NEW DATA SUGGEST ORAL LAQUINIMOD MAY CONFER NEUROPROTECTION IN ADDITION TO IMMUNOMODULATION IN THE TREATMENT OF MULTIPLE SCLEROSIS
(Thomson Reuters ONE) -
Contact: Elana Holzman Teva Pharmaceutical Industries Ltd. +972-(3)-926-7554
Kevin Mannix Teva North America +1-(215)-591-8912
Contact: Tomas Leanderson Active Biotech AB +46-46-19-20-95
Göran Forsberg Active Biotech AB +46-46-19-11-54
- Enhanced levels of brain derived neurotrophic factor, possibly
contributing to neuroprotection, were shown in laquinimod treated multiple
sclerosis (MS) patients
- Laquinimod significantly reduce demyelination and axonal damage as
shown in animal models
- Two ongoing pivotal, global phase III clinical trials are fully
enrolled and results are anticipated next year
Jerusalem, Israel and Lund, Sweden, April 15, 2010 - Teva Pharmaceutical
Industries Ltd. (NASDAQ: TEVA) and Active Biotech (NASDAQ OMX NORDIC: ACTI)
today announced results from several studies demonstrating that laquinimod, a
novel, investigational once-daily oral immunomodulator for relapsing remitting
multiple sclerosis (RRMS) may have neuroprotective properties in addition to its
anti-inflammatory effects. These studies were presented at the 62(nd) Annual
Meeting of the American Academy of Neurology (AAN).
New data from studies in RRMS patients demonstrate that treatment with
laquinimod results in a significant increase in brain derived neurotrophic
factor, a key protein responsible for the maintenance of mature neurons.
Additionally, data from new animal models show that following treatment with
laquinimod there were significant reduction in the extent of demyelination, and
more axonal preservation within spinal cord lesions. Furthermore, treatment with
laquinimod inhibited the infiltration of inflammatory cells, into the spinal
cord and brain as well as causing a positive shift in specific white blood cells
involved in MS pathology.
These findings suggest laquinimod may have neuroprotective properties in
addition to anti-inflammatory effects. Coupled with the Phase IIb study results,
which demonstrated oral laquinimod to be effective and safe in RRMS patients,
these data provide further insight into the contributing factors surrounding the
favorable benefit-risk profile associated with this compound to date.
"As MS research progresses, emphasis will not only be on delaying disease
progression, but on preventing permanent nerve damage," said Ralf Linker, MD,
Dept. of Neurology, St. Josef-Hospital/Ruhr-University Bochum. "These data are
encouraging and suggest that the mechanism of action of laquinimod may
contribute to neuroprotection in RRMS patients, in addition to providing
therapeutic benefit through immunomodulation."
Laquinimod received Fast Track designation from the U.S. Food and Drug
Administration (FDA) in February 2009. Two pivotal global Phase III clinical
trials, BRAVO and ALLEGRO, are fully enrolled and results are anticipated next
year.
ABOUT THE STUDIES
The studies evaluating the mechanism of action of laquinimod being presented at
AAN include:
- Laquinimod Induces Up-Regulation of BDNF in Serum of Patients with
Relapsing-Remitting Multiple Sclerosis (PD5.004, Poster Discussion Session V:
Thursday, April 15(th) from 7:30 AM-12:00 PM)
Jan Thöne, Silvia Seubert, Rebecca Conrad, Bochum, NRW, Germany, Giancarlo Comi,
Milan, Italy, Stefan Wiese, Bochum, NRW, Germany, Liat Hayardeny, Netanya,
Israel, Ralf Gold, Ralf Andreas Linker, Bochum, NRW, Germany
- Treatment with 0.6 mg of laquinimod for three months resulted in a significant
and specific increase (up to 11-fold) in brain derived neurotrophic factor
(BDNF) serum levels as compared to baseline or placebo treatment (Total amount
of mean SEM: 16088 760 pg/ml BDNF in the laquinimod-group vs. 12882 625 pg/ml
in the placebo-group, p < 0.05 and vs. 14436 778 pg/ml at baseline, p < 0.05).
This effect on BDNF was maintained at 9 months and when analyzing the
relapse-free subgroup. The increased levels of the neurotrophic factor BDNF in
vivo in laquinimod treatment groups possibly contributes to neuroprotection in
MS patients.
- Effect of Laquinimod on Monocyte Subsets (S41.005, Scientific Sessions:
Multiple Sclerosis: Clinical Immunology: Thursday, April 15, 2010 at 2:15 PM)
Tal Birnberg, Steffen Jung, Rehovot, Israel, Israel
- Results indicate a profound effect of laquinimod on the steady state
distribution of murine blood and bone-marrow (BM) monocytes. Short-term
treatment resulted in a significant shift of the monocyte subset balance towards
the Ly6C(hi) subset, established precursors of CNS dendritic cells (DCs) and
macrophages in EAE lesions, which are accumulating in the blood and CNS
immediately prior to EAE clinical episodes. Furthermore, the laquinimod-mediated
effect was significantly increased in EAE induced mice. Study authors conclude
the effect of laquinimod on autoimmune deviation might be due in part to its
impact on monocyte subsets.
- Axonal Protection Effect of Laquinimod Appears Partially Independent of Its
Inhibitory Effect on Inflammation and Demyelination in Experimental Autoimmune
Encephalomyelitis (P 06.208, Poster Session VI: Thursday, April 15, 2010 from
3:00 PM-7:30 PM)
Christiane Wegner, Christine Stadelmann, Goettingen, Germany, Emanuel Nathan
Raymond, Bracha Timan, Liat Hayardeny, Netanya, Israel, Wolfgang Brück,
Goettingen, Germany
- Histological analysis revealed a marked reduction of macrophage and T-cell
infiltration in the total white matter of mice with MOG-induced experimental
autoimmune encephalomyelitis (EAE) treated with laquinimod compared to control
mice. Pro-inflammatory cytokines were down-regulated and the extent of
demyelination was significantly reduced in laquinimod treated mice. In addition
after therapeutic treatment, laquinimod treated mice displayed significantly
less axonal damage (measured by APP immunohistochemistry) within spinal cord
lesions in comparison to control mice (697 185/mm2 vs. 892 205/mm2, p=0.014).
Treatment with laquinimod is effective in ameliorating the extent of macrophage
and T cell infiltration, demyelination and axonal damage. These findings
indicate that laquinimod might have axon-protection properties in addition to
its anti-inflammatory effect and may therefore play a role in future treatment
of MS.
ABOUT MULTIPLE SCLEROSIS
Multiple sclerosis (MS) is the leading cause of neurological disability in young
adults. It is estimated that more than 400,000 people in the United States are
affected by the disease and that two million people may be affected worldwide.
MS is a progressive, demyelinating disease of the central nervous system
affecting the brain, spinal cord and optic nerves. Demyelination is the
destructive breakdown of the fatty tissue that protects nerve endings.
ABOUT LAQUINIMOD
Laquinimod is a novel once-daily, orally administered immunomodulatory compound
that is being developed as a disease-modifying treatment for RRMS. Active
Biotech developed laquinimod and licensed it to Teva Pharmaceutical Industries,
Ltd. in June 2004. Results from a Phase IIb study in 306 patients were published
in June 2008 in The Lancet and reported that an oral 0.6 mg dose of laquinimod,
administered daily, significantly reduced MRI disease activity by a median of
60 percent (51 percent mean reduction) versus placebo in RRMS patients. In
addition, the study showed a favorable trend toward reducing annual relapse
rates and in the number of relapse-free patients compared with placebo.
Treatment was well tolerated, with some transient and dose-dependent increases
in liver enzymes reported, without clinically-evident liver damage.
In addition to the efficacy that laquinimod has shown in Phase IIb RRMS studies,
laquinimod has demonstrated potent therapeutic efficacy in preclinical models of
other autoimmune diseases such as rheumatoid arthritis, insulin-dependent
diabetes mellitus, Guillain Barré Syndrome, lupus and Inflammatory Bowel
Disease. The broad profile of efficacy in animal models of inflammatory diseases
suggests that laquinimod affects a pivotal pathway of inflammation and
autoimmunity. Laquinimod is currently in Phase II development for Crohn's
disease and Teva will initiate the clinical development of the compound for
Lupus Nephritis in the near future.
ABOUT TEVA
Teva Pharmaceutical Industries Ltd., headquartered in Israel, is among the top
15 pharmaceutical companies in the world and is the leading generic
pharmaceutical company. The company develops, manufactures and markets generic
and innovative pharmaceuticals and active pharmaceutical ingredients. Over 80
percent of Teva's sales are in North America and Western Europe.
ABOUT ACTIVE BIOTECH
Active Biotech AB (OMX NORDIC: ACTI), headquartered in Sweden, is a
biotechnology company with R&D focus on autoimmune/inflammatory diseases and
cancer. Projects in pivotal phase are laquinimod, an orally administered small
molecule with unique immunomodulatory properties for the treatment of multiple
sclerosis, as well as ANYARA for use in cancer targeted therapy, primarily renal
cancer. Further key projects in clinical development comprise the three orally
administered compounds TASQ for prostate cancer, 57-57 for SLE and RhuDex(TM)
for RA. Please visit www.activebiotech.com for more information.
Teva's Safe Harbor Statement under the U. S. Private Securities Litigation
Reform Act of 1995:
This release contains forward-looking statements, which express the current
beliefs and expectations of management. Such statements are based on
management's current beliefs and expectations and involve a number of known and
unknown risks and uncertainties that could cause our future results, performance
or achievements to differ significantly from the results, performance or
achievements expressed or implied by such forward-looking statements. Important
factors that could cause or contribute to such differences include risks
relating to: our ability to successfully develop and commercialize additional
pharmaceutical products, the introduction of competing generic equivalents, the
extent to which we may obtain U.S. market exclusivity for certain of our new
generic products and regulatory changes that may prevent us from utilizing
exclusivity periods, potential liability for sales of generic products prior to
a final resolution of outstanding patent litigation, including that relating to
the generic versions of Neurontin®, Lotrel® and Protonix®, the extent to which
any manufacturing or quality control problems damage our reputation for high
quality production, the effects of competition on sales of our innovative
products, especially Copaxone® (including potential generic and oral competition
for Copaxone®), the impact of continuing consolidation of our distributors and
customers, our ability to identify, consummate and successfully integrate
acquisitions, interruptions in our supply chain or problems with our information
technology systems that adversely affect our complex manufacturing processes,
intense competition in our specialty pharmaceutical businesses, any failures to
comply with the complex Medicare and Medicaid reporting and payment obligations,
our exposure to currency fluctuations and restrictions as well as credit risks,
the effects of reforms in healthcare regulation, adverse effects of political or
economical instability, major hostilities or acts of terrorism on our
significant worldwide operations, increased government scrutiny in both the U.S.
and Europe of our agreements with brand companies, dependence on the
effectiveness of our patents and other protections for innovative products, our
ability to achieve expected results through our innovative R&D efforts, the
difficulty of predicting U.S. Food and Drug Administration, European Medicines
Agency and other regulatory authority approvals, uncertainties surrounding the
legislative and regulatory pathway for the registration and approval of
biotechnology-based products, potentially significant impairments of intangible
assets and goodwill, potential increases in tax liabilities resulting from
challenges to our intercompany arrangements, our potential exposure to product
liability claims to the extent not covered by insurance, the termination or
expiration of governmental programs or tax benefits, current economic
conditions, any failure to retain key personnel or to attract additional
executive and managerial talent, environmental risks and other factors that are
discussed in this report and in our other filings with the U.S. Securities and
Exchange Commission ("SEC").
Active Biotech's Safe Harbor Statement in Accordance with the Swedish Securities
Market Act:
This press release contains certain forward-looking statements. Such
forward-looking statements involve known and unknown risks, uncertainties and
other important factors that could cause the actual results, performance or
achievements of the company, or industry results, to differ materially from any
future results, performance or achievement implied by the forward-looking
statements. The company does not undertake any obligation to update or publicly
release any revisions to forward-looking statements to reflect events,
circumstances or changes in expectations after the date of this press release.
Active Biotech is obligated to publish the information contained in this press
release in accordance with the Swedish Securities Market Act. . The information
was submitted for publication at 5:15 pm CET on April 15, 2010.
# # #
[HUG#1404285]
Press release (PDF): http://hugin.info/1002/R/1404285/358382.pdf
Unternehmensinformation / Kurzprofil:
Datum: 15.04.2010 - 18:31 Uhr
Sprache: Deutsch
News-ID 19130
Anzahl Zeichen: 0
contact information:
Town:
LUND
Kategorie:
Business News
Diese Pressemitteilung wurde bisher 881 mal aufgerufen.
Die Pressemitteilung mit dem Titel:
"NEW DATA SUGGEST ORAL LAQUINIMOD MAY CONFER NEUROPROTECTION IN ADDITION TO IMMUNOMODULATION IN THE TREATMENT OF MULTIPLE SCLEROSIS"
steht unter der journalistisch-redaktionellen Verantwortung von
Active Biotech (Nachricht senden)
Beachten Sie bitte die weiteren Informationen zum Haftungsauschluß (gemäß TMG - TeleMedianGesetz) und dem Datenschutz (gemäß der DSGVO).
