Victor L Marcheselli

6979682, Dec 27, 2005

Feb 25, 2002

10/082821

Jay D. Hunt - Slidell LA, US
Haydee E. Bazan - New Orleans LA, US
Victor L. Marcheselli - Covington LA, US
Julio Alvarez Builla Gomez - Madrid, ES
Nicholas G. Bazan - New Orleans LA, US

Board of Supervisors of Louisiana State University and Agricultural and Mechanical College - Baton Rouge LA

A61K031/55

514219, 514 77, 514 91, 514218

A novel use of platelet-activating factor antagonists that bind to intracellular PAF binding sites such as BN-50730 (tetrahedra-4,7,8,10 methyl-1 (chloro-1 phenyl)-6 (methoxy-4 phenyl-carbamoyl)-9 pyrido [4′,3′-4,5] thieno [3,2-f] triazolo-1,2,4 [4,3-a] diazepine-1,4) has been discovered. These intracellular-binding platelet-activating factor antagonists were found to inhibit both in vivo and in vitro tumor growth and angiogenesis where the angiogenesis is stimulated by basic fibroblast growth factor.

20050075398, Apr 7, 2005

Aug 5, 2004

10/911835

Nicolas Bazan - New Orleans LA, US
Charles Serhan - Needham MA, US
Victor Marcheselli - Covington LA, US
Pranab Mukherjee - Metairie LA, US
Sebastian Barreiro - Metairie LA, US
Walter Lukiw - Slidell LA, US
Song Hong - Brookline MA, US
Karsten Gronert - New Fairfield CT, US
Alberto Musto - New Orleans LA, US

A61K031/202

514560000

A unique DHA product, 10, 17S-docosatriene (“Neuroprotectin D1” or “NPD1”), was found to provide surprisingly effective neuroprotection when administered right after an experimental stroke. Moreover, both nerve cells and retinal pigment epithelial (RPE) cells were found to synthesize 10,17S-docosatriene (NPD1) from DHA. NPD1 also potently counteracted HO/TNFα oxidative stress-mediated cell apoptotic damage. Under the same oxidative-stress conditions, NPD1 up-regulated the anti-apoptotic Bcl-2 proteins, Bcl-2 and Bcl-xL, and decreased expression of the pro-apoptotic proteins, Bad and Bax. Moreover, in RPE cells NPD1 inhibited oxidative stress-induced caspase-3 activation, IL-1β-stimulated human COX-2 promoter expression, and apoptosis due to N-retinylidene-N-retinylethanolamine (A2E). Overall, NPD1 protected both nerve and retinal pigment epithelial cells from cellular apoptosis and damage due to oxidative stress. NPD1 concentration in the brain of Alzheimer's patients was found to be significantly decreased from that of controls. In cultured human brain cells, NPD1 synthesis was up-regulated by neuroprotective soluble β amyloid, and NPD1 was found to inhibit secretion of toxic β amyloid peptides.

20070042953, Feb 22, 2007

Oct 18, 2005

11/253483

Nicolas Bazan - New Orleans LA, US
Alberto Musto - Covington LA, US
Victor Marcheselli - Covington LA, US

A61K 38/26
A61K 31/202

514012000, 514560000

The infusion of an albumin-docosahexaenoic acid (DHA) complex was shown to inhibit the progression of kindling epileptogenesis. This was shown in mice using kindling as the experimental epilepsy model. The DHA-albumin complex was shown to affect the activity of the brain when administered intraperitoneally. This therapy could also be administered intravenously. This therapy would also be effective against chronic epilepsy.

6566359, May 20, 2003

May 20, 2002

10/151984

Nicholas G. Bazan - Baton Rouge LA
Carlos Sunkel - Madrid, ES
Victor L. Marcheselli - Covington LA
Julio Builla-G. - Madrid, ES

Board of Supervisors of Louisiana State University and Agricultural and Mechanical College - Baton Rouge LA

A61K 315377

5142322, 544 82, 5462727, 546321

A new series of derivatives of 2,4,6-trimethyl-1,4-dihydropyridine-3,5-dicarboxylic acid and their synthesis have been discovered. Surprisingly, by modifying the substituent of the 3-carboxylic acid group, new compounds were produced with high activity as PAF receptor antagonists. These compounds were shown to protect neurons from brain damage that normally occurs in response to stroke and other cerebrovascular diseases. These compounds are also protective against edema generation resulting from traumatic breakdown of the blood-brain barrier. Moreover, these compounds were found to be non-toxic and cytoprotective of cells undergoing oxidative stress that would normally trigger apoptotic cell death; and to have activity as (a) antagonists of an intracellular platelet activating factor (âPAFâ)-binding site, (b) inhibitors of PAF- and cytokine-mediated c-aminoterminal jun kinase (JNK) and extracellular regulated kinase (ERK), and (c) transcriptional inhibitors of COX-2 expression.