Alteon's Alagebrium Reverses Erectile Dysfunction In Preclinical Study
October 18 2004 - 8:30AM
PR Newswire (US)
Alteon's Alagebrium Reverses Erectile Dysfunction In Preclinical
Study Leading Investigators in ED Field Note Unique Mechanism of
Action PARSIPPANY, N.J., Oct. 18 /PRNewswire-FirstCall/ -- Alteon
Inc. (AMEX:ALT) announced today that its lead A.G.E. Crosslink
Breaker compound alagebrium (formerly known as ALT-711) has
demonstrated an ability to reverse erectile dysfunction (ED) in a
preclinical model of diabetes. The preclinical study, entitled
"Delayed Administration of ALT-711, but not of Aminoguanidine,
Improves Erectile Function in Streptozotocin Diabetic Rats:
Curative Versus Preventive Medicine," was presented today at the
11th World Congress of the International Society for Sexual and
Impotence Research in Buenos Aires. Independent study authors,
Mustafa F. Usta(1,3), Muammer Kendirci(1), Trinity J.
Bivalacqua(1,4), Serap Gur(1), Wayne J.G. Hellstrom(1), Neale A.
Foxwell(2), and Selim Cellek(2), conclude that alagebrium --
through what appears to be a unique mechanism of action -- offers
significant potential for the treatment of diabetic erectile
dysfunction. According to the investigative team, these data are
unlike results for existing ED drugs in similar experiments,
particularly due to a beneficial effect on the function of the
corpus cavernosum. "Alagebrium appears to have significant
therapeutic potential for the treatment of diabetic erectile
dysfunction, with a unique mechanism of action," said Wayne J.G.
Hellstrom, M.D., an author of this study and many of the seminal
studies in ED. An estimated 30-40 percent of diabetic and aged
patients with ED do not receive benefit from currently available
drugs, and patients with diabetes or severe vascular disease are
among the most refractory to such treatment. This occurs, in part,
because the corpus cavernosum, the structure that acts as an
expandable reservoir for blood, has become significantly glycated
and fibrotic, unable to properly dilate due to the accumulation and
crosslinking of pathological structures called advanced glycation
end-products (A.G.E.s). A.G.E.s have been implicated in the
fibrosis and stiffening of tissues and organs throughout the body
and have been shown to contribute to many inflammatory processes.
A.G.E.s have been demonstrated to impair erectile function in
diabetes by affecting the functional capabilities of the corpus
cavernosum and by interfering with the production of natural penile
vasodilating agents, endothelial and neuronal nitric oxide (NO).
Study authors investigated the effect of delayed administration of
alagebrium, a crosslink breaker of A.G.E.s, as compared to
aminoguanidine (pimagedine), an inhibitor of A.G.E.s, in a
well-established ED animal model. In previous preclinical and
clinical testing, alagebrium has demonstrated the ability to cleave
advanced glycation end-product crosslinks as well as diminish
deleterious inflammatory responses caused by A.G.E.s.
Aminoguanidine has previously been shown to prevent ED in diabetic
animals if given immediately after the induction of diabetes. In
the current study, both aminoguanidine and alagebrium were
initiated at the 6th week of diabetes and the two treated groups
were compared to a group of age-matched controls and a group of
untreated diabetic animals. Twelve weeks after diabetes induction,
in vivo intracavernosal pressure measurements were assessed, as
well as serum and penile A.G.E. levels. The diabetic rats had a
significant decrease in erectile function as assessed by the level
of intracavernosal pressure obtained after cavernosal nerve
stimulation and elevated A.G.E. levels when compared to the control
rats. The administration of alagebrium resulted in a significant
improvement in erectile function, as well as a decrease in serum
and tissue A.G.E. levels, while the delayed administration of
aminoguanidine did not correct either A.G.E. levels or erectile
dysfunction. In addition, alagebrium normalized other
diabetes-induced pathologies associated with ED, an effect unlike
any currently marketed therapies used to treat symptoms of the
condition. The results of the preclinical study have been submitted
for publication in a peer-reviewed medical journal. In prior
clinical and preclinical studies, alagebrium has been shown to have
a remodeling effect on the cardiovascular system(5) as well a
positive effect on systolic hypertension(6) and vascular
compliance(7). The drug is currently in Phase 2 studies in patients
with hypertension and heart failure. In addition, it is being
studied for its effect in endothelial dysfunction, a condition also
linked to erectile dysfunction. "We are actively evaluating a
clinical development pathway for the ED indication," said Kenneth
I. Moch, President and CEO. "Because ED is an early indicator of
vascular disease, this exciting research by world-renowned ED
investigators is fully consistent with, and supportive of, our
ongoing clinical development programs for alagebrium in
hypertension and heart failure. Should alagebrium's therapeutic
effect be seen in human studies in ED, this would not only
represent a breakthrough for ED, but would also be indicative of
alagebrium's potential to reverse pathologies in a number of other
human vascular diseases." Understanding the Link between Erectile
Dysfunction and Vascular Disease Erectile dysfunction is defined as
the persistent inability to attain and maintain an erection
sufficient to permit satisfactory sexual intercourse. ED has been
reported to affect as many as 20 to 30 million men in the United
States and 152 million men worldwide, according to the National
Institutes on Health. The risk for ED increases progressively with
advancing age, with an estimated 54 percent of men ages 65 to 70
reporting some degree of impotence (Nicolosi, 2003). It is believed
that 85-90 percent of ED cases are related to a physical or medical
condition, while 10-15 percent is due to psychological causes. Many
studies have identified ED as an early indicator of cardiovascular
diseases, including hypertension, heart attack and stroke, and
point to the underlying dysfunction of the arteries and vascular
system as a principal cause. ED is commonly associated with a
number of other conditions frequently occurring in aging men,
including prostatic hypertrophy, arterial hypertension, ischemic
heart disease, peripheral vascular disease, atherosclerosis,
hyperlipidemia, and diabetes mellitus. About Alteon Alteon is
developing several new classes of drugs that have shown the
potential to reverse or slow down diseases of aging and
complications of diabetes. These compounds have an impact on a
fundamental pathological process caused by the progressive
formation of protein-glucose complexes called Advanced Glycation
End-products (A.G.E.s). The formation and crosslinking of A.G.E.s
lead to a loss of flexibility and function in body tissues and
organs and have been shown to be a causative factor in many age-
related diseases and diabetic complications. Alteon has created a
library of novel classes of compounds targeting the A.G.E. Pathway.
Alteon's lead compound alagebrium chloride (formerly ALT-711), the
only A.G.E. Crosslink Breaker in advanced human testing, has
demonstrated safety and efficacy in several Phase 2 trials and is
actively being developed for systolic hypertension and heart
failure. Over 1200 patients have been involved in alagebrium's
human clinical trials to date, of whom approximately 900 have
received active compound. Ongoing clinical trials include the phase
2b systolic hypertension trial, SPECTRA (Systolic Pressure Efficacy
and Safety Trial of Alagebrium), and the phase 2a heart failure
trial, PEDESTAL (Patients with Impaired Ejection Fraction and
Diastolic Dysfunction: Efficacy and Safety Trial of ALagebrium), as
well as a third trial exploring mechanism of action in endothelial
dysfunction. For more detailed scientific information about
alagebrium and a copy of the full abstract, please visit the
scientific publications section of the Alteon website,
http://www.alteon.com/ . 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 (including the possibility that early clinical
trial results may not be predictive of results that will be
obtained in large-scale testing or that any clinical trials will
not demonstrate sufficient safety and efficacy to obtain requisite
approvals or will not result in marketable products), 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. The information contained in this press release is
accurate as of the date indicated. Actual results, events or
performance 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. 1 Department of Urology, Tulane Health
Sciences Centre, New Orleans, USA 2 Wolfson Institute for
Biomedical Research, University College London, London, UK 3
Present address: Urology Department, Akdeniz University, Antalya,
Turkey 4 Present address: Department of Surgery, Johns Hopkins
Hospital, Baltimore, USA 5 "Effect of ALT-711, a Novel Glucose
Cross-link Breaker, in the Treatment of Diastolic Heart Failure."
Poster presentation, European Society of Cardiology Congress 2003.
Dalane W. Kitzman, Michael Zile, William C. Little, W. Gregory
Hundley, Terrence X. O'Brien, Robert C. deGroof. 6 "A Clinical
Trial of an A.G.E. Cross-link Breaker, Alagebrium Chloride
(ALT-711), in Systolic Hypertension." Abstract presented at the
American Society of Hypertension Nineteenth Annual Scientific
Meeting, May 19, 2004. George L. Bakris, Alan Bank, David C. Kass,
Joel Neutel, Richard Preston. 7 "Improved Arterial Compliance by a
Novel Advanced Glycation End-Product Crosslink Breaker."
Circulation: 2001; 104: r8-r14. David A. Kass, Edward P. Shapiro,
Miho Kawaguchi, Anne R. Capriotti, Angelo Scuteri, Robert C.
deGroof, Edward G. Lakatta. DATASOURCE: Alteon Inc. CONTACT: Susan
M. Pietropaolo, Director, Corporate Communications & Investor
Relations, +1-201-818-5537(direct) for Alteon Inc. Web site:
http://www.alteonpharma.com/
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