DR. DAVID LEE STERN, M.D.
Osteopathic Medicine at Northern Blvd, Great Neck, NY

5227368, Jul 13, 1993

Feb 28, 1990

7/486311

Herwig Gerlach - New York NY
David Stern - Great Neck NY

The Trustees of Columbia University in the City of New York - NY

A61K 3700, C07K 300, C07K 700, C07K 1500

514 12

This invention provides a purified endotoxin-induced thrombosis factor, preferably an endotoxin-induced thrombosis factor characterized by an apparent molecular weight between about 50,000 and 65,000 daltons, more specifically about 55,000 daltons, on reduced and nonreduced SDS-polyacrylamide gels, by maximal recovery on elution from such gels at 52,000 to 58,000 daltons, by the ability to migrate as a single band on such gels, by the ability to precipitate in ammonium sulfate at saturations from 40% to 70%, by the ability to precipitate in polyethylene glycol at concentrations above 15%, by high hydrophobicity, by the ability to bind weakly to a hydroxylapatite column and to a lentil lectin column, by the ability to bind tightly to a hydrophobic interaction resin and smear off with ethylene glycol, and by the ability to bind tightly to a reverse-phase column and elute more effectively with isopropranol than with acetonitrile, by the ability to bind to an anion exchange resin over a pH range from 5 to 10, by the inability to bind to a cation exchange resin, by resistance to acid denaturation up to 30 minutes, resistance to polymyxin, sensitivity to heating at 95. degree. C. for 30 minutes, and sensitivity to trypsin exposure for 24 hours. Another characteristic of a purified endotoxin-induced thrombosis factor that it maximally induces tissue factor after six to eight hours, and continues to induce tissue factor for up to sixty hours.

7060870, Jun 13, 2006

Aug 14, 2000

09/638647

David M. Stern - Great Neck NY, US
Shi Du Yan - New York NY, US

The Trustees of Columbia University in the City of New York - New York NY

C12N 15/00, G01N 33/00

800 18, 800 3, 800 12

The present invention provides for a transgenic non-human animal whose cells contain a DNA sequence comprising: (a) a nerve tissue specific promoter operatively linked to a DNA sequence which encodes amyloid-beta peptide alcohol dehydrogenase (ABAD), and (b) a nerve tissue specific promoter operatively linked to a DNA sequence encoding a mutant human amyloid precursor protein hAPP695, hAPP751 and hAPP770 bearing mutations linked to familial Alzheimer's disease in humans, wherein the non-human animal exhibits at least one phenotype from the group consisting of: reduced basal synaptic transmission; inhibited synaptic plasticity; increased neuronal stress; elevated 4-hydroxynonenal in cerebral cortex; increased heme oxygenase type I in cerebral cortex; decreased synaptophysin in cerebral cortex; decreased micortubule-associated protein 2 in cerebral cortex; and increased levels of activated caspase 3 antigen in cortical neurons.

5968911, Oct 19, 1999

Feb 18, 1997

8/362571

Charles A. Lawson - Verona NJ
David J. Pinsky - Riverdale NY
Arthur Smerling - New Rochelle NY
David M. Stern - Great Neck NY

The Trustees of Columbia University in the City of New York - New York NY

C07H 19167, C07H 1920, A01N 4390

514 46

This invention provides a method of selectively decreasing pulmonary vascular resistance in a subject by administering endobronchially a drug chosen from among cAMP analogs, cGMP analogs, phosphodiesterase inhibitors, nitric oxide precursors, nitric oxide donors, and nitric oxide analogs.

6555340, Apr 29, 2003

Mar 5, 1999

09/263312

Ann Marie Schmidt - Franklin Lakes NJ
David Stern - Great Neck NY

The Trustees of Columbia University in the City of New York - New York NY

C12P 2106

435 691, 4353201, 435325, 536 235

The present invention provides for an isolated human EN-RAGE peptide. The present invention also provides for a method for determining whether a compound is capable of inhibiting the interaction of an EN-RAGE peptide with a RAGE peptide. The present invention also provides for a method for inhibiting inflammation in a subject which comprises administering to the subject a compound capable of interfering with the interaction between EN-RAGE peptide and receptor for advanced glycation endproduct (RAGE) in the subject thereby inhibiting inflammation in the subject.

6825164, Nov 30, 2004

Aug 14, 2000

09/638648

David M. Stern - Great Neck NY
Ann Marie Schmidt - Franklin Lakes NJ
Shi Du Yan - New York NY
Berislav Zlokovic - Rochester NY

The Trustees of Columbia University in the City of New York - New York NY

A01N 6100

514 1, 514 2, 514 44, 800 3, 5303871

The present invention provides a method for decreasing cerebral vasoconstriction in a subject suffering from chronic or acute cerebral amyloid angiopathy which comprises administering to the subject an inhibitor of receptor for advanced glycation endproduct (RAGE) in an effective amount to inhibit transcytosis of amyloid peptides across the blood-brain barrier in the subject, thereby decreasing cerebral vasoconstriction in the subject. The invention further provides for a method for ameliorating neurovascular stress in a subject which comprises administering to the subject an effective amount of an inhibitor of receptor for advanced glycation endproduct (RAGE), so as to increase cerebral blood flow in the subject, thereby ameliorating neurovascular stress in the subject.

6677299, Jan 13, 2004

Nov 5, 2001

09/992955

David M. Stern - Great Neck NY
Ann Marie Schmidt - Franklin Lakes NJ
Shi Du Yan - New York NY
Berislav Zlokovic - Rochester NY

The Trustee of Columbia University in the city of New York - New York NY

A01N 6100

514 1, 514 2, 514 44, 800 3, 800 8, 800 9, 800 12, 800 13, 800 18

The present invention provides a method for decreasing cerebral vasoconstriction in a subject suffering from chronic or acute cerebral amyloid angiopathy which comprises administering to the subject an inhibitor of receptor for advanced glycation endproduct (RAGE) in an effective amount to inhibit transcytosis of amyloid peptides across the blood-brain barrier in the subject, thereby decreasing cerebral vasoconstriction in the subject. The invention further provides for a method for ameliorating neurovascular stress in a subject which comprises administering to the subject an effective amount of an inhibitor of receptor for advanced glycation endproduct (RAGE), so as to increase cerebral blood flow in the subject, thereby ameliorating neurovascular stress in the subject.

7081241, Jul 25, 2006

Oct 6, 1998

09/167705

Ann Marie Schmidt - Franklin Lakes NJ, US
David Stern - Great Neck NY, US

The Trustees of Columbia University in the City of New York - New York NY

A61K 39/395

4241301, 4241411, 4241421, 4241431, 514 2, 514 12

The present invention provides for an isolated human EN-RAGE peptide. The present invention also provides for a method for determining whether a compound is capable of inhibiting the interaction of an EN-RAGE peptide with a RAGE peptide, which comprises: (a) admixing: (i) a RAGE peptide or an sRAGE peptide or a fragment of either thereof, (ii) an EN-RAGE peptide or a fragment thereof, and (iii) the compound; (b) measuring the level of interaction between the peptide of step (a)(i) and the peptide of step (a)(ii), and (c) comparing the amount of interaction meausred in step (b) with the amount measured between the peptide of step (a) (i) and the peptide of step (a) (ii) in the absence of the compound, thereby determining whether the compound is capable of inhibiting the interaction of the EN-RAGE peptide with the RAGE peptide, wherein a reduction in the amount of interaction in the presence of the compound indicates that the compound is capable of inhibiting the interaction. The present invention also provides for a method for inhibiting inflammation in a subject which comprises administering to the subject a compound capable of interfering with the interaction between EN-RAGE peptide and receptor for advanced glycation endproduct (RAGE) in the subject thereby inhibiting inflammation in the subject.

2004012, Jun 24, 2004

Sep 19, 2003

10/665867

Ann Schmidt - Franklin Lakes NJ, US
David Stern - Great Neck NY, US

The Trustees of Columbia University in the City of New York

C12Q001/68, C07H021/04, C07K014/705

435/006000, 435/069100, 435/320100, 435/252300, 435/325000, 530/350000, 536/023500

The present invention provides for an isolated human EN-RAGE peptide. The present invention also provides for a method for determining whether a compound is capable of inhibiting the interaction of an EN-RAGE peptide with a RAGE peptide, which comprises: (a) admixing: (i) a RAGE peptide or an sRAGE peptide or a fragment of either thereof, (ii) an EN-RAGE peptide or a fragment thereof, and (iii) the compound; (b) measuring the level of interaction between the peptide of step (a) (i) and the peptide of step (a) (ii), and (c) comparing the amount of interaction meausred in step (b) with the amount measured between the petpide of step (a)(i) and the peptide of step (a) (ii) in the absence of the compound, thereby determining whether the compound is capable of inhibiting the interaction of the EN-RAGE peptide with the RAGE peptide,, wherein a reduction in the amount of interaction in the presence of the compound indicates that the compound is capable of inhibiting the interaction. The present invention also provides for a method for inhibiting inflammation in a subject which comprises administering to the subject a compound capable of interfering with the interaction between EN-RAGE peptide and receptor for advanced glycation endproduct (RAGE) in the subject thereby inhibiting inflammation in the subject.

5552267, Sep 3, 1996

Dec 5, 1994

8/350319

David M. Stern - Great Neck NY
Mehmet C. Oz - Fort Lee NJ
Roman Nowygrod - Teaneck NJ
Shin Koga - New York NY
David J. Pinsky - Riverdale NY

The Trustees of Columbia University in the City of New York - New York NY

A01N 102

435 11

An aqueous solution for organ preservation or maintenance, which contains: a vasodilator in an amount sufficient to maintain vascular homeostasis; D-glucose in an amount sufficient to support intracellular function and maintenance of cellular bioenergetics; magnesium ions in an amount sufficient to support intracellular function and maintenance of cellular bioenergetics; macromolecules of molecular weight greater than 20,000 daltons in an amount sufficient to maintain endothelial integrity and cellular viability; potassium ions in a concentration greater than about 110 mM; and a buffer in an amount sufficient to maintain the average pH of the organ preservation or maintenance solution during the period of organ preservation at about physiologic pH or above.

6268479, Jul 31, 2001

Mar 12, 1997

8/815225

David M. Stern - Great Neck NY
Shi Du Yan - New York NY

The Trustees of Columbia University in the City of New York - New York NY

C07K 14435

530350

The present invention provides an isolated nucleic acid encoding an endoplasmic reticulum associated amyloid-beta peptide binding (ERAB) polypeptide. The ERAB polypeptide may comprise human ERAB polypeptide. The present invention provides a purified ERAB polypeptide, as well as a method for treating a neurodegenerative condition in a subject which comprises administering to the subject an agent in amount effective to inhibit ERAB polypeptide binding to amyloid-beta peptide so as to thereby treat the neurodegenerative condition.