Creative Biomolecules, Inc.

Curis, Inc.

Hoffmann-la Roche Inc.

Stryker Corporation

The State University of New York

John E Smart

Thangavel Kuberasampath

Hermann Oppermann

David C Rueger

Charles M Cohen

Engin Ozkaynak

Roy H Pang

Roy H L Pang

Marc F Charette

Donald F Jin

Peter C Keck

Pascal Sebastian Bailon

Herrmann Oppermann

David V Weber

Kuber T Sampath

Dennis Higgins

Disclosed are methods and compositions for maintaining the integrity of the gastrointestinal tract luminal lining in a mammal, including (1) limiting epithelial cell proliferation, (2) inhibiting ulcerative lesion formation, (3) inhibiting inflammation normally associated with ulcerative diseases, and (4) stimulating the repair of ulcerative lesions and the regeneration of the luminal tissue. The methods and compositions include a therapeutically effective amount of a morphogen as defined herein.

Morphogen treatments for limiting proliferation of epithelial cells

The invention is a treatment for increasing the bone mass or preventing bone loss in an individual afflicted with a bone disease which includes administering to the individual a morphogen in a therapeutically effective amount so as to maintain or stimulate bone formation.

Treatment to prevent loss of and/or increase bone mass in metabolic bone diseases

Disclosed are methods and compositions for maintaining neural pathways in a mammal including: enhancing survival of neurons at risk of dying; inducing cellular repair of damaged neurons and neural pathways; stimulating neurons to maintain their differentiated phenotype; and promoting dendritic outgrowth, including maintaining dendritic arbors and regenerating dendritic architecture. In one embodiment, the invention provides means for stimulating CAM expression in neurons. The invention also provides means for evaluating the status of nerve tissue, including means for detecting and monitoring neuropathies in a mammal. The methods, devices and compositions include a morphogen or morphogen-stimulating agent provided to the mammal in a therapeutically effective concentration. In another embodiment, the invention provides methods and compositions which include a morphogen or morphogen-stimulating agent, and a nerve trophic factor or nerve trophic factor-stimulating agent at concentrations effective for stimulating dendrite outgrowth. The morphogen and the nerve trophic factor can be admixed in combination.

Morphogen-induced dendritic growth

Disclosed are a family of single-chain polypeptide constructs designed to agonize or mimic members of the TGF-&bgr; superfamily by binding to a cell surface receptor complementary to the superfamily member. The single-chain constructs of the invention called &ldquo;morphons&rdquo; contain in a single biologically active subunit interacting finger and heel regions which together define a tertiary protein structure complimentary to the ligand binding surface of a receptor that binds a TGF-&bgr; superfamily member . Also disclosed are truncated versions of the morphon constructs. Methods are disclosed for making and using single-chain morphons that have binding affinity for predetermined receptors of the TGF-&bgr; superfamily.

Single chain analogs of the TGF-&bgr; superfamily (morphons)

Disclosed are (1) nucleic acid sequences, amino acid sequences, homologies, structural features and various other data characterizing a morphogen cell surface receptor; (2) methods for producing receptor proteins, including fragments thereof, using recombinant DNA technology; (3) methods for identifying novel morphogen receptors and their encoding DNAs; (4) methods for identifying compounds capable of modulating endogenous morphogen receptor levels; and (5) methods for identifying morphogen receptor binding analogs useful in the design of morphogen agonists and antagonists for therapeutic, diagnostic and experimental uses.

Morphogen cell surface receptor and screening for morphogen analogs

The present invention is directed to methods and compositions for enhancing viability of organs and living tissues to be transplanted in a mammal. The methods and compositions provide a therapeutically effective concentration of a morphogen or morphogen-stimulating agent to the tissue or organ to be transplanted, sufficient to substantially protect the tissue or organ from tissue damage.

Morphogen treatment of organ implants

The present invention is directed to methods and compositions for alleviating tissue destructive effects associated with the inflammatory response to tissue injury in a mammal. The methods and compositions include administering a therapeutically effective concentration of a morphogen or morphogen-stimulating agent sufficient to alleviate immune cell-mediated tissue destruction.

Method for reducing tissue damage associated with ischemia-reperfusion

Disclosed are a family of single-chain polypeptide constructs designed to agonize or mimic members of the TGF-.beta. superfamily by binding to a cell surface receptor complementary to the superfamily member. The single-chain constructs of the invention called 'morphons' contain in a single biologically active subunit interacting finger and heel regions which together define a tertiary protein structure complimentary to the ligand binding surface of a receptor that binds a TGF-.beta. superfamily member. Also disclosed are truncated versions of the morphon constructs. Methods are disclosed for making and using single-chain morphons that have binding affinity for predetermined receptors of the TGF-.beta. superfamily.

Single chain analogs of the TGF-.beta. superfamily (morphons)

Disclosed is a method of screening candidate compounds for the ability to modulate the level of morphogenic protein in mammalian system. The method includes determining a parameter indicative of the level of production of a morphogenic in a cell culture known to produce the morphogen, incubating a candidate compound with the culture for a time sufficient to allow the compound to affect the production of the morphogenic protein, and then assaying the culture again to detect a change in the level of morphogenic protein production.

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Weston, MA, United States of America

John E Smart