Patents (1436 Stem Cell Patents)

Compounds and methods for increasing neurogenesis

Patent Number: 6969702

Date of First Priority Issue: Wednesday November 20th, 2002
Date Issued: Tuesday November 29th, 2005
Assignee: NeuroNova AB (Stockholm, SE)
Inventors: Bertilsson, Goran (Vasterhaninge, SE); Erlandsson, Rikard (Sundyberg, SE); Frisen, Jonas (Stockholm, SE); Haegerstrand, Anders (Danderyd, SE); Heidrich, Jessica (.ANG.rsta, SE); Hellstrom, Nina (Sodertalje, SE); Haggblad, Johan (Vastgotagrand, SE); Jansso

From Class: Expansion

This patent deals with administration of compounds, some which I believe are already in the clinic, for stimulation of neurogenesis in a patient suffering from a neurodegenerative condition. The patent has 2 independent claims, the first covers the administration of calcitonin, or exendin or analogues thereof that intracellular cAMP levels. The second independent claim covers administration of thyrocalcitonin, calcitonin, exendin-3, exendin-4, and analogs to increase neurogenesis. Exendin-4 is called Exenatide (Amylin) and is approved for diabetes patients.

View this patent on the USPTO website.

Added to StemCellPatents.com on Monday October 16th, 2006

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1 Comment | Add Comment

Zap70 said...

Created 2006-12-10 15:13:18 EST

This patent is owned by the company

NeuroNova AB
Fiskartorpsvägen 15 A-D
S-114 33 Stockholm
Sweden

They have developed some interesting technology that they call "neurogenesis qualifier" which is used to screen compounds for ability to generate new neurons...I guess they must have used this technology to identify the exendin compounds as potential neurogenesis stimulators.

There are several similar small molecule peptides that could be of relevance for this invention. One is GLP-1 (ironically also developed by Amylin).

GLP-1 is generated following food intake and has the ability to stimulate islet proliferation. Exendin-4 is an endogenous analog of GLP that stimulates the same receptor. Most importantly, both exendin and GLP are protective against neuronal toxicity mediated by amyloid beta peptides and gluatamate induced cytotoxicity.

In vivo studies with stimulators of GLP-1 receptors have demonstrated that it is possible to protect against cholinergic neuron deterioration in the basal forebrain of the rat following glutamate induced toxicity.



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