BARBARA L. HEMPSTEAD, MD, PHD
Osteopathic Medicine at 68 St, New York, NY

2003008, May 8, 2003

May 24, 2002

10/155886

Barbara Hempstead - New York NY, US
Ramee Lee - New York NY, US
Kenneth Teng - New York NY, US
Pouneh Kermani - Great Neck NY, US

A01N037/18, A61K038/00, C07K001/00, C07K014/00, C07K017/00

514/002000, 530/350000

The present invention provides an isolated protein comprising a pro-domain of a proneurotrophin, methods for producing the protein, and pharmaceutical compositions containing the isolated protein. The invention also provides a nucleic acid molecule which encodes the protein and a vector containing the nucleic acid molecule. The present invention further provides a method for cleaving a proneurotrophin protein to a mature neurotrophin. In addition, the invention relates to methods for inducing apoptosis in a cell of a mammal expressing p75 surface receptors or p75 and trk receptors. The methods include causing the p75 receptor to bind a pharmaceutical composition containing a pro-domain of a proneurotrophin or administering to the mammal an effective amount of a cleavage-resistant proneurotrophin and an inhibitor of trk activation. The invention also relates to a method for inhibiting apoptosis of a cell in a mammal by administering an effective amount of a molecule which inhibits binding of a proneurotrophin to a p75 receptor. Also provided, are kits and methods for screening a human for a condition associated with undesired apoptosis.

2010022, Sep 9, 2010

May 21, 2010

12/785183

Barbara L. HEMPSTEAD - New York NY, US
Rosemary KRAEMER - Brooklyn NY, US
Shahin RAFII - Great Neck NY, US
Phi WIEGN - New York NY, US
Michael J. DONOVAN - Brookline MA, US

CORNELL RESEARCH FOUNDATION, INC. - Ithaca NY
CHILDREN'S MEDICAL CENTER CORPORATION - Boston MA

A61K 38/12, A61P 7/00

514 12

The present invention relates to methods of inducing or inhibiting the angiogenic process and promoting vessel growth or stabilization in an organ by modulating the trk receptor pathway. The present invention also relates to a method for treating a pathological disorder in a patient which includes administering a trk receptor ligand or an inhibitor or expression or activity of a trk receptor ligand. The present invention also relates to a method of screening for a modulator of angiogenesis, vessel growth, or vessel stabilization. Another aspect of the present invention is a method of diagnosing or monitoring a pathological disorder in a patient which includes determining the presence or amount of a trk receptor ligand or activation of a trk receptor ligand in a biological sample.

2010024, Sep 23, 2010

Jan 19, 2007

12/223053

Francis S. Lee - New York NY, US
Barbara L. Hempstead - New York NY, US
Kevin G. Bath - New York NY, US

C12Q 1/68, A61K 31/138, A61P 25/24

514651, 435 6

The invention provides a method for determining whether a patient suffering from a condition that is susceptible to treatment with a compound that activates the brain serotonin system is resistant to treatment with the compound. The method comprises observing whether the genome of the patient contains at least one copy of the BDNF allele containing a genetic alteration, and correlating the presence of the allele containing the genetic alteration with patients who are resistant to treatment with the compound. In another embodiment, the method comprises observing whether the patient expresses a BDNF protein containing an amino acid alteration, and correlating the expression of the BDNF protein containing the amino acid alteration with patients who are resistant to treatment with the compound.

2011020, Aug 25, 2011

Jun 16, 2009

12/999581

Francis S. Lee - New York NY, US
Barbara Hempstead - New York NY, US
James Kocsis - Roxbury CT, US
Kevin Bath - New York NY, US

CORNELL UNIVERSITY - Ithaca NY

A61K 31/135, C12Q 1/68, A61P 25/24

514651, 435 613, 435 611

The invention relates to a method for determining whether a patient suffering from a condition that is susceptible to treatment with a compound that activates the brain serotonin system is susceptible or resistant to treatment with the compound. The method includes establishing whether the patient is a pre-adult, a transition age patient, or an adult and observing whether the genome of the patient contains at least one copy of a BDNF allele having a genetic alteration. The method further includes correlating the presence of the allele containing the genetic alteration with susceptibility or resistance of the patient to the treatment with the compound, wherein a pre-adult patient containing the genetic alteration is correlated as being susceptible to the treatment; a transition age patient containing the genetic alteration is correlated as being susceptible or resistant to the treatment; and an adult patient containing the genetic alteration is correlated as being resistant to the treatment.

7723293, May 25, 2010

Oct 30, 2006

11/589659

Barbara L. Hempstead - New York NY, US
Rosemary Kraemer - Brooklyn NY, US
Shahin Rafii - Great Neck NY, US
Phi Wiegn - New York NY, US
Michael L. Donovan - Brookline MA, US

Cornell Research Foundation, Inc. - Ithaca NY
Children's Medical Center Corporation - Boston MA

A61K 38/18

514 2, 514 12, 530399

The present invention relates to methods of inducing or inhibiting the angiogenic process and promoting vessel growth or stabilization in an organ by modulating the trk receptor pathway. The present invention also relates to a method for treating a pathological disorder in a patient which includes administering a trk receptor ligand or an inhibitor or expression or activity of a trk receptor ligand. The present invention also relates to a method of screening for a modulator of angiogenesis, vessel growth, or vessel stabilization. Another aspect of the present invention is a method of diagnosing or monitoring a pathological disorder in a patient which includes determining the presence or amount of a trk receptor ligand or activation of a trk receptor ligand in a biological sample.

2011018, Aug 4, 2011

Oct 8, 2009

13/122483

Barbara L. Hempstead - New York NY, US

CORNELL UNIVERSITY - Ithaca NY

A61K 33/00, A61K 31/12, A61K 31/198, A61K 31/366, A61P 25/28, A61P 25/24, A61P 25/14, A61P 9/00, A61P 9/10

424722, 514689, 514567, 514460

The present invention relates to a method of inhibiting cellular uptake of pro-nerve growth factor (proNGF) in a cell expressing neurotrophin p75 receptor in a mammal in need thereof. Such mammals include, for example, those suffering from neuropathological conditions. In another aspect, the invention relates to a method of promoting cellular uptake of proNGF in a cell expressing p75receptor in a mammal in need thereof. Such mammals include, for example, those suffering from conditions relating to human and other mammalian hair follicle cycling.

2013011, May 9, 2013

Jun 15, 2011

13/704404

Barbara Hempstead - New York NY, US
Chia-Jen Siao - New York NY, US

Cornell University - Ithaca NY

A61K 39/395, A61K 31/713

4241581, 514 44 A, 514 84, 4241721, 514 11

This disclosure has identified a new ligand-receptor system, proNGF and p75NTR/SorCS2, which is found to be involved in the microvascular functions of the heart. This disclosure provides methods for limiting microvascular damage following acute myocardial ischemia based on administration of an antagonist of this newly identified system, thereby promoting myocardial recovery.

2013033, Dec 19, 2013

Nov 17, 2011

13/988193

Barbara L. Hempstead - New York NY, US
Taeho Kim - Palo Alto CA, US
Katrin Deinhardt - Southampton, GB
Moses Victor Chao - New York NY, US
Jianmin Yang - Forest Hills NY, US

NEW YORK UNIVERSITY - New York NY
CORNELL UNIVERSITY - Ithaca NY

A61K 39/395, A61K 38/08, A61K 31/713, A61K 31/7088

4241581, 4241721, 514 44 R, 514 177, 514 44 A

This disclosure relates to modulation of the interactions between proNTs and p75/SorCS2 expressed on neuronal cells. Inhibition of such interactions is useful for reducing unwanted synaptic elimination, neurite pruning and/or other neuronal structural collapses, and for treating early stage and mild neurological disorders including mild cognitive impairment.