Data presented at the 26th Congress of the European Committee for Treatment and
Research in Multiple Sclerosis (ECTRIMS)

Jerusalem, Israel and Lund, Sweden, October 15, 2010 - Teva Pharmaceutical
Industries Ltd. (NASDAQ: TEVA) and Active Biotech (NASDAQ OMX NORDIC: ACTI)
announced today that data providing further evidence of the neuroprotective
properties of laquinimod in animal studies were presented at the 26th Congress
of the European Committee for Treatment and Research in Multiple Sclerosis
(ECTRIMS) in Gothenburg, Sweden. Laquinimod is an investigational, once-daily
oral immunomodulator for the treatment of relapsing remitting multiple sclerosis

These results, generated from several pre-clinical studies evaluating the
mechanism of action (MOA) of oral laquinimod, demonstrated that:

  * Laquinimod reverts the disruption of neurogenic processes that can occur
    with chronic
                inflammation in the central nervous system (CNS), and is
    associated with a significant reduction
                in the percentage of demyelination and axonal damage.

  * Laquinimod differentially influenced the activity of select immune cells,
    reducing their pro-
                inflammatory characteristics while increasing the production of
    neurotrophic factors known to be
                involved in neuroprotection and repair mechanisms.

  * Laquinimod treatment is associated with an increase in brain-derived
    neurotrophic factor (BDNF),
                a pivotal factor in the development and maintenance of the CNS.

"These results add to the accumulating body of data establishing the novel MOA
of laquinimod. These MOA studies suggest that laquinimod has the potential to
prevent demyelination, which is associated with multiple sclerosis, and
therefore may provide neuroprotection in the treatment of RRMS," said Prof. Ralf
Gold, Department of Neurology, St. Josef-Spital, Ruhr University Bochum,
Germany. "Research is ongoing to further evaluate laquinimod, and we look
forward to additional data, including the forthcoming results from the Phase III
clinical development program."

Laquinimod received Fast Track designation from the U.S. Food and Drug
Administration (FDA) in February 2009. Two global Phase III clinical studies,
ALLEGRO and BRAVO, have completed enrollment and are currently ongoing, with
results anticipated in 2011.


  * [P885] Laquinimod prevents the inflammation-induced derangement of
    neurogenic niches
                in experimental autoimmune encephalomyelitis mice.

Poster Session: Neuroprotection 2, October 15, 3:30pm-5:00pm CET (F. Ruffini, A.
Bergamaschi, C. Marinaro, R. De Ceglia, L. Muzio, R. Furlan, L. Hayardeny, G.
Comi, G. Martino)

      * To determine if laquinimod is capable of reverting non-cell autonomous
        dysfunction of endogenous neural stem cells following chronic
        inflammation within the central nervous system (CNS), C57Bl/6 mice were
        immunized with myelin oligodendrocytes glycoprotein (MOG) peptide 35-55
        and treated subcutaneously (s.c.) with increasing doses of laquinimod
        (1, 5, 10 or 25 mg/kg laquinimod). At the end of the study (day 25
        p.i.), CNS of EAE mice was collected for pathological and molecular
        studies. Pathological and molecular study results in mice with EAE
        suggest that treatment with 25 mg/kg of laquinimod administered after
        EAE onset resulted in a significant reduction in the percentage of
        demyelination and axonal damage as well in the number of inflammatory
        responses.   An in vivo increase in cell proliferation was also
    [P881] Laquinimod ameliorates experimental autoimmune encephalomyelitis via
                dependent mechanisms.

Poster Session: Neuroprotection 2, October 15, 3:30pm-5:00pm CET (J. Thöne, D.
Lee, S. Seubert, L. Hayardeny, R. Linker, R. Gold)

      * To further elucidate the mechanism of action of laquinimod and to
        examine its potential neuroprotective capacity via modulation of BDNF
        secretion, laquinimod was tested in myelin oligodendrocyte glycoprotein
        (MOG) induced EAE experiments using mice at 6-8 weeks of age on C57Bl/6J
        background, and with a conditional deficiency for BDNF in T cells and
        monocytes (LLF mice). Histological analyses reveal that mice with BDNF
        deficiency, treated with laquinimod, had more severe experimental
        autoimmune encephalomyelitis (EAE), or animal model of MS progression,
        than mice not BDNF deficient, and actually experience an increase in
        BDNF levels. This suggests that the mechanism of action of laquinimod is
        BDNF dependent and may contribute to neuroprotection.
    [P882] Differential activity of laquinimod on production of inflammatory
    molecules and
                neurotrophic factors by human microglia and macrophages.

Poster Session: Neuroprotection 2, October 15th, 3:30pm-5:00pm CET (C. Silva, J.
Wang, M. Mishra, V.W. Yong)

      * To determine whether laquinimod modulates the production of inflammatory
        molecules and growth factors by microglia and macrophages, the cells
        were isolated from the peripheral blood of healthy adult human
        volunteers and cultured from the brains of human fetal samples or from
        adult human surgical brain resections.  Cytokines and matrix
        metalloproteinase-9 (MMP-9) were measured by ELISA of cell-conditioned
        media and growth factor transcripts were determined using PCR of
        cellular extracts. Treatment with laquinimod reduces the expression of
        inflammatory responses by autoimmune microglia and in healthy human
        cells and increases production of the neuroprotective BDNF by threefold.

    [P251] Laquinimod rescue therapy in mice with experimental autoimmune

Poster Session: Experimental Models 1, October 14th, 2010, 3:30pm-5:00pm CET (C.
Wegner, R. Pförtner, W. Brück)

      * To test whether laquinimod could improve EAE symptoms as a late-stage
        rescue therapy. The next goal was to assess if this late-stage treatment
        alters the extent of demyelination and inflammation in MOG induced EAE.
        Laquinimod rescue therapy given from days 30 to 60 improved clinical
        disease scores in the majority of animals in comparison to the control
        group. Findings indicate that late stage therapy with laquinimod is
        effective in ameliorating the disease severity. Results indicate that
        laquinimod may have a role in future treatment of MS.


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.


Laquinimod is a novel once-daily, orally administered immunomodulatory drug
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 mean of 51
percent (p<0.0001) and median of 60 percent (p=0.01) versus placebo in RRMS
patients. Some transient and dose-dependent increases in liver enzymes were
reported, without clinically-evident liver damage.

Two pivotal, global Phase III studies of laquinimod for the treatment of RRMS,
ALLEGRO and BRAVO, are nearing completion. ALLEGRO, a 24-month multinational,
double-blind, placebo-controlled study, designed to evaluate the efficacy,
safety and tolerability of laquinimod versus placebo in the treatment of RRMS,
enrolled 1,106 patients and data from the study are expected in Q1 2011.  BRAVO,
 a 24-month multinational, multi-center, randomized, parallel-group study
designed to evaluate laquinimod compared to placebo, as well as to provide risk-
benefit data for laquinimod compared to a currently available injectable
treatment, Avonex®, has enrolled 1,332 patients and will be complete in Q3 2011.

In addition to the ongoing RRMS clinical studies, laquinimod is currently in
Phase II development for Crohn's disease and Lupus, and is being studied in
other autoimmune diseases.


Teva Pharmaceutical Industries Ltd. (NASDAQ:TEVA) is a leading global
pharmaceutical company, committed to increasing access to high-quality
healthcare by developing, producing and marketing affordable generic drugs as
well as innovative and specialty pharmaceuticals and active pharmaceutical
ingredients. Headquartered in Israel, Teva is the world's largest generic drug
maker, with a global product portfolio of more than 1,250 molecules and a direct
presence in approximately 60 countries. Teva's branded businesses focus on
neurological, respiratory and women's health therapeutic areas as well as
biologics. Teva's leading innovative product, Copaxone®, is the number one
prescribed treatment for multiple sclerosis. Teva employs more than 40,000
people around the world and reached $13.9 billion in net sales in 2009.


Active Biotech AB (NASDAQ OMX NORDIC: ACTI) is a biotechnology company with
focus on autoimmune/inflammatory diseases and cancer. Projects in or entering
pivotal phase are laquinimod, an orally administered small molecule with unique
immunomodulatory properties for the treatment of multiple sclerosis, TASQ for
prostate cancer as well as ANYARA for use in cancer targeted therapy, primarily
of renal cell cancer. In addition, laquinimod is in Phase II development for
Crohn's and Lupus. Further projects in clinical development comprise the two
orally administered compounds, 57-57 for SLE & Systemic Sclerosis and RhuDex(TM)
for RA. Please visit www.activebiotech.comfor more information.

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Reform Act of 1995:
This release contains forward-looking statements, which express the current
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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
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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 3:30 pm CEST on October 15, 2010.

Teva Contacts                       Active Biotech Contacts

Investor Relations:
                                    Tomas Leanderson, President & CEO,      +46-
Elana Holzman                       46-19-20-95
Teva Pharmaceutical Industries Ltd.
972 (3) 926-7554                    Media and Investors:

Kevin Mannix                        Göran Forsberg, +46-46-19-11-54
Teva North America
(215) 591-8912


Yossi Koren
Teva Pharmaceutical Industries Ltd.
972 (3) 926-7590

Denise Bradley
Teva North America
(215) 591-8974



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