Copaxone® Demonstrated Protective Effect in Patients with Clinically Isolated Syndrome Suggestive of Multiple Sclerosis

PreCISe Data Presented at World Congress on Treatment and Research in Multiple Sclerosis

Jerusalem, Israel, September 19, 2008 - New data from PreCISe, in clinically isolated syndrome patients, have demonstrated that COPAXONE® (glatiramer acetate injection) significantly improved neuro-axonal integrity in patients presenting with a first clinical event suggestive of multiple sclerosis (MS) versus patients who received placebo (p=0.03), as measured by proton magnetic resonance spectroscopy (MRS). This effect was maintained over two years of treatment.

The data represent the first evidence of neuro-axonal protection by a disease modifying therapy in patients presenting with a first clinical event suggestive of MS.

Data were derived from an ancillary study from the Phase III, randomized, placebo-controlled PreCISe trial, which demonstrated that patients treated with COPAXONE® (n=243) had a 45 percent reduction in the risk of developing clinically definite multiple sclerosis (CDMS) compared to those on the placebo (n=238).

"These newly announced data, so far shown in RRMS patients treated with COPAXONE®, provide more evidence that treatment may control the neuronal damage associated with MS disease pathology," said Douglas Arnold, M.D., Professor of Neurology, McGill University and the primary investigator of this ancillary study. "The PreCISe trial demonstrated a significant benefit of COPAXONE® on both clinical and MRI disease activity, along with further reinforcing the excellent safety profile."

The data were presented along with two other presentations from the PreCISe study at the World Congress on Treatment and Research in Multiple Sclerosis, in Montreal, Canada. Additional data derived from the PreCISe study demonstrated that COPAXONE® significantly delayed time to conversion to CDMS and reduced magnetic resonance imaging (MRI) disease activity. The effect was robust among the PreCISe study population (n=481), as a whole and also in subgroups of patients (segmented by gender, age, type of unifocal manifestation as well as steroid treatment for the initial attack, and MRI findings at study baseline). Based on these data, applications for marketing authorization for the extension of its indication to include the treatment of patients with a first clinical event suggestive of MS were submitted in Europe and in the U.S. and are currently under review.

About the PreCISe Data
The study, "Treatment with glatiramer acetate protects axons in patients with clinically isolated syndromes: evidence from the PreCISe trial," determined that patients with clinically isolated syndrome (CIS) who received COPAXONE® showed improvement in their cerebral neuro-axonal integrity relative to patients treated with placebo.

Proton MRS was performed in a subgroup of patients in the PreCISe trial (n=34) to measure the concentration of N-acetulaspartate (NAA) levels. NAA/CR measurements were acquired each year from each patient enrolled at 10 clinical sites in seven countries. Patients terminated at the time of relapse.

Patients who received COPAXONE® showed significant improvement in their cerebral neuro-axonal integrity compared to patients treated with placebo, who showed the decline expected from natural history studies. Paired changes in NAA/CR ratio differed significantly between both patients treated with COPAXONE® (+0.14, n=11) compared to those treated with placebo (-0.33, n=9, p=0.03) at one year, and the change maintained at two years (COPAXONE® n=6, +0.17; placebo n=3, -0.23, p=0.15).

Previously announced PreCISe studies included:

"Treatment with glatiramer acetate reduces MRI-detectable disease activity in patients at presentation with CIS suggestive of MS"

* Demonstrated that early treatment with COPAXONE® is effective in both delaying time to conversion to CDMS and reducing MRI activity in patients presenting with CIS


"Treatment with glatiramer acetate delays conversion to CDMS in patients with CIS: subgroup analyses"

* Demonstrated that COPAXONE® treatment effect was robust among the PreCISe study population (n=481) as a whole ,as well as in subgroups of patients (broken down by gender, age and type of unifocal manifestation and steroid treatment for the initial attack, and MRI findings at study baseline)



About COPAXONE®
COPAXONE® is indicated for the reduction of the frequency of relapses in RRMS. The most common side effects of COPAXONE® are redness, pain, swelling, itching, a lump or an indentation at the site of injection, weakness, infection, pain, nausea, joint pain, anxiety, and muscle stiffness.

COPAXONE® is now approved in 51 countries worldwide, including the United States, Canada, Mexico, Australia, Israel, and all European countries. In North America, COPAXONE® is marketed by Teva Neuroscience, Inc., which is a subsidiary of Teva Pharmaceutical Industries Ltd. (NASDAQ:TEVA). In Europe, COPAXONE® is marketed by Teva Pharmaceutical Industries Ltd. and sanofi-aventis. COPAXONE® is a registered trademark of Teva Pharmaceutical Industries Ltd.

See additional important information at http://www.copaxone.com/pi/index.html or call 1-800-887-8100 for electronic releases. For hardcopy releases, please see enclosed full prescribing information.

About Teva
Teva Pharmaceutical Industries Ltd., headquartered in Israel, is among the top 20 pharmaceutical companies in the world and is the world's leading generic pharmaceutical company. The Company develops, manufactures and markets generic and innovative human pharmaceuticals and active pharmaceutical ingredients, as well as animal health pharmaceutical products. Over 80 percent of Teva's sales are in North America and Europe.

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, competition from brand-name companies that are under increased pressure to counter generic products, or competitors that seek to delay the introduction of generic products, the impact of consolidation of our distributors and customers, potential liability for sales of generic products prior to a final resolution of outstanding patent litigation, including that relating to the generic versions of Allegra® , Neurontin®, Lotrel® and Protonix®, the effects of competition on our innovative products, especially Copaxone® sales, the impact of pharmaceutical industry regulation and pending legislation that could affect the pharmaceutical industry, the difficulty of predicting U.S. Food and Drug Administration, European Medicines Agency and other regulatory authority approvals, the regulatory environment and changes in the health policies and structures of various countries, our ability to achieve expected results though our innovative R&D efforts, our ability to successfully identify, consummate and integrate acquisitions, including the pending acquisition of Barr Pharmaceuticals Inc., potential exposure to product liability claims to the extent not covered by insurance, dependence on the effectiveness of our patents and other protections for innovative products, significant operations worldwide that may be adversely affected by terrorism, political or economical instability or major hostilities, supply interruptions or delays that could result from the complex manufacturing of our products and our global supply chain, environmental risks, fluctuations in currency, exchange and interest rates, and other factors that are discussed in this report and in our other filings with the U.S. Securities and Exchange Commission ("SEC").



Company Contacts:
Company Contacts:
Elana Holzman
Kevin Mannix

Teva Pharmaceutical Industries Ltd.
Teva North America

972 (3) 926-7554
(215) 591-8912

New Data on Disease-modifying Therapies for Multiple Sclerosis

Mark J. Tullman, MD

Introduction

New data from key clinical trials of disease-modifying therapy were presented at the 60th Annual Meeting of the American Academy of Neurology. The results of some of these studies, along with the potential clinical implications of those results, are presented below.

Efficacy of Interferon Beta-1b and Glatiramer Acetate in Patients With Relapsing-Remitting Multiple Sclerosis: The BEYOND Trial

Results of the Betaferon/Betaseron Efficacy Yielding Outcomes of a New Dose (BEYOND) trial, which was funded by Bayer Healthcare Pharmaceuticals, were presented in a late-breaking session by Paul O'Connor, MD.[1] This trial was designed to compare the efficacy of 250 micrograms (mcg) and 500 mcg of interferon beta-1b given subcutaneously (SC) every other day in patients with relapsing-remitting multiple sclerosis (RRMS). The efficacy of these two doses of beta interferon-1b was also compared with glatiramer acetate (20 mg SC administered daily).

The trial randomized treatment-naive patients with RRMS with Expanded Disability Status Scale (EDSS) scores equal to or less than 5. Patients also had to have at least one relapse in the year prior to entry into the study. A total of 2244 patients were randomized in a 2:2:1 ratio to the 500-mcg dose of beta interferon-1b (n = 899), the 250-mcg dose of interferon beta-1b (n = 899) or to the 20-mg dose of glatiramer acetate (n = 448) for a period of 104 weeks or longer. Patients underwent clinical evaluations every 3 months and brain magnetic resonance imaging (MRI) scans annually.

The trial's primary endpoint was relapse risk. A per-protocol analysis and an intent-to-treat analysis were performed on the data. The clinical efficacy of each of the 3 treatment groups (beta interferon-1b 250 mcg, beta interferon-1b 500 mcg, and glatiramer acetate 20 mg) was similar in each of the analyses.

There were several supportive endpoints, including relapse rate, proportion of relapse-free patients, and time to first relapse. Secondary outcome variables were time to confirmed EDSS progression and T1 black hole development. Other endpoints of interest included the number and volume of T2 lesions. The annualized relapse rate fell by nearly 80% compared with the year prior to enrollment in the study, but there were no significant differences among the treatment groups.

There were some MRI endpoints that showed statistically significant differences between the treatment groups. The cumulative number of T2 lesions up to the last scan was significantly higher in the group receiving glatiramer acetate compared with the groups receiving 250 mcg (P = .17) or 500 mcg (P = .001) beta interferon-1b. Additionally, patients receiving 250 mcg or 500 mcg beta interferon-1b had a significantly lower increase in T2-lesion volume compared with the group receiving glatiramer acetate (P < .001 and P = .001, respectively). The authors note that it is unclear whether there is any long-term clinical significance to these findings.

All 3 treatments were generally well-tolerated. Dropout rates for 250 mcg interferon beta-1b, 500 mcg interferon beta-1b, and glatiramer acetate were 13%, 19%, and 17%, respectively. It is important to note that although this was a double-blind study for the interferon beta-1b groups (ie, they were unaware which dose they were receiving), this was not a double-blind trial for the patients who received glatiramer acetate. This may explain the higher dropout rate in the group receiving glatiramer acetate (17%) compared with the group receiving 250 mcg interferon beta-1b (13%) because the patients receiving interferon beta-1b were aware that there was a 50% chance that they could be receiving the higher, and potentially more effective, dose of interferon beta-1b.

The adverse events observed were similar to the known adverse event profiles of these compounds. Flulike symptoms were more common with interferon beta-1b and injection-site reactions (eg, pain, pruritis) were more common with glatiramer acetate.

The Results of the BEYOND trial[1] are similar to the recently presented results from the REGARD trial[2] that compared interferon beta-1a 44 mcg SC 3 times a week to glatiramer acetate. In these 2 studies, more than 2000 patients were randomized to either high-dose interferon or glatiramer acetate. Patients did very well and there were no major differences in terms of efficacy between the therapies. Unfortunately, the 500-mcg dose of interferon beta-1b was no more effective than the 250-mcg dose. In the absence of clear superior efficacy data between the high-dose interferons and glatiramer acetate, it seems to me that a high-dose interferon and glatiramer acetate are both reasonable initial treatment options for most patients with RRMS. Patients should be well informed and part of the treatment decision process. Some patients may prefer starting with a daily injection with fewer side effects and others would rather take a medication that has fewer injections but the potential to cause more side effects and requires periodic blood work.

Furthermore, for patients on a high dose interferon of glatiramer acetate who experience persistent side effects, switching from one agent to the other might improve tolerability and enhance quality of life without sacrificing efficacy.

Efficacy of Glatiramer Acetate in Delaying Conversion to Clinically Definite Multiple Sclerosis: The PreCISe Trial

Results from the Study to Evaluate the Effect of Early Glatiramer Acetate Treatment in Delaying the Conversion to CDMS of Subjects Presenting With a Clinically Isolated Syndrome (CIS) (PreCISe) trial, were presented in a late-breaking session by Giancarlo Comi.[3] The PreCISe trial was a randomized, double-blind, placebo-controlled, multicenter, 3-year study designed to evaluate the efficacy of early treatment with glatiramer acetate in delaying the progression to clinically definite MS (CDMS) in patients with clinically isolated syndromes (CIS), which are considered to be first events suggestive of MS.

The study randomized 481 patients who had a minimum of 2 T2-weighted brain lesions at least 6 mm in diameter shown on MRI and who had experienced a first clinical event to receive glatiramer acetate 20 mg/day SC (n = 243) or placebo (n = 238). Only patients with a unifocal disease manifestation were included. Key baseline characteristics were: age (31.1 ± 6.9 years), time from first event to randomization (74.0 ± 14.9 days), and corticosteroid use for first attack (64% of patients). There was no difference between the study arms in EDSS (1.0 ± 1.0), number (31.5 ± 30.7) and volume (6.0 ± 6.2ml) of T2 weighted lesions, and number (1.5±2.9) and volume (0.3 ± 0.6ml) of gadolinium enhanced lesions.

The primary endpoint of the study was time to CDMS based on a second clinical attack. The trial was stopped prematurely by the data and safety monitoring committee after a preplanned interim analysis. The group initially receiving placebo was then switched to active treatment on an open-label basis. At this point, about 80% of the planned drug exposure had been given, and CDMS had developed in about 43% of those patients in the placebo group compared with just 25% in the glatiramer acetate group. The odds ratio for progression to CDMS was 0.41 (P < .0001) and the hazard ratio for progression to CDMS was 0.55 (95% CI 0.40-0.77; P = .0005) in the group taking glatiramer acetate compared with the placebo group. This translates in to a 45% risk reduction for progression to CDMS in the group on active treatment compared with the group on placebo. Additionally, the 25th percentile time to CDMS was prolonged from 336 days in the placebo group to 722 days (115% increase in time to CDMS onset) in the group receiving glatiramer acetate.

The results of MRI scans also favored the group receiving glatiramer acetate compared with the group receiving placebo. The mean number of new T2-weighted lesions was reduced by 61% in the patients receiving glatiramer acetate compared with the patients receiving placebo (P < .0001). Similarly, patients receiving glatiramer had a 61% reduction in new T1 gadolinium-enhancing lesions compared with the group receiving placebo (P < .0001).

Glatiramer acetate was well tolerated, and side effects were similar to those previously reported in patients with CDMS, including local injection-site reactions and transient postinjection reactions including chest pain, flushing, dyspnea, palpitations, and anxiety.

The open-label extension phase of the study will continue to a 5-year follow-up to evaluate the potential for glatiramer acetate to prevent or delay clinical progression of the disease. Patients will receive glatiramer acetate and will be followed until the development of CDMS.

The PreCISe study results are really not surprising. However, we now have strong evidence that the interferons and glatiramer acetate are effective when initiated after a first MS attack in patients with at least minimally abnormal brain MRI. The 5-year PreCISe data may provide additional evidence that early treatment with MS immunomodulatory therapy prevents the development of disability.

This activity is supported by an independent educational grant from Teva Neuroscience.

EARLY TREATMENT WITH COPAXONE® SIGNIFICANTLY DELAYED

Teva Seeks Approval for the Extension of its Indication to Include the Treatment of Patients with a First Clinical Event Suggestive of MS

Jerusalem, April 16, 2008 - Teva Pharmaceutical Industries Ltd. (NASDAQ: TEVA) today announced new results from the PreCISe study, which demonstrated that early treatment with COPAXONE® (glatiramer acetate injection) significantly reduced the risk of developing clinically definite multiple sclerosis (CDMS) by 45 percent compared to placebo (hazard ratio 0.55, p=0.0001). These data were presented as late-breaking science at the 60th Annual Meeting of the American Academy of Neurology (AAN) in Chicago.


Based on the PreCISE results, an application for marketing authorization in Europe to the Medicines and Healthcare products Regulatory Agency (MHRA) for the extension of its indication to include the treatment of patients with a first clinical event suggestive of MS, was submitted and is currently under review. A similar application requesting an expanded label for COPAXONE® will also be submitted shortly with the U.S. Food and Drug Administration (FDA).


"Clinically isolated syndrome, or CIS, is a first neurologic episode, usually caused by inflammation or demyelination, which is indicative of possible development of multiple sclerosis," said Giancarlo Comi, M.D., University Vita-Salute San Raffaele, Scientific Institute San Raffaele, Milan, Italy, and principal investigator. "The PreCISe study results clearly demonstrate that early treatment with COPAXONE®, as early as CIS, reduces the risk of developing MS" he added.


COPAXONE®, currently indicated for RRMS, is a unique disease modifying treatment with a dual mode of action that has over 10 years of prospective clinical trial data demonstrating long-term clinical treatment benefits and good safety profile. The PreCISe results now extend COPAXONE® effect to CIS patients, demonstrating a reduced risk of developing Clinically Definite MS (CDMS). Furthermore, the safety profile of COPAXONE® in the PreCISe study was consistent with the well-established safety profile of the product based on many years of post-marketing surveillance and over 100,000 patients treated globally with COPAXONE®.

Moshe Manor, Group Vice President, Global Innovative Resources of Teva Pharmaceutical Industries, Ltd., said, "These impressive results clearly demonstrate the potency of COPAXONE® in treating early phases of multiple sclerosis. Along with its lasting efficacy, confirmed over 10 years, it positions COPAXONE® as the preferred treatment option for multiple sclerosis patients".


About the Study
The multi-national, multi-center, prospective, double-blind, randomized, Phase III study was conducted in approximately 100 centers located in the U.S., Europe, Argentina, Israel, Nordic countries, Australia and New Zealand. It included a total of 481 patients presenting with a single clinical episode and MRI suggestive of MS. Patients included were those who had a unifocal disease manifestation (i.e., clinical evidence of a single lesion). Patients received either COPAXONE® 20mg/day or placebo as a subcutaneous injection and continued treatment for up to 36 months, unless a second attack was experienced and they were diagnosed with CDMS. Patients who converted to CDMS continued the trial on active treatment for an additional two years. The primary efficacy outcome was time to CDMS, based on a second clinical attack.

COPAXONE® (glatiramer acetate injection) was also demonstrated to be very well tolerated in the PreCISe study, with only 16 percent overall dropouts during the up to three-year study period, similar to that observed in RRMS patients treated with COPAXONE®. All patients in the study participated in a follow-up study with COPAXONE® to prospectively assess the impact of early versus delayed treatment with COPAXONE® on the long-term course of the disease for a total observation time of up to five years.

A pre-planned interim analysis was performed on data accumulated from approximately 80 percent of the three-year placebo-controlled study exposure. Results of the interim analysis, announced in December 2007, demonstrated the proportion of patients developing CDMS was reduced from 43 percent in the placebo group to only 25 percent in the COPAXONE® group (p< 0.0001). The PreCISe study also demonstrated that the 25th percentile of number of days to conversion to CDMS has more than doubled by COPAXONE® from 336 days to 722 days (hazard ratio 0.55, p=0.0005) compared with placebo.

At the time of this analysis, the data monitoring committee (DMC) stopped the placebo arm of the study, as COPAXONE® successfully met the efficacy endpoint of the study.


About COPAXONE®
Current data suggest COPAXONE® is a selective MHC (Major Histocompatability Complex) class II modulator. COPAXONE® is indicated for the reduction of the frequency of relapses in RRMS. COPAXONE® is very well tolerated and the most common side effects of COPAXONEv are redness, pain, swelling, itching, or a lump or an indentation at the site of injection, weakness, infection, pain, nausea, joint pain, anxiety, and muscle stiffness.

COPAXONE® is now approved in 51 countries worldwide, including the United States, all European countries, Canada, Mexico, Australia, and Israel. In Europe, COPAXONE® is marketed by Teva Pharmaceutical Industries Ltd. and sanofi-aventis. In North America, COPAXONE® is marketed by Teva Neuroscience, Inc.

See additional important information at http://www.COPAXONE.com/pi/index.html or call 1-800-887-8100 for electronic releases. For hardcopy releases, please see enclosed full prescribing information.

About Teva
Teva Pharmaceutical Industries Ltd., headquartered in Israel, is among the top 20 pharmaceutical companies in the world and is the world's leading generic pharmaceutical company. The Company develops, manufactures and markets generic and innovative human pharmaceuticals and active pharmaceutical ingredients, as well as animal health pharmaceutical products. Over 80 percent of Teva's sales are in North America and Europe. Teva's innovative R&D focuses on developing novel drugs for diseases of the central nervous system.

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 Teva's 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: when and whether the proposed acquisition will be consummated, Teva's ability to rapidly integrate Bentley's operations with its own operations and achieve expected synergies, the diversion of management time on merger-related issues, Teva's ability to accurately predict future market conditions, potential liability for sales of generic products prior to a final resolution of outstanding patent litigation, including that relating to the generic versions of Allegra®, Neurontin®, Lotrel®, Famvir® and Protonix®, Teva's ability to successfully develop and commercialize additional pharmaceutical products, the introduction of competing generic equivalents, the extent to which Teva may obtain U.S. market exclusivity for certain of its new generic products and regulatory changes that may prevent Teva from utilizing exclusivity periods, competition from brand-name companies that are under increased pressure to counter generic products, or competitors that seek to delay the introduction of generic products, the impact of consolidation of our distributors and customers, the effects of competition on our innovative products, especially Copaxone® sales, the impact of pharmaceutical industry regulation and pending legislation that could affect the pharmaceutical industry, the difficulty of predicting U.S. Food and Drug Administration, European Medicines Agency and other regulatory authority approvals, the regulatory environment and changes in the health policies and structures of various countries, our ability to achieve expected results though our innovative R&D efforts, Teva's ability to successfully identify, consummate and integrate acquisitions, potential exposure to product liability claims to the extent not covered by insurance, dependence on the effectiveness of our patents and other protections for innovative products, significant operations worldwide that may be adversely affected by terrorism, political or economical instability or major hostilities, supply interruptions or delays that could result from the complex manufacturing of our products and our global supply chain, environmental risks, fluctuations in currency, exchange and interest rates, and other factors that are discussed in Teva's Annual Report on Form 20-F and its other filings with the U.S. Securities and Exchange Commission. Forward-looking statements speak only as of the date on which they are made and the Company undertakes no obligation to update or revise any forward-looking statement, whether as a result of new information, future events or otherwise.




Company Contacts:
Elana Holzman
Kevin Mannix
Teva Pharmaceutical Industries Ltd.
Teva North America
972 (3) 926-7554
(215) 591-8912

Early Treatment with COPAXONE® Demonstrated Robust Protection against Progression to Clinically Definite Multiple Sclerosis in the PreCISe Study

Efficacy Is Attained and the Study Is Stopped after Interim Analysis and Supports Filing of COPAXONE® For Patients with a First Clinical Event Suggestive of MS

Jerusalem, Israel, December 3, 2007 - Teva Pharmaceutical Industries Ltd. (NASDAQ: TEVA) today announced the positive results from a pre planned interim analysis of the PreCISe trial in patients presenting with a first clinical event and MRI features suggestive of multiple sclerosis (MS). The results showed that treatment with COPAXONE® (glatiramer acetate injection) reduced the risk of developing clinically definite MS (CDMS) by 44 percent versus placebo, and prolonged the quartile time to disease conversion to 722 days versus 336 days (+386 days, +115%) in those patients receiving placebo (hazard ratio 0.56, p=0.0005). At the time of the interim analysis, the proportion of patients who had developed CDMS was reduced from 43 percent in the placebo group to only 25 percent in the COPAXONE® group. Based on these results, Teva plans to file a request for marketing authorization of COPAXONE® in Europe, the U.S. and Canada for the treatment of patients with a first clinical event suggestive of MS.

Professor Paul O'Connor, Neurology Division Chief at St. Michael's Hospital, Toronto, Canada and the chairman of the study's independent data monitoring committee (DMC), said, "We are deeply impressed by Teva's commitment to continue developing COPAXONE® for patients presenting with a first clinical event and MRI suggestive of MS. After analyzing the data from the PreCISe study at the interim analysis, the DMC recommended that the placebo arm of the trial be stopped, as COPAXONE® successfully met the efficacy endpoint of the study; all placebo patients will now be given the opportunity to receive active treatment with COPAXONE® for two years."

This study further demonstrated the beneficial effect of early treatment with COPAXONE® on disease activity and burden, also in its early stages, as measured by both short-term clinical and magnetic resonance imaging (MRI) disease outcomes. COPAXONE® is the only relapsing remitting MS (RRMS) treatment with data from a long-term, prospective, ongoing study which demonstrated that in those patients adhering to therapy, 92 percent still walk unassisted after a mean of 10 years of therapy and 18 years of disease duration.

Professor Giancarlo Comi, Department of Neurology, San Raffaele Scientific Institute, Milan, Italy, and principal investigator of the study said, "We are very pleased by the results of this trial. These data on COPAXONE® demonstrated the importance of treating patients early on to provide rapid, early control of progression to CDMS, and stand to improve therapy options for the treatment of patients with first clinical event and a high risk to develop MS."

Moshe Manor, Group Vice President - Global Innovative Resources of Teva Pharmaceutical Industries, Ltd., said "The interim results of this study, which showed that early treatment with COPAXONE® delayed progression to CDMS, together with the unmatched long-term efficacy, tolerability and favorable safety profile supporting COPAXONE®, position it now also as the outstanding treatment option for patients with a first clinical event suggestive of MS and RRMS patients."


About the Study
The multi-national, multi-center, prospective, double-blind, randomized, Phase III PreCISe study was conducted in approximately 100 centers located in the U.S., Europe, Argentina, Israel, Nordic countries, Australia and New Zealand and included a total of 481 patients presenting with a single clinical episode and MRI suggestive of MS. Patients included are those who had a unifocal disease manifestation (i.e., clinical evidence of a single lesion). Patients received either COPAXONE® 20mg/day or placebo as a subcutaneous injection and continued treatment for up to 36 months, unless a second attack was experienced and they were diagnosed with clinically definite MS. Patients who converted to CDMS continued the trial on active treatment for additional two years. The primary efficacy outcome was time to CDMS, based on a second clinical attack. The pre-planned interim analysis was performed on data accumulated from approximately 80 percent of the three-year placebo-controlled study exposure. Over the period up to the interim analysis, the proportion of patients developing CDMS was reduced from 43 percent in the placebo group to only 25 percent in the COPAXONE® group (p< 0.0001).

COPAXONE® was also very well tolerated in the PreCISe study, with only 13 percent overall dropouts during the up to three-year study period, similar to that observed in RRMS patients treated with COPAXONE®. All patients in the study participate in a follow-up study with COPAXONE® to prospectively assess the impact of early versus delayed treatment with COPAXONE® on the long-term course of the disease for a total observation time of up to five years.

About COPAXONE®
Current data suggest COPAXONE® is a selective MHC (Major Histocompatability Complex) class II modulator. COPAXONE® is indicated for the reduction of the frequency of relapses in RRMS. COPAXONE® is very well tolerated and the most common side effects of COPAXONE® are redness, pain, swelling, itching, or a lump or an indentation at the site of injection, weakness, infection, pain, nausea, joint pain, anxiety, and muscle stiffness.

COPAXONE® is now approved in 47 countries worldwide, including the United States, all European countries, Canada, Mexico, Australia, and Israel. In Europe, COPAXONE® is marketed by Teva Pharmaceutical Industries Ltd. and sanofi-aventis. In North America, COPAXONE® is marketed by Teva Neuroscience, Inc.

See additional important information at http://www.copaxone.com/pi/index.html or call 1-800-887-8100 for electronic releases. For hardcopy releases, please see enclosed full prescribing information.


About Teva
Teva Pharmaceutical Industries Ltd., (NASDAQ: TEVA) headquartered in Israel, is among the top 20 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. Teva's innovative R&D focuses on developing novel drugs for diseases of the central nervous system.




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 Teva�s 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: Teva`s ability to successfully develop and commercialize additional pharmaceutical products, the introduction of competing generic equivalents, the extent to which Teva may obtain U.S. market exclusivity for certain of its new generic products and regulatory changes that may prevent Teva from utilizing exclusivity periods, competition from brand-name companies that are under increased pressure to counter generic products, or competitors that seek to delay the introduction of generic products, the impact of consolidation of our distributors and customers, potential liability for sales of generic products prior to a final resolution of outstanding patent litigation, including that relating to the generic versions of Allegra®, Neurontin®, Lotrel®, and Famvir®, the effects of competition on our innovative products, especially Copaxone® sales, the impact of pharmaceutical industry regulation and pending legislation that could affect the pharmaceutical industry, the difficulty of predicting U.S. Food and Drug Administration, European Medicines Agency and other regulatory authority approvals, the regulatory environment and changes in the health policies and structures of various countries, our ability to achieve expected results though our innovative R&D efforts, Teva�s ability to successfully identify, consummate and integrate acquisitions, potential exposure to product liability claims to the extent not covered by insurance, dependence on the effectiveness of our patents and other protections for innovative products, significant operations worldwide that may be adversely affected by terrorism, political or economical instability or major hostilities, supply interruptions or delays that could result from the complex manufacturing of our products and our global supply chain, environmental risks, fluctuations in currency, exchange and interest rates, and other factors that are discussed in Teva�s Annual Report on Form 20-F and its other filings with the U.S. Securities and Exchange Commission. Forward-looking statements speak only as of the date on which they are made and the Company undertakes no obligation to update or revise any forward-looking statement, whether as a result of new information, future events or otherwise.
Company Contacts:
Dan Suesskind, Chief Financial Officer
Teva Pharmaceutical Industries Ltd.
972-2-941-1717

George Barrett,
Corp. E. V.P. - Global pharmaceutical Markets
Chief Executive Officer
Teva Pharmaceutical Industries Ltd.
Teva North America
(215) 591-3030

Liraz Kalif /
Kevin Mannix, Investor Relations
Teva Pharmaceutical Industries Ltd.
Teva North America
972-3-926-7281
(215) 591-8912