Myriad Genetics Reports Results of U.S. Phase 3 Trial of Flurizan™ in Alzheimer's Disease
19 july 2008-- Myriad Genetics, Inc. today announced results of the Act-Earli-AD trial, an 18-month Phase 3 study of Flurizan (tarenflurbil) in patients with mild Alzheimer's disease. The study did not achieve statistical significance on either of its primary endpoints -- cognition and activities of daily living.
"We are disappointed that Flurizan failed to achieve significance in this study, and we will now discontinue development of this compound," said Peter Meldrum, President and Chief Executive Officer of Myriad Genetics, Inc. "The discontinuation of Flurizan will reduce our pharmaceutical development spend substantially and should enable Myriad to achieve profitability next year, ending June 30, 2009."
During fiscal 2008, Myriad spent approximately $60 million on development of Flurizan. The remaining expenses to wrap up its Flurizan program are projected to be approximately $8 million in total, spread primarily over the next two fiscal quarters.
About Myriad
Myriad Genetics, Inc. is a leading healthcare company focused on the development and marketing of novel therapeutic and molecular diagnostic products. Myriad's news and other information are available on the Company's Web site at www.myriad.com.
This press release contains "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995. These forward looking statements include the statement regarding the Company's discontinued development of Flurizan, the statement regarding the Company's anticipated profitability for the fiscal year ending June 30, 2009, and the statement regarding projected expenses to wrap up the Flurizan program. These forward-looking statements are subject to risks and uncertainties that could cause actual results to differ materially from management's expectations. Such risks and uncertainties, include, but are not limited to, the risk that we may not identify and accurately estimate costs associated with wrapping up the Flurizan program; risks and uncertainties associated with our ability to maintain or increase revenue growth for our molecular diagnostic products; the risk that development and introduction of competing products and services may adversely affect our business; uncertainty as to our ability to protect our proprietary technologies; the risk of patent-infringement claims; risks of new, changing and competitive technologies and regulations in the United States and internationally; and other factors discussed under the heading "Risk Factors" contained in Item 1A in our Annual Report on Form 10-K for the year ended June 30, 2007, which has been filed with the Securities and Exchange Commission, as well as any updates to those risk factors filed from time to time in our Quarterly Reports on Form 10-Q or Current Reports on Form 8-K. All information in this press release is as of the date of the release, and Myriad undertakes no duty to update this information unless required by law.
Showing posts with label Flurizan. Show all posts
Showing posts with label Flurizan. Show all posts
Saturday, July 19, 2008
Sunday, July 06, 2008
Myriad Genetics Reports Results of U.S. Phase 3 Trial of Flurizan™ in Alzheimer's Disease
5 july 2008-- Myriad Genetics, Inc. (NASDAQ: MYGN) today announced results of the Act-Earli-AD trial, an 18-month Phase 3 study of Flurizan (tarenflurbil) in patients with mild Alzheimer's disease. The study did not achieve statistical significance on either of its primary endpoints -- cognition and activities of daily living.
"We are disappointed that Flurizan failed to achieve significance in this study, and we will now discontinue development of this compound," said Peter Meldrum, President and Chief Executive Officer of Myriad Genetics, Inc. "The discontinuation of Flurizan will reduce our pharmaceutical development spend substantially and should enable Myriad to achieve profitability next year, ending June 30, 2009."
During fiscal 2008, Myriad spent approximately $60 million on development of Flurizan. The remaining expenses to wrap up its Flurizan program are projected to be approximately $8 million in total, spread primarily over the next two fiscal quarters.
About Myriad
Myriad Genetics, Inc. is a leading healthcare company focused on the development and marketing of novel therapeutic and molecular diagnostic products. Myriad's news and other information are available on the Company's Web site at www.myriad.com.
This press release contains "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995. These forward looking statements include the statement regarding the Company's discontinued development of Flurizan, the statement regarding the Company's anticipated profitability for the fiscal year ending June 30, 2009, and the statement regarding projected expenses to wrap up the Flurizan program. These forward-looking statements are subject to risks and uncertainties that could cause actual results to differ materially from management's expectations. Such risks and uncertainties, include, but are not limited to, the risk that we may not identify and accurately estimate costs associated with wrapping up the Flurizan program; risks and uncertainties associated with our ability to maintain or increase revenue growth for our molecular diagnostic products; the risk that development and introduction of competing products and services may adversely affect our business; uncertainty as to our ability to protect our proprietary technologies; the risk of patent-infringement claims; risks of new, changing and competitive technologies and regulations in the United States and internationally; and other factors discussed under the heading "Risk Factors" contained in Item 1A in our Annual Report on Form 10-K for the year ended June 30, 2007, which has been filed with the Securities and Exchange Commission, as well as any updates to those risk factors filed from time to time in our Quarterly Reports on Form 10-Q or Current Reports on Form 8-K. All information in this press release is as of the date of the release, and Myriad undertakes no duty to update this information unless required by law.
5 july 2008-- Myriad Genetics, Inc. (NASDAQ: MYGN) today announced results of the Act-Earli-AD trial, an 18-month Phase 3 study of Flurizan (tarenflurbil) in patients with mild Alzheimer's disease. The study did not achieve statistical significance on either of its primary endpoints -- cognition and activities of daily living.
"We are disappointed that Flurizan failed to achieve significance in this study, and we will now discontinue development of this compound," said Peter Meldrum, President and Chief Executive Officer of Myriad Genetics, Inc. "The discontinuation of Flurizan will reduce our pharmaceutical development spend substantially and should enable Myriad to achieve profitability next year, ending June 30, 2009."
During fiscal 2008, Myriad spent approximately $60 million on development of Flurizan. The remaining expenses to wrap up its Flurizan program are projected to be approximately $8 million in total, spread primarily over the next two fiscal quarters.
About Myriad
Myriad Genetics, Inc. is a leading healthcare company focused on the development and marketing of novel therapeutic and molecular diagnostic products. Myriad's news and other information are available on the Company's Web site at www.myriad.com.
This press release contains "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995. These forward looking statements include the statement regarding the Company's discontinued development of Flurizan, the statement regarding the Company's anticipated profitability for the fiscal year ending June 30, 2009, and the statement regarding projected expenses to wrap up the Flurizan program. These forward-looking statements are subject to risks and uncertainties that could cause actual results to differ materially from management's expectations. Such risks and uncertainties, include, but are not limited to, the risk that we may not identify and accurately estimate costs associated with wrapping up the Flurizan program; risks and uncertainties associated with our ability to maintain or increase revenue growth for our molecular diagnostic products; the risk that development and introduction of competing products and services may adversely affect our business; uncertainty as to our ability to protect our proprietary technologies; the risk of patent-infringement claims; risks of new, changing and competitive technologies and regulations in the United States and internationally; and other factors discussed under the heading "Risk Factors" contained in Item 1A in our Annual Report on Form 10-K for the year ended June 30, 2007, which has been filed with the Securities and Exchange Commission, as well as any updates to those risk factors filed from time to time in our Quarterly Reports on Form 10-Q or Current Reports on Form 8-K. All information in this press release is as of the date of the release, and Myriad undertakes no duty to update this information unless required by law.
Wednesday, April 30, 2008
Investigational Drug Slows Functional Decline in Early Alzheimer's
By John Gever
OXFORD, England, 30 april 2008-- The investigational anti-amyloid drug tarenflurbil (Flurizan) significantly slowed declines in the overall ability to function among mild Alzheimer's disease patients, researchers here said.
"This phase II study provides preliminary evidence of a possible therapeutic effect of tarenflurbil, the first selective [amyloid] lowering agent to complete a phase II evaluation," wrote Gordon K. Wilcock, D.M., of the University of Oxford, and colleagues online in Lancet Neurology.
Highlights of the data were presented two weeks ago at the American Academy of Neurology meeting in Chicago (See: AAN: Investigational Amyloid Inhibitor Slows Early Alzheimer's Progression).
Tarenflurbil inhibits the gamma-secretase enzyme that cleaves beta-amyloid protein from a larger precursor molecule. In particular, it blocks production of the Ab42 species of beta-amyloid that forms fibrillary plaques in the brains of Alzheimer's patients.
Expectations are that the drug will prevent additional deposits of amyloid plaques in the brain, but it is unlikely to eliminate existing plaques.
The agent is a chemical sibling (specifically, the R-enantiomer) of the nonsteroidal anti-inflammatory drug flurbiprofen (Ansaid).
Dr. Wilcock and colleagues tested two doses of tarenflurbil (800 and 400 mg twice daily) against placebo in 210 patients with mild to moderate Alzheimer's disease, as defined by scores of 15 to 26 on the Mini-Mental State Exam.
The placebo-controlled study, conducted in Britain and Canada, lasted one year. Canadian patients could then participate in a one-year extension trial in which those previously assigned to tarenflurbil continued at the same doses, and those taking placebo were re-randomized to one of the two doses of active drug. The double-blind was maintained.
Primary outcomes were rates of decline in three standardized measures used to assess Alzheimer's disease:
Alzheimer's Disease Assessment Scale, cognitive subscale
Alzheimer's Disease Cooperative Study Group Activities of Daily Living
Clinical Dementia Rating-Sum of Boxes (assesses global function)
Dr. Wilcock and colleagues found that neither dose of tarenflurbil had a significant effect in patients with moderate Alzheimer's disease, defined by scores of 15 to 19 on the Mini-Mental State Exam.
However, during the first year of treatment, global function and daily activities scores showed lower decline in patients receiving 800 mg of tarenflurbil twice daily versus those taking placebo.
When Activities of Daily Living scores were graphed, Dr. Wilcock and colleagues found a difference in slope of 3.98 (95% CI 0.33 to 7.72) points per year between high-dose tarenflurbil and placebo. This difference translated into a reduction of 46.4% from the decline rate with placebo (Cohen's d 0.45, P=0.033).
Similarly, the difference in slope for global function scores was -0.80 points per year (95% CI -1.57 to -0.03), translating into an effect size of 35.7% (d 0.42, P=0.042).
Cognitive subscale also suggested a benefit with high-dose tarenflurbil, with an effect size of 33.7%, but it was not significant (d 0.20, P=0.327).
But cognitive decline was significantly slowed according to results in the extension trial, comparing 22 patients receiving 24 months of high-dose tarenflurbil with 11 patients initially on placebo and then switched to high-dose tarenflurbil in the extension.
Mean change in cognition scores was 2.9 points (SD 1.7) among patients continuously taking high-dose tarenflurbil for two years, versus 11.5 points (SD 2.4) among those initially in the placebo group (P=0.005).
Patients also showed significantly better scores on the other two primary outcome measures at the end of the extension.
The lower dose showed no significant benefit on any outcome measure.
Few significant differences in adverse effects were seen among groups receiving either of the tarenflurbil doses or placebo. At the higher drug dose, significantly more patients had eosinophilia compared with the placebo group.
On the other hand, patients in the placebo group had higher rates of urinary incontinence.
About 85% to 90% of patients in all groups had some type of adverse event. Among patients in the high-dose tarenflurbil group, the most common were diarrhea and nausea, each seen in 10% of patients. These were not significantly less common in the placebo group (seen in 8% and 6% of patients, respectively).
In an accompanying commentary, Paul S. Aisen, M.D., of the University of California San Diego, noted that the drug failed to meet the original primary endpoint in the study, significant slowing in cognitive and functional decline in patients with moderate as well as mild Alzheimer's disease.
He chalked up the failure to the difficulties of proving benefit in a phase II trial with this type of drug.
"Disease-modifying interventions are expected to slow the progressive decline of cognitive and clinical measures without any short-term effect," he pointed out. "Proof of efficacy, or even proof of mechanism, might be impossible in a phase II study."
Indeed, the phase II results with tarenflurbil are "hardly conclusive," Dr. Aisen wrote.
Nevertheless, he said it was good that the drug's sponsor, Myriad Pharmaceuticals, has gone ahead with phase III testing.
Two phase III trials are now underway. Data from a U.S.-based trial of 1,684 patients are now being analyzed and are expected to be reported later this year. An international study involving 840 patients is scheduled to end in October.
Wrote Dr. Aisen, "With the need so enormous, and the potential benefit suggested (although not proven) by these phase II results, the effort is indeed justified despite the substantial uncertainty. In a few months, we will learn whether tarenflurbil will be the first anti-amyloid intervention to be efficacious in a pivotal trial."
The phase II study was funded by Myriad Pharmaceuticals.
Study co-authors reported relationships with Myriad.
Dr. Aisen reported that he was a site investigator on a phase III trial of tarenflurbil but has not had a consultant relationship with Myriad.
Primary source: Lancet NeurologySource reference:Wilcock G, et al "Efficacy and safety of tarenflurbil in mild to moderate Alzheimer's disease: A randomised phase II trial" Lancet Neurology 2008; DOI: 10.1016/S1474-4422(08)70090-5 Additional source: Lancet NeurologySource reference: Aisen P, "Tarenflurbil: A shot on goal," Lancet Neurology 2008; DOI: 10.1016/S1474-4422(08)70091-7
By John Gever
OXFORD, England, 30 april 2008-- The investigational anti-amyloid drug tarenflurbil (Flurizan) significantly slowed declines in the overall ability to function among mild Alzheimer's disease patients, researchers here said.
"This phase II study provides preliminary evidence of a possible therapeutic effect of tarenflurbil, the first selective [amyloid] lowering agent to complete a phase II evaluation," wrote Gordon K. Wilcock, D.M., of the University of Oxford, and colleagues online in Lancet Neurology.
Highlights of the data were presented two weeks ago at the American Academy of Neurology meeting in Chicago (See: AAN: Investigational Amyloid Inhibitor Slows Early Alzheimer's Progression).
Tarenflurbil inhibits the gamma-secretase enzyme that cleaves beta-amyloid protein from a larger precursor molecule. In particular, it blocks production of the Ab42 species of beta-amyloid that forms fibrillary plaques in the brains of Alzheimer's patients.
Expectations are that the drug will prevent additional deposits of amyloid plaques in the brain, but it is unlikely to eliminate existing plaques.
The agent is a chemical sibling (specifically, the R-enantiomer) of the nonsteroidal anti-inflammatory drug flurbiprofen (Ansaid).
Dr. Wilcock and colleagues tested two doses of tarenflurbil (800 and 400 mg twice daily) against placebo in 210 patients with mild to moderate Alzheimer's disease, as defined by scores of 15 to 26 on the Mini-Mental State Exam.
The placebo-controlled study, conducted in Britain and Canada, lasted one year. Canadian patients could then participate in a one-year extension trial in which those previously assigned to tarenflurbil continued at the same doses, and those taking placebo were re-randomized to one of the two doses of active drug. The double-blind was maintained.
Primary outcomes were rates of decline in three standardized measures used to assess Alzheimer's disease:
Alzheimer's Disease Assessment Scale, cognitive subscale
Alzheimer's Disease Cooperative Study Group Activities of Daily Living
Clinical Dementia Rating-Sum of Boxes (assesses global function)
Dr. Wilcock and colleagues found that neither dose of tarenflurbil had a significant effect in patients with moderate Alzheimer's disease, defined by scores of 15 to 19 on the Mini-Mental State Exam.
However, during the first year of treatment, global function and daily activities scores showed lower decline in patients receiving 800 mg of tarenflurbil twice daily versus those taking placebo.
When Activities of Daily Living scores were graphed, Dr. Wilcock and colleagues found a difference in slope of 3.98 (95% CI 0.33 to 7.72) points per year between high-dose tarenflurbil and placebo. This difference translated into a reduction of 46.4% from the decline rate with placebo (Cohen's d 0.45, P=0.033).
Similarly, the difference in slope for global function scores was -0.80 points per year (95% CI -1.57 to -0.03), translating into an effect size of 35.7% (d 0.42, P=0.042).
Cognitive subscale also suggested a benefit with high-dose tarenflurbil, with an effect size of 33.7%, but it was not significant (d 0.20, P=0.327).
But cognitive decline was significantly slowed according to results in the extension trial, comparing 22 patients receiving 24 months of high-dose tarenflurbil with 11 patients initially on placebo and then switched to high-dose tarenflurbil in the extension.
Mean change in cognition scores was 2.9 points (SD 1.7) among patients continuously taking high-dose tarenflurbil for two years, versus 11.5 points (SD 2.4) among those initially in the placebo group (P=0.005).
Patients also showed significantly better scores on the other two primary outcome measures at the end of the extension.
The lower dose showed no significant benefit on any outcome measure.
Few significant differences in adverse effects were seen among groups receiving either of the tarenflurbil doses or placebo. At the higher drug dose, significantly more patients had eosinophilia compared with the placebo group.
On the other hand, patients in the placebo group had higher rates of urinary incontinence.
About 85% to 90% of patients in all groups had some type of adverse event. Among patients in the high-dose tarenflurbil group, the most common were diarrhea and nausea, each seen in 10% of patients. These were not significantly less common in the placebo group (seen in 8% and 6% of patients, respectively).
In an accompanying commentary, Paul S. Aisen, M.D., of the University of California San Diego, noted that the drug failed to meet the original primary endpoint in the study, significant slowing in cognitive and functional decline in patients with moderate as well as mild Alzheimer's disease.
He chalked up the failure to the difficulties of proving benefit in a phase II trial with this type of drug.
"Disease-modifying interventions are expected to slow the progressive decline of cognitive and clinical measures without any short-term effect," he pointed out. "Proof of efficacy, or even proof of mechanism, might be impossible in a phase II study."
Indeed, the phase II results with tarenflurbil are "hardly conclusive," Dr. Aisen wrote.
Nevertheless, he said it was good that the drug's sponsor, Myriad Pharmaceuticals, has gone ahead with phase III testing.
Two phase III trials are now underway. Data from a U.S.-based trial of 1,684 patients are now being analyzed and are expected to be reported later this year. An international study involving 840 patients is scheduled to end in October.
Wrote Dr. Aisen, "With the need so enormous, and the potential benefit suggested (although not proven) by these phase II results, the effort is indeed justified despite the substantial uncertainty. In a few months, we will learn whether tarenflurbil will be the first anti-amyloid intervention to be efficacious in a pivotal trial."
The phase II study was funded by Myriad Pharmaceuticals.
Study co-authors reported relationships with Myriad.
Dr. Aisen reported that he was a site investigator on a phase III trial of tarenflurbil but has not had a consultant relationship with Myriad.
Primary source: Lancet NeurologySource reference:Wilcock G, et al "Efficacy and safety of tarenflurbil in mild to moderate Alzheimer's disease: A randomised phase II trial" Lancet Neurology 2008; DOI: 10.1016/S1474-4422(08)70090-5 Additional source: Lancet NeurologySource reference: Aisen P, "Tarenflurbil: A shot on goal," Lancet Neurology 2008; DOI: 10.1016/S1474-4422(08)70091-7
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