GenoMed Announces Potential Therapy for SARS
ST. LOUIS, Fla., Apr 25, 2003 /PRNewswire-FirstCall via COMTEX/ -- GenoMed,
Inc. (OTC Pink Sheets: GMED) ("the Company" or "GenoMed"), a St. Louis,
Missouri-based medical genomics and Next Generation Disease Management(TM)
company, announced today a novel anti-viral therapy that may decrease mortality
in the current epidemic of SARS (severe acute respiratory syndrome). The Company
is looking for patient and physician collaborators.
SARS is caused by a coronavirus. However, it is not the virus which kills
people, but their own exuberant immune response. Down-modulating their immune
response in a precise, not general, fashion, should convert coronavirus to just
another viral infection, no more serious than the common cold.
GenoMed has case reports showing the ability of angiotensin II receptor blockers
(AT1 Receptor blockers, or ARB's) to arrest the excessive immune responses in
autoimmune diseases such as alopecia areata and psoriasis. Alopecia areata is
particularly instructive. In this disease, patients lose the hair from their
scalp as well as the rest of their body because of an autoimmune attack on their
hair follicles by their own T cells. Others have shown that helper T cells of
the CD4+ variety make excessive interferon-gamma (IFN-gamma). The IFN-gamma
turns off proliferation of the cells in the dermal papilla that normally become
part of the growing strand of hair. The hair follicle becomes quiescent as a
result of excessive IFN-gamma production.
IFN-gamma is the key cytokine (cell stimulator) in viral infections, such as
coronavirus. In viral infections, CD4+ T cells recruit CD8+ cytotoxic T
lymphocytes to the site of infection. The recruitment and activation of
cytotoxic T cells is due in large part to secretion of IFN-gamma. IFN-gamma is
also made by antigen-presenting cells like macrophages, and by the infected
epithelial cells themselves.
GenoMed believes that angiotensin II stimulates CD4+ helper T cells and
antigen-presenting cells, and perhaps even infected epithelial cells, to secrete
more IFN-gamma. The rate-limiting enzyme for angiotensin II production is the
angiotensin II-converting enzyme (ACE). ACE is expressed on the surface membrane
of T cells as well as activated macrophages. Angiotensin II likely also
stimulates production of other cytokines, either directly or indirectly, such as
interleukin-1 and tumor necrosis factor-alpha (TNF-alpha). These last two are
the pyrogens which cause the high fevers seen in SARS patients.
Angiotensin II may also be responsible for the increased vascular permeability
in the lungs of SARS patients, as well as their respiratory insufficiency.
Angiotensin II probably normally causes vasoconstriction of pulmonary
arterioles, and directs blood away from alveoli that no longer are involved in
gas exchange. Alveoli full of immune cells fighting virally infected epithelial
cells are no longer good at gas exchange, since they're essentially under water.
GenoMed has filed a patent application for the use of "sartans" for SARS. A
"sartan" is a drug that specifically inhibits the angiotensin II type 1 receptor
(AT1R). It appears that angiotensin II operates through the AT1 receptor to
activate lymphocytes and macrophages, but that the type 2 angiotensin II
receptor promotes death ("apoptosis") of these cells. Thus, an AT1 receptor
blocker might be ideal for selectively turning off an overly exuberant host
immune response.
A number of "sartans" are already on the market, where they are used to treat
high blood pressure. They require a prescription. Examples include valsartan,
irbesartan, candesartan, losartan, telmisartan, and eprosartan. Since SARS
patients are dehydrated and their blood pressure is low to start with, the
smallest dose of the "sartan" should be broken in half and then used once a day
to avoid an excessive drop in blood pressure.
GenoMed has applied for patent protection on this approach but is now recruiting
patients and physicians to collaborate in a world-wide trial of its efficacy.
Participating patients and physicians will be able to license the treatment for
free in exchange for agreeing to contribute their outcomes to an eventual
publication.
In particular, GenoMed predicts that the patients who are the sickest SARS
patients will have the ACE deletion/deletion (D/D) genotype. This genotype is
associated with the highest expression of ACE on T cell membranes. It is
interesting that 10% of Asians die of SARS, and 10% of Asians are ACE D/D. Other
populations have a higher frequency of ACE D/D. For example, 25% of Caucasians
are ACE D/D, about 32% of African Americans have the ACE D/D genotype, and 45%
of Africans are ACE D/D. This suggests that SARS may become much more lethal if
it spreads to non-Asian populations. (Incidentally, the high population
frequency of the ACE D/D genotype could also help explain why HIV has been so
successful at infecting people of African descent, and why African Americans
have 8-fold more HIV-associated nephropathy than Caucasians infected with HIV).
GenoMed would also welcome the participation of any of the manufacturers of the
sartans in this worldwide trial, e.g. through donation of their drug or other
financial help.
If this novel approach to anti-viral therapy works, the Company's next target
will be patients with HIV and those who are at risk for HIV.
About GenoMed
GenoMed, Inc. is a medical genomics company whose mission is to improve patient
outcomes by identifying the gene pathways that cause disease. A St. Louis
Business Journal article
(http://www.stlouis.bizjournals.com/stlouis/stories/2002/05/13/story8.html )
first reported that the company has applied for patents based on its finding
that the ACE gene is associated with a large number of common diseases. The
Company has filed worldwide patent applications on its new treatments, and is
eager to license them globally. GenoMed's research results are more fully
described on its website, www.genomedics.com
For questions, please contact GenoMed at 314-977-0110, FAX 314-977-0042, email:
dwmoskowitz@genomedics.com, or visit GenoMed at genomedics.com.
SOURCE GenoMed, Inc.
CONTACT: Dave Moskowitz, GenoMed, Inc., +1-314-977-0110, or fax, +1-314-977-0042, or dwmoskowitz@genomedics.com
URL: genomedics.com |
