comprising an endothelial cell-specific promoter sequence capable of directing endothelial cell-specific transcription of a polypeptide-encoding sequence or an antisense template to which it is operably linked.

Endothelial-cell specific promoter

The present invention relates to a treatment for myocardial infarction and blood clots within a patient, and more specifically to a therapy which enhances clot lysis comprising administering to a patient an antibody directed to .alpha.2-antiplasmin crosslinked to fibrin (.alpha.2AP-FX) which does not inhibit plasma .alpha.2-antiplasmin (.alpha.2AP). The invention also relates to a treatment for enhancing clot lysis comprising administering an antibody directed toward .alpha.2-antiplasmin crosslinked to fibrin which does not inhibit plasma .alpha.2AP together with a thrombolytic agent.

Antibodies that bind to .alpha.2-antiplasmin crosslinked to fibrin which

Hybrid immunoglobulin-enzyme molecules are provided which are composed of antibodies, or derivatives or fragments thereof, which specifically bind an arterial or venous thrombus that are operably linked to the enzymatically active portions of thrombolytic enzymes such as plasminogen activators. In a preferred embodiment the hybrid molecules specifically bind to fibrin and have fibrinolytic activity. The hybrid molecules of the present invention may be produced by any means, including chemical conjugation, or by means of recombinant DNA, genetic engineering and/or hybridoma technology. Methods for making and using the molecules in diagnosis and therapy are also disclosed.

Hybrid immunoglobulin-thrombolytic enzyme molecules which specifically

A mouse model for transplant arteriosclerosis useful for identifying compounds which reduce or prevent such arteriosclerosis, consisting of a mouse engrafted with a histoincompatible artery which exhibits detectable arteriosclerosis within 30 days of transplantation. Also disclosed are therapeutic methods for inhibiting the development of transplant arteriosclerosis in mammalian recipients of allografted organs.

Cellular basis of transplant arteriosclerosis in mice

Methods of inhibiting the activation of Factor XIII

The present invention relates to a treatment for myocardial infarction and blood clots within a patient, and more specifically to a therapy which enhances clot lysis comprising administering to a patient an antibody directed to .alpha.2-antiplasmin crosslinked to fibrin (.alpha.2AP-Fx) which does not inhibit plasma .alpha.2-antiplasmin (.alpha.2AP). The invention also relates to a treatment for enhancing clot lysis comprising administering an antibody directed toward .alpha.2-antiplasmin crosslinked to fibrin which does not inhibit plasma .alpha.2AP together with a thrombolytic agent.

A method of inhibiting arteriosclerosis or smooth muscle cell proliferation by identifying an animal having an artery suspected of needing such inhibition and contacting the artery with an apoptosis-inducing amount of an antioxidant.

Antioxidant-induced apoptosis in vascular smooth muscle cells

Heterobifunctional antibodies having dual specificities, one specificity directed against a thrombus, and the other specificity directed against a thrombolytic agent are disclosed. The invention also relates to methods of using these heterobifunctional antibodies to lyse a thrombus.

Growing community of inventors

Salisbury, NH, United States of America

Edgar Haber