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Biotech / Medical : Alteon (ALT)
ALT 3.860-3.0%Dec 26 3:59 PM EST

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To: Bill Tomko who wrote (293)11/5/2000 8:09:48 PM
From: tnsaf  Read Replies (1) of 318
 
Two news releases from the past few weeks.

Jason

Tuesday October 10, 8:30 am Eastern Time

Press Release

SOURCE: Alteon Inc.

Alteon Partners with University of Pittsburgh Spinout to
Develop New Cardiovascular Therapy

- Novel Tissue Perfusion Technology Pioneered at McGowan Center for Artificial Organ Development
-

RAMSEY, N.J., Oct. 10 /PRNewswire/ -- Alteon Inc. (Amex: ALT - news) announced today that it has entered into an
agreement with HemoMax, LLC, for the development of a novel tissue perfusion technology for enhanced blood circulation.
The technology, also called HemoMax, was developed at the McGowan Center for Artificial Organ Development at the
University of Pittsburgh, and has recently been licensed to HemoMax, LLC, so that formal preclinical development programs
can be initiated.

The HemoMax technology is focused on the restoration or enhancement of impaired microcirculation and tissue oxygenation,
an area where existing therapies have had only limited results. Impaired microcirculation and low tissue perfusion have been
known to occur as a result of a variety of conditions, including hemorrhage, severe trauma, ischemic heart disease, diabetes,
acute myocardial infarction, acute transient cerebral ischemic attack, sickle cell disease and atherosclerosis.

Under the agreement, HemoMax, LLC will fund the preclinical development of compounds arising from the technology, and
Alteon will directly manage these development programs. HemoMax has granted Alteon an exclusive right of first refusal to
acquire the HemoMax technology. In addition, Alteon will receive 15% ownership of HemoMax, LLC.

``We are pleased to be involved in the preclinical development of this exciting new technology, because it directly
complements Alteon's cardiovascular activities with ALT-711,'' said Kenneth I. Moch, President and CEO of Alteon. ``The data
which has been generated thus far indicates that the HemoMax technology may have broad clinical potential in the treatment
of cardiovascular diseases.''

HemoMax, LLC has been funded by Three Rivers Medical Technologies, LLC, a seed fund recently formed by Pittsburgh area
investors to invest in early stage life science technologies developed in Western Pennsylvania. The HemoMax technology was
developed at the McGowan Center for Artificial Organ Development at the University of Pittsburgh.

About the McGowan Center

The University of Pittsburgh McGowan Center for Artificial Organ Development is one of the world's most advanced academic
programs investigating the use of bioengineered organ devices for treating human illness and disease. HemoMax is one of the
novel technologies created at the McGowan Center. There is a portfolio of engineered organ projects currently being
researched at the McGowan Center.

``The McGowan Center is at the intersection of the campus and the company,'' said Dr. Griffith, McGowan Center Director, the
Henry T. Bahnson Professor of Surgery and Chief of Cardiothoracic Surgery at the University of Pittsburgh School of
Medicine. The Center officially began operation in 1992, bringing together a number of the University of Pittsburgh's
pioneering artificial organ activities.

McGowan Center investigators work closely with the leading device developers to provide expertise in organ transplantation
and bioengineering. As a result, more heart-assist devices and artificial organs have been transplanted in Pittsburgh than any
other transplant center in the United States.

About Alteon

Alteon is a leader in the discovery and development of pharmaceuticals for the treatment of cardiovascular and renal diseases
and other disorders of diabetes and aging, based on slowing or reversing a fundamental pathological process caused by
protein-glucose complexes called Advanced Glycosylation End-Products (A.G.E.s).

A.G.E.s ultimately form crosslinks with adjacent proteins, leading to a loss of flexibility and function in body tissues, organs
and cells. This A.G.E. pathway represents one of several pathological processes believed to be responsible for aging, including
regulation of telomere length, DNA turnover, and build-up of senescent products, among others. A.G.E.s have been shown to
be causative factors in many of the complications of diabetes and age-related diseases, including cardiovascular disease,
kidney disease, nerve damage and retinopathy. Alteon's unique approach is to inhibit or break A.G.E.s and their chemical
crosslinks.

Alteon's lead A.G.E. crosslink breaker, ALT-711, is in Phase IIa clinical testing to evaluate its effect on cardiovascular
compliance, with results from this trial anticipated near year-end. Additional indications being evaluated include
non-obstructive uropathy, peritoneal dialysis and scleroderma. The company is seeking a corporate partner to help fund the
continued development of its A.G.E.-formation inhibitor, Pimagedine, based on the results of a Phase II/III trial in Type 1
diabetic patients with progressive kidney disease. Alteon is also pursuing the development of a novel series of glucose
lowering agent (GLA) compounds.

Any statements contained in this press release that relate to future plans, events or performance are forward-looking
statements that involve risks and uncertainties including, but not limited to, those relating to technology and product
development, regulatory approval processes, intellectual property rights and litigation, competitive products, ability to obtain
financing, and other risks identified in Alteon's filings with the Securities and Exchange Commission. Actual results, events or
performances may differ materially. Alteon undertakes no obligation to publicly release the result of any revision to these
forward-looking statements that may be made to reflect events or circumstances after the date hereof or to reflect the
occurrence of unanticipated events.

More information is available on Alteon's web site, alteonpharma.com; or the McGowan Center Website
upmc.edu.

SOURCE: Alteon Inc.
===============================================
Tuesday October 17, 11:01 am Eastern Time

Press Release

SOURCE: Alteon Inc.

Alteon Granted Patent on New Class of A.G.E. Crosslink
Breakers; Compounds Have Potential to Reverse Age-Related Diseases

- Company Granted Several Patents Covering A.G.E. Technology -

RAMSEY, N.J., Oct. 17 /PRNewswire/ -- Alteon Inc. (Amex: ALT - news) announced today that it has received a patent
covering a new class of A.G.E. crosslink breaker compounds. A.G.E. crosslink breakers offer the possibility of the first
therapeutic approach to reverse cardiovascular disease and other age-related disorders by cleaving Advanced Glycosylation
End-product, or A.G.E., crosslinks between proteins, thereby restoring flexibility and elasticity to stiffened tissues. Alteon now
has a library of over 375 A.G.E. crosslink breaker compounds in several classes. U.S. Patent #6,121,300, ``Reversing Advanced
Glycosylation Cross-links Using Heterocyclic Substituted Thiazolium Salts,'' brings Alteon's total number of U.S. patents to
104, the majority covering A.G.E. technology. Alteon is evaluating the new class of compounds for possible clinical use.

``This patent clearly adds to our leadership position in the A.G.E. field,'' said Kenneth I. Moch, President and Chief Executive
Officer. ``We have been aggressively patenting and developing this technology with the belief that it will play an important
role in the future treatment of many diseases, and are pleased to have coverage on an entirely new class of compounds.''
Alteon's lead A.G.E. crosslink breaker, ALT-711, is in Phase IIa clinical trials in patients with measurable cardiovascular
stiffening, with results anticipated near year-end.

Other patents recently issued include U.S. patent #6,114,323, ``Methods for Inhibiting the Advanced Glycosylation of
Proteins,'' and U.S. patent #6,110,968, ``Methods for Treatment Predicated on the Presence of Advanced Glycosylation
End-products in Tobacco and its Combustion Byproducts.''

Alteon's Technology Platform - The A.G.E. Pathway
The Pathological Role of A.G.E. Crosslinks in Aging and Diabetes
Decreased elasticity of the cardiovascular system and the stiffening of

tissues and organs is one of the hallmarks of the normal aging process. The
resulting loss of flexibility and function ultimately leads to diseases or
disorders involving tissues that depend on elastic properties, including
vascular disorders, cardiomyopathies, ophthalmologic diseases and skin aging.

A key mechanism involved in this aging process is the reaction of a simple sugar, glucose, with natural proteins such as
collagen and elastin. This non-enzymatic chemical reaction results in the formation throughout the body of ``molecular
glue-like'' complexes called Advanced Glycosylation End-products (A.G.E.s). While the formation of A.G.E.s in the human body
usually takes place at a slow, progressive rate that results in disease later in life, A.G.E. formation can be significantly
accelerated by conditions such as diabetes where glucose levels are increased. This same chemical process of A.G.E. formation
occurs during cooking, where it is called the Maillard or ``browning'' reaction. As with humans, this cooking process results in
the toughening and discoloration of food, and can be accelerated by increased temperature and sugar levels.

The A.G.E. pathway may provide the scientific explanation for how and why many of the complications of the aging process
occur with higher frequency and earlier in life in diabetic patients. Once A.G.E.s form on proteins, they eventually crosslink to
other proteins, forming pathological complexes that have been shown in preclinical models to be responsible for many
age-related and diabetic disorders. In tissues and organs that depend on elastic properties to function, normal physiologic
functions are compromised by A.G.E. formation and crosslinking.

Because A.G.E.s have been implicated in a broad range of pathologies, therapeutic intervention may provide relief for many
medical conditions where A.G.E. crosslinking has contributed to a loss of normal function, elasticity and/or flexibility.

ALT-711:

A Drug for Reversing Cardiovascular Disease and Other Diseases of Aging and Diabetes

How ALT-711 Works

Recent discoveries at Alteon have indicated that many of the diseases that are caused by A.G.E.s, and which were previously
believed to be permanent and irreversible pathologies, may in the future be treatable.

Alteon's lead A.G.E. Crosslink Breaker, ALT-711, is the first in a new class of novel pharmaceuticals that have been shown to
``break'' A.G.E. crosslinks, thereby restoring more normal function to organs and tissues that have lost flexibility. Through a
unique mechanism of action, ALT-711 restores normal elastic function to stiffened arteries and heart tissue in diabetic and
aging animal models. In rodents, canines and in primates, medical researchers have documented important improvements to the
cardiovascular system using ALT-711; in effect, ALT-711 has demonstrated the ability to restore the cardiovascular system to
a more youthful state.

In cardiovascular disease, restoring normal arterial wall function is an important therapeutic goal in preventing the subsequent
development of serious cardiomyopathies. By breaking the pathological A.G.E. crosslinks, thereby restoring normal arterial
function, ALT-711 may treat cardiovascular disease itself, not just the symptoms. ALT-711 is currently undergoing Phase II
human clinical testing for cardiovascular disease, and is being evaluated in several other conditions where the loss of tissue
flexibility and function leads to pathology.

About Alteon

Alteon is a leader in the discovery and development of pharmaceuticals for the treatment of cardiovascular and renal diseases
and other disorders of diabetes and aging, based on slowing or reversing a fundamental pathological process caused by
protein-glucose complexes called Advanced Glycosylation End-Products (A.G.E.s).

A.G.E.s ultimately form crosslinks with adjacent proteins, leading to a loss of flexibility and function in body tissues, organs
and cells. This A.G.E. pathway represents one of several pathological processes believed to be responsible for aging, including
regulation of telomere length, DNA turnover, and build-up of senescent products, among others. A.G.E.s have been shown to
be causative factors in many of the complications of diabetes and age-related diseases, including cardiovascular disease,
kidney disease, nerve damage and retinopathy. Alteon's unique approach is to inhibit or break A.G.E.s and their chemical
crosslinks.

Alteon's lead A.G.E. crosslink breaker, ALT-711, is in Phase IIa clinical testing to evaluate its effect on cardiovascular
compliance, with results from this trial anticipated near year-end. Additional indications being evaluated include
non-obstructive uropathy, peritoneal dialysis and scleroderma. The company is seeking a corporate partner to help fund the
continued development of its A.G.E.-formation inhibitor, Pimagedine, based on the results of a Phase II/III trial in Type 1
diabetic patients with progressive kidney disease. Alteon is also pursuing the development of a novel series of glucose
lowering agent (GLA) compounds.

Any statements contained in this press release that relate to future plans, events or performance are forward-looking
statements that involve risks and uncertainties including, but not limited to, those relating to technology and product
development, regulatory approval processes, intellectual property rights and litigation, competitive products, ability to obtain
financing, and other risks identified in Alteon's filings with the Securities and Exchange Commission. Actual results, events or
performances may differ materially. Alteon undertakes no obligation to publicly release the result of any revision to these
forward-looking statements that may be made to reflect events or circumstances after the date hereof or to reflect the
occurrence of unanticipated events.

More information on Alteon is available at the corporate web site, alteonpharma.com.

SOURCE: Alteon Inc.
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