[extropy-chat] weak and non-functional estrogens-mitokor-com

Fri Dec 26 21:27:18 UTC 2003

Will go get their SEC filings and find out more about them
Still reading but it fits...   weak estrogens  have been useful beyond the
traditional hormone function.  Example-  Estriol   It has  weak estrogenic,
immunomodulatory as well as antioxidant properties.

@MitoKor.com

Compounds

 MitoKor's drug development efforts include estrogen and novel, non-feminizing,
 polycyclic phenolic estrogen analogs, that protect cells and mitochondria under

 the pathological conditions occurring during a stroke or myocardial infarction.

 MitoKor has entered into a strategic alliance with Wyeth Corporation related to
the
 development of estrogens and estrogen-like compounds for treatment of
 Alzheimer's disease. Wyeth is funding a Phase III clinical trial evaluating the
use of
 estrogens in the prevention and treatment of Alzheimer's disease in
 post-menopausal women. This trial is part of the Women's Health Initiative
Study,
 and has enrolled over 7,500 women. MitoKor has also successfully completed a
Phase I clinical trial of a non-feminizing estrogen analog.

Damien Broderick wrote:

> From: "Brett Paatsch" <bpaatsch at bigpond.net.au>
> Sent: Friday, December 26, 2003 8:02 AM
> Subject: Re: [extropy-chat] BIO: Stem Cell Genes
>
> [Rafal Smigrodzki wrote:]
> > > ### Oh, the technology is patented already (as a preliminary
> > > patent)
>
> > "Preliminary patent" seems like slightly confused lay-speak to me.
> > I think the process that would be used in the circumstance you've
> > 'outlined' would have been a provisional application for patent.
>
> My JD legal adviser informs me that `provisional patent' is indeed what
> Rafal would be writing about.
>
> Meanwhile, here's an interesting patent that was granted more than two and
> half years ago. It'll fix hangnails, cancer, migrims, Alzheimers, and a
> gallon or two should have your car running like new. :)
>
> http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1
> &u=/netahtml/srchnum.htm&r=1&f=G&l=50&s1=6,268,398.WKU.&OS=PN/6,268,398&RS=P
> N/6,268,398
>
> Compounds and methods for treating mitochondria-associated diseases
>
> Abstract
> Compounds, compositions and methods are disclosed for treating
> mitochondria-associated diseases, such as cancer, psoriasis, stroke,
> Alzheimer's Disease and diabetes. The compounds of this invention have
> structure (I) below, including stereoisomers, prodrugs and pharmaceutically
> acceptable salts thereof, wherein Ar and L are as defined herein. The
> methods of this invention are directed to treating a mitochondria-associated
> disease by administering to a warm-blooded animal in need thereof an
> effective amount of a compound of structure (I), typically in the form of a
> pharmaceutical composition. ##STR1##
>
> .......
> a sample from the lengthy text:
>
> < Oxidatively stressed mitochondria may release a pre-formed soluble factor
> that can induce chromosomal condensation, an event preceding apoptosis
> (Marchetti et al., Cancer Res. 56:2033-38, 1996). In addition, members of
> the Bcl-2 family of anti-apoptosis gene products are located within the
> outer mitochondrial membrane (Monaghan et al., J. Histochem. Cytochem.
> 40:1819-25, 1992) and these proteins appear to protect membranes from
> oxidative stress (Korsmeyer et al, Biochim. Biophys. Act. 1271:63, 1995).
> Localization of Bcl-2 to this membrane appears to be indispensable for
> modulation of apoptosis (Nguyen et al., J. Biol. Chem. 269:16521-24, 1994).
> Thus, changes in mitochondrial physiology may be important mediators of
> apoptosis. To the extent that apoptotic cell death is a prominent feature of
> neuronal loss in AD. mitochondrial dysfunction may be critical to the
> progression of this disease and may also be a contributing factor in other
> mitochondria associated diseases.
>
> Focal defects in energy metabolism in the mitochondria, with accompanying
> increases in oxidative stress, may be associated with AD.  > etc etc
>
> Damien Broderick
>
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