TPTX » Topics » The Posiphen Development Program

This excerpt taken from the TPTX 10-Q filed Aug 8, 2006.

The Posiphen™ Development Program

                Posiphen™ is the positive isomer of Phenserine. It appears to decrease the formation of beta-amyloid (Aß) with potential application in the treatment of AD progression. The build-up of beta-amyloid (Aß) is generally believed to be causative of the dementia of Alzheimer’s disease and its progression. Posiphen’s mechanism of action is potentially through RNA translational inhibition and possibly beta secretase inhibition. Posiphen™ has been shown to lower beta amyloid precursor protein (beta-APP) and beta-amyloid levels in pre-clinical studies. The primary mechanism of action results in a dose dependent reduction of beta-amyloid, which may result in slowing AD progression. The initial pre-clinical side effect rates potentially allow for higher clinical doses. On August 1, 2005 we announced that the US Food and Drug Administration (FDA) approved our investigational new drug (IND) application allowing Phase I clinical testing of Posiphen™. The first Phase I single ascending dose clinical study commenced in August 2005 and evaluated the safety of Posiphen™ in healthy volunteers.


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                In January 2006, we completed a single ascending dose Phase I trial with Posiphen™. This double-blind, placebo controlled study of Posiphen™ in healthy men and women sought to establish well tolerated doses. Posiphen™ appears to be well tolerated at single doses up to and including 80mg. Blood levels of Posiphen™ associated with this study were higher than those associated with beneficial effects on beta-amyloid metabolism in animal models. The build-up of beta-amyloid (Aß) is generally believed to be causative of the dementia of AD. No serious adverse events were reported at any dose level. We initiated a Phase I multiple ascending dose study in the first quarter of 2006.

                On April 24, 2006, we announced the results of an independent research study showing that Posiphen increased the ability of transplanted human neuronal stem cells (HNSC) to differentiate into neurons in APP transgenic mice, a model of Alzheimer’s disease (AD) in humans.

                On May 15, 2006 we announced the completion of a multiple dose Phase I study with Posiphen™ in clinical development for the treatment of Alzheimer’s disease progression.

                This double-blind, placebo-controlled multiple ascending dose safety and pharmacokinetic study of Posiphen in healthy volunteers sought to establish well tolerated doses. The initial review of the clinical adverse event data appears to be generally consistent with the results of the earlier single ascending dose Phase I study that suggested that the mean Posiphen blood levels associated with well tolerated doses in humans are higher than those associated with potentially beneficial effects on beta-amyloid metabolism in animal models. No serious adverse events were reported at any dose level in this second Phase I study.

                This multiple ascending-dose study examined the effects of Posiphen 20, 40 and 60mg given four times daily, for a period of 7, 7 and 10 days respectively. On the first and last day of each dosing period one single dose of Posiphen was given. Each dose period was completed and evaluated for safety and tolerance before the next higher dose level was initiated. Each cohort was composed of a different set of 16 subjects, comprised of 12 who received Posiphen and 4 who received placebo, with equal numbers of males and females in each.

                The necessary detailed safety, pharmacokinetic and pharmacodynamic analyses are ongoing. Based on this favorable clinical outcome, we are evaluating plans regarding the further clinical development steps for Posiphen.

This excerpt taken from the TPTX 10-Q filed May 10, 2006.
The Posiphen™ Development Program  

Posiphen™ is the positive isomer of Phenserine. It appears to decrease the formation of beta-amyloid with potential application in the treatment of AD progression. Posiphen’s mechanism of action is potentially through RNA translational inhibition as well as beta secretase inhibition. Posiphen™ has been shown to lower beta amyloid precursor protein (beta-APP) and beta-amyloid levels in pre-clinical studies. The primary mechanism of action results in a dose dependent reduction of beta-amyloid, which may result in slowing AD progression. The initial pre-clinical side effect rates potentially allow for higher clinical doses. On August 1, 2005 we announced that the US Food and Drug Administration (FDA) approved our investigational new drug (IND) application allowing Phase I clinical testing of Posiphen™. The first Phase I single ascending dose clinical study commenced in August 2005 and evaluated the safety of Posiphen™ in healthy volunteers.

In January 2006, we completed a single ascending dose Phase I trial with Posiphen™. This double-blind, placebo controlled study of Posiphen™ in healthy men and women sought to establish well tolerated doses. Posiphen™ appears to be well tolerated at single doses up to and including 80mg. Blood levels of Posiphen™ associated with this study were higher than those associated with beneficial effects on beta-amyloid metabolism in animal models. The build-up of beta-amyloid (Aß) is generally believed to be causative of the dementia of AD. No serious adverse events were reported at any dose level. We initiated a Phase I multiple ascending dose study in the first quarter of 2006.

 

On April 24, 2006, we announced the results of an independent research study showing that Posiphen increased the ability of transplanted human neuronal stem cells (HNSC) to differentiate into neurons in APP transgenic mice, a model of Alzheimer’s disease (AD) in humans.

This excerpt taken from the TPTX 10-K filed Mar 16, 2006.

The Posiphen™ Development Program

          Posiphen™ is the positive isomer of Phenserine. It appears to decrease the formation of beta-amyloid with potential application in the treatment of AD progression. Posiphen’s mechanism of action is potentially through RNA translational inhibition as well as beta secretase inhibition. Posiphen™ has been shown to lower beta amyloid precursor protein (beta-APP) and beta-amyloid levels in pre-clinical studies. The primary mechanism of action

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results in a dose dependent reduction of beta-amyloid, which may result in slowing AD progression. The initial pre-clinical side effect rates potentially allow for higher clinical doses. On August 1, 2005 we announced that the US Food and Drug Administration (FDA) approved our investigational new drug (IND) application allowing Phase I clinical testing of Posiphen™. The first Phase I single ascending dose clinical study commenced in August 2005 and evaluated the safety of Posiphen™ in healthy volunteers.

          In January 2006, we completed a single ascending dose Phase I trial with Posiphen™. This double-blind, placebo controlled study of Posiphen™ in healthy men and women sought to establish well tolerated doses. Posiphen™ appears to be well tolerated at single doses up to and including 80mg. Blood levels of Posiphen™ associated with this study were higher than those associated with beneficial effects on beta-amyloid metabolism in animal models. The build-up of beta-amyloid (Ab) is generally believed to be causative of the dementia of AD. No serious adverse events were reported at any dose level. We anticipate initiating a Phase I multiple ascending dose study in the first quarter of 2006.

This excerpt taken from the TPTX 10-Q filed Nov 9, 2005.
The Posiphen Development Program

Posiphen has been shown to lower beta amyloid precursor protein (beta-APP) levels in pre-clinical studies. The primary mechanism of action results in a dose dependent reduction of beta amyloid, which may result in slowing AD progression. The initial pre-clinical side effect rates potentially allow for higher clinical doses. On August 1, 2005 the Company announced that the US Food and Drug Administration (FDA) has approved its investigational new drug (IND) application allowing Phase I clinical testing of Posiphen. The first Phase I clinical study commenced in August 2005 and will primarily evaluate the safety of Posiphen in healthy volunteers. This study is ongoing.

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