Peter Daniel Canoll

20080153167, Jun 26, 2008

Jun 21, 2007

11/821086

Peter Canoll - New York NY, US
James Goldman - White Plains NY, US
Marcela Assanah - East Elmhurst NY, US
Sanja Ivkovic - New York NY, US

THE TRUSTEES OF COLUMBIA UNIVERSITY IN THE CITY OF NEW YORK - New York NY

A61K 35/30
C12N 5/02
C12N 15/87
G01N 33/53
A61P 25/00
A01K 67/027
A61K 31/7088

435464, 435375, 514 44, 424 9321, 800 10, 800 3

The invention is directed to methods for in vivo amplification of neural progenitor cells using the proliferative environment of glial neoplasms in adult brain. The progenitor cells have the capacity to proliferate and differentiate into mature brain cells which can be used for cell replacement therapies. The invention also provides cell replacement therapy methods for treating central nervous system diseases or injuries, including multiple sclerosis, stroke, Alzheimer's disease and Parkinson's disease.

20070213286, Sep 13, 2007

Sep 6, 2006

11/516204

Richard Vallee - Dobbs Ferry NY, US
Peter Canoll - New York NY, US
James Goldman - White Plains NY, US

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

A61K 48/00
C07H 21/02

514044000, 536023100

The invention provides antagonists and agonists of dynein mediated activity, for example specific inhibitory RNAs and dominant negative cDNAs which function as antagonists of LIS1 and dynein, and compositions comprising such antagonist and agonists. Provided are also methods for treating unwanted cell proliferation of neural progenitor cells such as cancers of the CNS, including gliomas, by administering the antagonists of the invention.

20220211752, Jul 7, 2022

Nov 26, 2021

17/535969

- New York NY, US
Dominique Higgins - New York NY, US
Jeffrey N. Bruce - New York NY, US
Simon Cheng - New York NY, US
Kunal Chaudhary - New York NY, US
Peter Canoll - New York NY, US
Brent Stockwell - New York NY, US
Athanassios Dovas - New York NY, US

A61K 33/26
A61K 31/355
A61K 31/198
A61K 33/04
A61K 38/05
A61K 31/201
A61K 31/202
A61P 35/00

Ferroptosis (cell death mediated by iron-dependent lipid peroxide accumulation) results from lipid peroxidation of phospholipids containing polyunsaturated fatty acyl moieties. Glutathione, the key cellular antioxidant capable of inhibiting lipid peroxidation via the activity of the enzyme glutathione peroxidase 4 (GPX-4), is generated directly from the sulfur-containing aminoacid cysteine, and indirectly from methionine via the transsulfuration pathway. Cysteine and methionine deprivation (CMD) in the diet can synergistically increase RSL3-mediated cell death and lipid peroxidation in both murine and human glioma cell lines and in ex-vivo organotypic slice cultures. A cysteine-depleted, methionine-restricted diet can improve survival in an syngeneic orthotopic murine glioma model. This CMD diet leads to profound in-vivo metabolomic, proteomic and lipidomic alterations, leading to improvements in the efficacy of ferroptotic therapies in glioma treatment with a non-invasive dietary modification.