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Milestones 2008 2009
10K Update Targacept
Our lead product candidate is a novel small molecule that we have historically referred to as TC-1734 and that our strategic collaborator, AstraZeneca, refers to as AZD3480. AZD3480 (TC-1734) modulates the activity of the †4ß2 NNR. In December 2005, we entered into a collaborative research and license agreement with AstraZeneca AB for the development and worldwide commercialization of AZD3480 (TC-1734) as a treatment for Alzheimer's disease, cognitive dysfunction in schizophrenia and potentially other conditions characterized by cognitive impairment such as ADHD, AAMI and MCI. AstraZeneca is currently conducting two Phase 2b clinical trials of AZD3480 (TC-1734), one in mild to moderate Alzheimer's disease, which is referred to as the "Sirocco" trial, and one in cognitive dysfunction in schizophrenia, which is referred to as the "HALO" trial. Based on information provided to us by AstraZeneca, we expect that both trials will be completed by the end of 2008.
We and AstraZeneca are also conducting a preclinical research collaboration under the agreement that is designed to discover and develop additional compounds that, like AZD3480 (TC-1734), act on the †4ß2 NNR as treatments for conditions characterized by cognitive impairment. AstraZeneca pays us research fees, based on a reimbursement rate specified under the agreement, for research services rendered in the preclinical research collaboration, subject to specified limits. The research term began in January 2006 and has a planned term of four years.
In July 2007, we entered into a product development and commercialization agreement with GlaxoSmithKline. The agreement sets forth the terms of an alliance designed to discover, develop and market product candidates that selectively target specified NNR subtypes in five therapeutic focus areas: pain, smoking cessation, addiction, obesity and Parkinson's disease.
Our other clinical-stage product candidates, in addition to AZD3480 (TC-1734), are described below.
• TC-5619. TC-5619 is a novel small molecule that we plan to develop for cognitive dysfunction in schizophrenia and potentially one or more other conditions characterized by cognitive impairment. TC-5619 modulates the activity of the †7 NNR. We are currently conducting a Phase 1 single rising dose clinical trial of TC-5619 and plan to initiate a Phase 1 multiple rising dose clinical trial of TC-5619 in the second quarter of 2008. Following our completion of Phase 1 clinical development and a Phase 2 clinical proof of concept trial of TC-5619, AstraZeneca has the right to license TC-5619 for any or all of schizophrenia and various conditions characterized by cognitive impairment on terms specified in our agreement.
• TC-5214. TC-5214 is one of the two enantiomers of mecamylamine hydrochloride. Enantiomers are mirror images of each other that have the same chemical but potentially different biological properties and together form a chemical mixture known as a racemate. TC-5214 inhibits the activity of various NNR subtypes, including the †4ß2 NNR. We are currently developing TC-5214 as an augmentation treatment for major depression. We initiated a Phase 1 single rising dose clinical trial of TC-5214 in healthy volunteers in the first quarter of 2008.
In 2006, we completed a Phase 2 clinical trial of the racemate mecamylamine hydrochloride as an augmentation treatment to citalopram hydrobromide, a commonly prescribed treatment for depression marketed as Celexa in the United States, in patients who did not respond adequately to first-line treatment with citalopram. We refer to this treatment combination as TRIDMAC. In our preclinical evaluation, TC-5214 has exhibited a more favorable overall safety and efficacy profile than mecamylamine. We have no current plans to conduct further clinical development of mecamylamine and intend instead to pursue the development of TC-5214.
• TC-2216. Our depression and anxiety program also includes the novel small molecule TC-2216. TC-2216 inhibits the activity of the † 4ß2 NNR. We completed a Phase 1 single rising dose clinical trial of this product candidate in the first quarter of 2008. We may in the future elect to develop one of the enantiomers of TC-2216 in lieu of further development of TC-2216. However, based on our anticipated development of TC-5214 and our current budget management plans, we do not expect that we will conduct further clinical development of TC-2216 or either of its enantiomers in 2008.
• TC-6499. TC-6499 is novel small molecule that we plan to develop as a treatment for neuropathic pain. TC-6499 modulates the activity of the †4ß2 NNR. We initiated a Phase 1 single rising dose clinical trial of TC-6499 in the fourth quarter of 2007. TC-6499 is subject to a contingent future option of GlaxoSmithKline under the terms of our alliance
Targacept strikes loan agreement with BB&TThe Business Journal of the Greater Triad Area
Targacept has established a new loan facility with BB&T to help it acquire new, more efficient drug-discovery lab equipment.
The Winston-Salem-based Targacept (NASDAQ: TRGT) will be able to borrow up to $5.3 million under the loan agreement from BB&T (NYSE: BBT), which is also headquartered in the Twin City.
Targacept is already "well capitalized," said Chief Financial Officer Alan Musso, with $87 million of cash in the bank according to its most recent quarterly earnings report. But Musso said the company is upgrading its lab equipment to speed the drug discovery process in conjunction with its two major pharmaceutical partners, AstraZeneca and GlaxoSmithKline.
To conserve cash Targacept had been drawing on a line of credit last year, "but the interest rate environment has become much more favorable since then, so we're seeing some real interest savings" under the new loan terms, Musso said.
Musso said the expansion Targacept underwent in its Piedmont Triad Research Park headquarters last year has sufficient space for the new equipment, so no further expansions are planned for now.
Every two weeks a change with ORG24448
Org 24448 to Treat Depression
This study is currently recruiting participants.
Source: http://www.clinicaltrials.gov/ct2/show/NCT00113022?term=24448&rank=1
Have a nice day
Erbse
Comment NeuroInvestment
EPIX Pharmaceuticals
From NI February 2008
Epix's Epic Embarrassment: "Michael G. Kauffman, M.D., Ph.D., chief executive officer of EPIX Pharmaceuticals stated, “We are very excited by the measurable impact on memory and cognition, achieved in such a short period of time, in a trial that was designed primarily to assess safety and tolerability."
--Press release from Epix Pharmaceuticals, 12/18/07
"When things seem to be too good to be true, they usually are (too good to be true): Epix's Alzheimer's trial for its 5HT-4 drug PRX-03140 showed an amazing 5.7 point ADAS-cog improvement in just two weeks...albeit in just one 10 patient dose cohort, with two 14 point responders, the mean change for the others was 3.3 points, and the other six cohorts did not show significant benefit. And there was no benefit if the patients also received Aricept--Epix states that these patients hadn't been washed out, and thus were already at the cholinergic ceiling (dubious trial design and execution). But other than that, these were revolutionary results. So revolutionary, in fact, that NI strongly doubts that they will be replicated. Because they are not only revolutionary, they make no sense."
--NeuroInvestment 1/06/08
"The updated results described below reflect the correction of previously undetected errors that were included in the trial results as provided to the company from a third party contract research organization (CRO) and as reported by the company in a recent press release, as well as newly available data on other measures of cognition.
As a result of errors made in the transcription of data and calculation of the Alzheimer’s Disease Assessment Scale cognitive subscale (ADAS-cog) score, an independent re-analysis of the data has been conducted. The corrected results show that patients receiving 150 mg of PRX-03140 orally once daily as monotherapy achieved a mean 3.6 point improvement on the ADAS-cog versus a 0.9 point worsening in patients on placebo, which continues to be statistically significant (p= 0.021).
--Press release from Epix Pharmaceuticals, 1/15/08
"Oh. That's very different. Never mind."
--Gilda Radner 1976
Perhaps in the future, if circumstances warrant, Epix will conduct the "independent re-analysis' of suspect data before broadcasting them.
Patent Life Ampakines for RD = 2027
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Erbse
Cortex Pipeline Overview (in German)
Nicotine improves cognitive deficits of dopamine transporter knockout mice without long-term tolerance.
Weiss S, Nosten-Bertrand M, McIntosh JM, Giros B, Martres MP.
Inserm, U513, Laboratoire de Neurobiologie et Psychiatrie, University Paris 12, Créteil, France.
Various studies suggest a dysfunction of nicotinic neurotransmission in schizophrenia and establish that patients suffering from schizophrenia and attention deficit hyperactivity disorder (ADHD) have a high tobacco consumption, potentially for the purpose of self-medication. Owing to its neuroprotective and procognitive effects, transdermal nicotine was proposed to be an effective treatment of some neurodegenerative and psychiatric diseases. Mice deficient in the dopamine transporter (DAT KO) exhibit a phenotype reminiscent of schizophrenia and ADHD, including hyperdopaminergia, hyperactivity, paradoxical calming by methylphenidate and cognitive deficits, some of which being improved by antipsychotic agents. We recently demonstrated that nicotinic receptor content and function were profoundly modified in DAT KO mice. In this study, we assessed the effects of a chronic nicotine treatment in the drinking water on the nicotine-induced locomotion, anxiety status and learning performance. Chronically nicotine-treated DAT KO mice were always hypersensitive to the hypolocomotor effect of nicotine without tolerance and did not exhibit the anxiogenic effect of nicotine treatment observed in WT mice. Very interestingly, both acute and chronic nicotine treatments greatly improved their deficits in the cued and spatial learning, without eliciting tolerance. We speculate that the procognitive effects of nicotine in DAT KO mice are related to the upregulation of alpha7 nicotinic receptors in the hippocampus, amygdala, and prelimbic cortex, all areas involved in cognition. Data from our studies on DAT KO mice shed light on the nicotine self-medication in psychiatric patients and suggest that nicotinic agonists could favorably lead to additional therapy of psychiatric diseases.
ORG-26576 Abstract from Neuroscience Meeting 2007
Electrophysiological effects of farampator (Org 24448) and Org 26576, two novel allosteric modulators of AMPA receptors, in rat hippocampal neurones
Pharmacological enhancement of glutamatergic neurotransmission through AMPA receptors may have potential for therapeutic utility in the treatment of psychiatric disorders. The current study was aimed at characterizing the in vitro and in vivo electrophysiological properties of farampator and Org 26576, novel positive allosteric modulators of AMPA receptor function, in rat hippocampus.
Whole-cell patch-clamp recordings were performed in rat cultured hippocampal neurons at room temperature. Glutamate (0.5 mM) was applied for 1s either alone or with the test compound. Effects of compounds on the synaptic transmission were studied in submerged rat hippocampal slices at room temperature. Field excitatory postsynaptic potentials (fEPSPs) were recorded from stratum radiatum of CA1 area in response to Schaffer-commissural stimulation. In vivo experiments were performed in the CA1 region of hippocampus in rats under anaesthesia. AMPA-evoked single neurone activity was induced by iontophoretically applied AMPA and fEPSPs were evoked by anterior commisure/fimbria stimulation.
Co-application of farampator (3-300μM) or Org 26576 (1-300μM) with glutamate decreased desensitisation leading to increases in steady-state current in a reversible and concentration dependent manner: maximum increases were 19±4% (n=9) and 11±2% (n=6), respectively and the EC50 values were 14 μM (5μM to 40μM) 13 μM (4μM to 36μM), respectively (values in brackets indicate 95% confidence intervals). In the absence of glutamate, the test compounds were without effect. Bath applications of farampator (300 μM, n=9) and Org 26576 (300 μM, n=7) increased the slope of fEPSPs by 36±9% and 29±6%, respectively (mean±S.E.M) (p<0.05, Student’s t test).
Farampator and Org 26576-induced potentiation of AMPA receptor activity was also confirmed in vivo: farampator and Org 26576 (1 mg/kg, i.v.) enhanced the AMPA-induced neuronal activity which lasted at least 30 minutes (by 22±5% and 68±5%, respectively n=6, p<0.01). Iontophoretic applications of NBQX depressed the AMPA-evoked neuronal activity by 83.2±4.2% (n=4) confirming that evoked excitation was mediated mainly by activation of AMPA receptors. Effects of Org 26576 on endogenously released glutamate-mediated AMPA receptor responses were also studied: in 3 rats Org 26576 (3 mg/kg, i.v.) enhanced the slope of fEPSP by 26±0.4% (p<0.05). These results indicate that farampator and Org 26576 are allosteric modulators of AMPA receptor function in hippocampal neurones. Thus they represent interesting tools for investigating the therapeutic potential of glutamatergic enhancement in psychiatric disorders
New study in ADHD and Depression with Ampakines
Trial to Determine the Maximum Tolerated Dose (MTD,) Based on Safety and Tolerability, of Org 26576 in Patients With Major Depressive Disorder.
This study is currently recruiting participants.
http://investorshub.advfn.com/boards/post_new.asp?board_id=3252
Dose Finding Study in Adults With Attention Deficit Hyperactivity Disorder (ADHD)
This study is currently recruiting participants.
http://www.clinicaltrials.gov/ct2/show/NCT00610441?term=26576&rank=2
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Erbse
Org 24448 to Treat Depression
This study is currently recruiting participants.
http://www.clinicaltrials.gov/ct2/show/NCT00113022?term=ampakine&rank=5
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Erbse
Cortex Pharmaceuticals presents at Roth Capital Partners to Hold 20th Annual OC Growth Stock Conference February 18-21, 2008
http://www.pr-inside.com:80/roth-capital-partners-to-hold-20th-r405085.htm
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Erbse
Org 24448 to Treat Depression
This study has been completed.
http://www.clinicaltrials.gov/ct2/show/NCT00113022?term=24448&rank=1
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Erbse
Targacept Announces Exercise of Underwriters’ Overallotment Option and Closing of $30.9 Million Public Offering
Winston-Salem, North Carolina
January 24, 2008
Targacept, Inc. (Nasdaq: TRGT), a clinical-stage biopharmaceutical company developing a new class of drugs known as NNR Therapeutics (TM), today announced that it has completed the previously announced underwritten public offering of shares of its common stock. The completed offering included 570,000 shares purchased by the underwriters upon exercise of their overallotment option. Targacept issued and sold a total of 4,370,000 shares in the offering, resulting in gross proceeds, before deducting underwriting discounts, commissions and offering expenses, of $30.9 million.
Deutsche Bank Securities Inc. was the sole book-running manager for the offering. Lazard Capital Markets LLC, Oppenheimer & Co. Inc. and Pacific Growth Equities, LLC were co-managers for the offering.
Targacept Announces the Pricing of a Public Offering of 3.8 Million Shares of its Common Stock
Thursday January 17, 8:55 am ET
WINSTON-SALEM, N.C.--(BUSINESS WIRE)--Targacept, Inc. (Nasdaq: TRGT) today announced the pricing of an underwritten public offering of 3.8 million shares of its common stock at a price to the public of $7.07 per share, which was the closing bid price of Targacept’s shares on the Nasdaq Global Market on January 16, 2008. Targacept has granted to the underwriters for the offering a 30-day option to purchase up to 570,000 additional shares of common stock to cover over-allotments, if any. All of the shares are being offered by Targacept. The closing of the offering is expected to take place on January 23, 2008, subject to satisfaction of customary closing conditions. Deutsche Bank Securities Inc. is the sole book-running manager for the offering. Lazard Capital Markets LLC, Oppenheimer & Co. Inc. and Pacific Growth Equities, LLC are co-managers for the offering.
The offering is being made pursuant to an effective shelf registration statement that Targacept previously filed with the Securities and Exchange Commission. This press release does not and shall not constitute an offer to sell or the solicitation of an offer to buy, nor shall there be any sale of these securities in any state or jurisdiction in which such offer, solicitation or sale would be unlawful prior to the registration or qualification under the securities laws of any such state or jurisdiction. Any offer will only be made by means of a prospectus, including a prospectus supplement, forming a part of the effective registration statement. Copies of the final prospectus, including the prospectus supplement when filed, can be obtained from Deutsche Bank Securities Prospectus Department, 100 Plaza One, Second Floor, Jersey City, NJ 07311, telephone: 800-503-4611
EPIX Pharmaceuticals Announces Updated Results from Phase 2a Clinical Trial of PRX-03140 in Alzheimer's Disease
Data Continue to Show Statistically Significant Improvements in Cognitive Function and Favorable Safety Profile
EPIX , a biopharmaceutical company focused on discovering and developing novel therapeutics through the use of its proprietary and highly efficient in silico drug discovery platform, today announced revised results from its Phase 2a clinical trial of PRX-03140, its novel 5-HT4 agonist, in Alzheimer's disease. The trial was designed to assess the effects of PRX-03140 following two weeks of treatment as monotherapy and separately in combination with donepezil (Aricept(R)) in patients with mild Alzheimer's disease and the company announced initial findings on December 18, 2007. The updated results described below reflect the correction of previously undetected errors that were included in the trial results as provided to the company from a third party contract research organization (CRO) and as reported by the company in a recent press release, as well as newly available data on other measures of cognition.
As a result of errors made in the transcription of data and calculation of the Alzheimer's Disease Assessment Scale cognitive subscale (ADAS-cog) score, an independent re-analysis of the data has been conducted. The corrected results show that patients receiving 150 mg of PRX-03140 orally once daily as monotherapy achieved a mean 3.6 point improvement on the ADAS-cog versus a 0.9 point worsening in patients on placebo, which continues to be statistically significant (p= 0.021). Data for the patients on a 50 mg dose of PRX-03140 showed a 1.0 point improvement on the ADAS-cog. The monotherapy dose response (150 mg versus 50 mg versus placebo) continues to be statistically significant with p=0.026. There were no substantive changes in the results from the combination arms of the study.
The previously reported safety results from the trial are unchanged. In the Phase 2a clinical trial, PRX-03140 appeared to be well tolerated, both alone and in combination with donepezil (Aricept(R)). No serious drug-related adverse events occurred during the trial.
The two-week study also utilized other cognitive tests including Mindstreams, an automated battery of computerized cognitive function tests. Patients on monotherapy demonstrated significant (pless than0.04) improvements in memory and visual-spatial indices as measured using Mindstreams when compared with placebo.
Based upon the compelling improvements in cognition demonstrated over such a short duration of time, EPIX has received requests from certain patients, caregivers and clinical trial investigators for continued access to PRX-03140. EPIX has been able to accommodate such requests on a case-by-case basis by extending the study to allow these patients to continue on PRX-03140. To date, one patient has completed 11 additional weeks of study treatment, and additional patients have initiated extended dosing.
"We are very excited by the measurable impact on memory and cognition achieved with PRX-03140 in a two-week study that was designed primarily to assess tolerability and safety. While we were disappointed that these errors were not detected during the CRO clinical monitoring or data verification processes, EPIX moved as quickly and efficiently as possible to reassess these data, reanalyze the findings and release the updated results of the trial to the public," stated Michael G. Kauffman, M.D., Ph.D., chief executive officer of EPIX. "With our partner, GlaxoSmithKline, we are continuing with our plans to initiate a Phase 2b clinical trial program in Alzheimer's patients in the first half of this year."
gfp927z, i am sorry. I have no slides from this presentation. The link from the Cortex homepage doesn`t work.
Have a nice day
Erbse
Comment from NeuroInvestor Homepage
(from NI January 2008)
Comment 1: Having recovered from Neurology's imposition of a clinical hold on CX717, a hold that was lifted, with dose limitations subsequently removed as well, Cortex was battered when the FDA's Psychiatry Division refused to allow their IND for ADHD. As has been discussed at length in NI, the refusal appears to be fear-driven; the fear that the post-mortem artifact cleared in the eyes of Neurology might eventually prove to be a genuine problem, a risk they were not willing to take with ADHD. The stock price was savaged, a process inflamed by Rodman & Renshaw's call for the quick sale of the company, and a bizarre price target of 30 cents (!). On the positive side, CX717 and other Ampakines were found by a U. Alberta group to provide unique and highly specific activation of normal respiration via AMPA receptors in the pre-Botzinger Complex. The specific application would be in the treatment of analgesic-induced respiratory depression, where CX717 appears (in four species so far) to restore respiration without attenuating analgesia. A Phase IIa trial will begin this month in Germany. Cortex also made progress with other compounds, bringing CX701 close to its IND, and developing 'high-impact' neurotrophic compounds that are not epileptogenic (unlike many of the high impacts developed elsewhere, like Lilly). This opens the door to partnering for neurodegenerative conditions.
Comment 2: In the past two years, Cortex has had two setbacks, the CX717 artifact and the IND rejection, which have twice completely blown up solid share appreciation. Had the first not occurred, the second never would have, and the share price would be near 10. Every company has bad luck and unexpected setbacks, but Cortex seems to have had more than its share. Will this be the year their luck changes? Or are they forever snakebitten? With high probability of success with the respiratory depression program, and some resolution of Schering-Plough's Ampakine intentions, we believe that it will be the former, Of course, we have said that every year since 1946, or so it sometimes seems. Our target is 5; set low because Cortex also has the burden of swimming upstream against the wishes of their former banker, and because some degree of battle fatigure has set in. If they reach that price level, we suspect that they might be amenable to a buyout, and with a high-impact Ampakine now approaching the clinic by year-end, we cannot believe that there is not a Big Pharma out there smart enough to know a bargain platform when they see one.
Hi gfp927z, here another article about Enbrel
Amgen, Wyeth Arthritis Treatment Eases Alzheimer's (Update3)
By Elizabeth Lopatto
Jan. 10 (Bloomberg) -- Alzheimer's symptoms improved in just 10 minutes in a single patient injected with Amgen Inc. and Wyeth's anti-inflammatory drug Enbrel, according to a case report by University of California scientists.
The patient, an 81-year-old physician, could remember facts such as the year and the state he lived in after one spinal shot of Enbrel, according to researchers from the University of California, Los Angeles. Before the shot, he couldn't recall such details. After the treatment he was also ``noticeably calmer, less frustrated and more attentive,'' the authors wrote.
In 2006, the same researchers reported that 15 Alzheimer's patents with mild to severe symptoms showed ``sustained cognitive improvement'' after six months of weekly Enbrel injections. Studies suggest an excess of the inflammation protein blocked by Enbrel, called TNF-alpha, is involved in the disorder's development, the authors reported in the Journal of Neuroinflammation.
``This absolutely has the potential to be a disease- modifying treatment,'' said Edward Tobinick, one of the study's authors and an associate professor at the UCLA School of Medicine. ``Since this report, our patient has received several other doses, and he's continued to show a therapeutic benefit.''
No other patients were involved in this latest research, so there was no control group. Also, the patient, his family and the doctor were aware of the treatment.
``The concept is interesting,'' said Michael Lampe, a spokesman for Madison, New Jersey-based Wyeth, in a telephone interview today. ``In general, we don't discuss early stage research.''
``There is insufficient scientific data to support pursuit of a TNF inhibitor as a means of treating Alzheimer's,'' said Sonia Fiorenza, a spokeswoman for Thousand Oaks, California- based Amgen, in an e-mailed statement.
Inflammation Interrupted
Enbrel and similar medications may interrupt the inflammation that produces a substance called beta amyloid, which causes Alzheimer's characteristic tangles in the brain. TNF-alpha, or tumor necrosis factor alpha, may also interfere with the way neurons communicate, so Enbrel may help brain cells transmit their messages, said Tobinick, who disclosed in the report he owns stock in Amgen and has patents for giving TNF treatments to patients with Alzheimer's.
Tobinick hasn't tested other TNF-alpha-blockers, though they too may aid in treatment, he said.
``My natural inclination would be to be highly skeptical,'' said Thomas Finucane, a professor of geriatric medicine at Johns Hopkins School of Medicine in Baltimore. He noted the limited sample size.
More Study Warranted
Amgen and Wyeth's Enbrel, approved in 1998, was the first rheumatoid arthritis drug from proteins instead of chemicals, a biotechnology class of TNF-inhibitors that includes Abbott Laboratories' Humira, Johnson & Johnson's Remicade and Bristol- Myers Squibb Co.'s Orencia.
Enbrel and similar medications ``are worthy of further investigation, and may lead to earlier therapeutic intervention which may have the potential to favorably affect the natural history of Alzheimer's disease,'' the researchers said in the report.
Amgen fell 9 cents, or less than 1 percent, to $47.56, at 4 p.m. New York time in Nasdaq Stock Market composite trading. Wyeth fell 22 cents, or less than a percent, to $47.14 in New York Stock Exchange composite trading.
To contact the reporter on this story: Elizabeth Lopatto in New York at elopatto@bloomberg.net .
Source: http://www.bloomberg.com/apps/news?pid=20601082&sid=aM.UlJAdl8mc&refer=canada
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Jogging your memory
http://bulletin.ninemsn.com.au:80/article.aspx?id=334191
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Erbse
Jogging your memory
http://bulletin.ninemsn.com.au:80/article.aspx?id=334191
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Erbse
EPIX Have Been Added To Naked Short List
http://www.tradingmarkets.com:80/.site/news/Stock%20News/948279/
Happy new year from Germany
Erbse
Inside the Brain: An Interactive Tour
What happens in the brain of a person with Alzheimer’s disease? This tour explains how the brain works and how Alzheimer's affects it.
Taking the tour: There are 16 interactive slides. Move forward or back one slide at a time by clicking on the arrows. You can also jump to any slide by clicking on its number at the top of each page.
Start Tour: http://www.alz.org/brain/overview.asp
Update Pipeline Targacept
EPIX Pharmaceuticals Makes a Significant Altzheimer's Discovery
posted on: December 23, 2007
EPIX Pharmaceuticals (EPIX) is a bio-pharmaceutical company that is focused on discovering and developing novel therapeutics through the use of its proprietary and highly efficient silico drug discovery platform. Last week, the company made a huge breakthrough relating to Alzheimer’s. As we all know some of the greatest inventions were stumbled upon accidentally. We all know about Ben Franklin, and what happened when chocolate met peanut butter - the rest is history.
It is just possible that what EPIX stumbled upon is extremely important to humanity.
The company initiated a phase 2A study of its Alzheimer’s disease drug, PRX-03140, to get safety and tolerability information. What happened? The company actually found that the drug had a profound impact on the Alzheimer’s Disease Assessment Scale cognitive subscale. While it usually takes drugs between 12 and 24 weeks to show an improvement, after only 2 weeks with PRX-03140, sufferers showed a marked improvement.
Even the CEO was surprised by the findings. Epix Chief Executive Officer Michael Kauffman said the company was surprised by the compound’s swift effectiveness.
“No drug has been shown to work this quickly, as far as we are aware,” said Kauffman, adding that other Alzheimer’s drugs generally must be taken for at least 12 weeks before any significant improvement can be observed.
With 5 million Americans Alzheimer’s the opportunity for EPIX is huge. It is also important to consider that with an aging population this could be absolutely huge for the little Biotech company with a market-cap of only $141 million.
After seeing the stock surge more than 50% on the news, it has fallen way back. With this potential revolutionary, blockbuster drug, this is a stock that should be trading much higher than the $4 range. For investors looking to take a swing at an up and coming drug company, EPIX is worth the look.
Source: http://seekingalpha.com/article/58205-epix-pharmaceuticals-makes-a-significant-altzheimer-s-discovery?source=yahoo
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Erbse
Lundbeck expands agreement with PAION for desmoteplase
http://www.foxbusiness.com/markets/industries/health-care/article/lundbeck-expands-agreement-paion-desmoteplase_416985_10.html
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Erbse
What Was That Clinical Trial For?
By Brian Orelli December 20, 2007
EPIX Pharmaceuticals (Nasdaq: EPIX) initiated a phase 2A study of its Alzheimer's disease drug, PRX-03140, to get safety and tolerability information. Instead, it got much more than it had bargained for.
In a two-week trial, the 150 mg dose of PRX-03140 achieved a mean 5.7 point improvement on the Alzheimer's Disease Assessment Scale cognitive subscale (ADAS-cog). That's pretty darn impressive -- Alzheimer's drugs usually demonstrate a three- to four-point improvement after a full 12 to 24 weeks in clinical studies.
With only 10 subjects receiving each dose level of the drug (150 mg, 50 mg, placebo), the 150 mg treatment arm showed a statistically significant improvement compared to subjects receiving the placebo. The latter had a 0.2 point worsening in their ADAS-cog score.
The data point I like even more is the 50 mg dose of PRX-03140, which showed a 1.1 point improvement on the ADAS-cog. While that's not as impressive as the 150 mg dose -- and the smaller dose won't likely be used in future studies -- it demonstrates that there's a dose response to the drug, which lends confidence to the argument that the effects of the 150 mg dose aren't a fluke.
In the study, PRX-03140 was also tested in combination with Eiasi's and Pfizer's (NYSE: PFE) Aricept, but the addition of PRX-03140 didn't statistically change the ADAS-cog score. Aricept is thought to act by preventing the loss of acetylcholine, a molecule that improves cognitive symptoms of Alzheimer's disease.
PRX-03140, on the other hand, is believed to increase the production of acetylcholine. The idea of putting the two together made perfect sense, and it was hoped that the combination would have a stronger effect than either one alone. Unfortunately, that didn't happen. One explanation is that the patients taking Aricept were already in better shape, and therefore it would take a longer study to show any improvement from adding PRX-03140.
As for the original safety goals? It passed.
EPIX plans to initiate a larger and longer phase 2B clinical trial of PRX-3140 in the first half of 2008. If that data is as strong as the phase 2A data, GlaxoSmithKline (NYSE: GSK) will almost certainly exercise its option to pick up the compound for further development. With compounds such as Novartis' (NYSE: NVS) Exelon and Johnson & Johnson's (NYSE: JNJ) Razadyne producing fair but certainly not stellar results, PRX-03140 could pick up a substantial chunk of the $4 billion market.
Even after the run-up in stock price Tuesday, Epix has a market cap of less than $150 million. That's a pretty fair value for a company with a few phase 2 candidates, including one that could storm onto the Alzheimer's-disease marketplace if it keeps up these strong results.
Slide PRX-03140 150mg
Hi snottymal, here the information from the Epix homepage. I have no other information.
Here are some information in german and english
http://www.erbse.vm-elsig.de/form/base/YaBB.pl?num=1190489775
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Erbse
Vasovist™ is an injectable intravascular contrast agent discovered internally at EPIX and is designed to provide improved imaging of the vascular system using magnetic resonance angiography (MRA). EPIX's initial target indication for Vasovist is for use in MRA imaging of peripheral vascular disease, providing a breakthrough in the physician's ability to visualize the human vascular system and improve disease diagnosis and treatment.
In October 2005, the European Medicines Agency granted marketing approval of Vasovist for the 25 member states of the E.U. and Bayer Schering Pharma AG, Germany, EPIX's partner for Vasovist, began marketing Vasovist in Europe in the second quarter of 2006. With the addition of Bulgaria and Romania to the E.U. in 2007, Vasovist is now approved in all 27 member states. Vasovist is currently marketed in 16 countries, including Germany, the Netherlands, Norway, Sweden, Denmark, United Kingdom and Switzerland. In August 2006, the Australian Drug Evaluation Committee (ADEC) recommended to the Therapeutic Goods Administration (TGA) that Vasovist be registered for sale in Australia. Vasovist was approved for use in Switzerland in February 2006, Australia in September 2006 and Canada in November 2006.
In December 2003, EPIX Pharmaceuticals submitted a New Drug Application (NDA) to the FDA for the use of Vasovist in detection of vascular disease. In January 2005, EPIX received an approvable letter from the FDA for Vasovist pending additional clinical trials. In May 2005, EPIX submitted a response to the FDA, which was accepted as a complete response the following month. EPIX received a second approvable letter from the FDA in November 2005. The Company met with the FDA twice in early 2006 to discuss the path forward for Vasovist in the U.S.
In August 2006, EPIX received a letter from the U.S. Food and Drug Administration (FDA) denying the formal appeal to approve its novel blood-pool imaging agent Vasovist and turning down EPIX's request for an Advisory Committee to review Vasovist. In its response letter, the Office of New Drugs (OND) of the FDA also suggested that if EPIX decides to conduct additional clinical research to support approval, then rather than relying on a blinded re-read of previously submitted data and data from a new clinical trial, a safer course of action would be to conduct two new clinical trials to support the application for approval. EPIX submitted the appeal to the OND on June 30, 2006 in response to two prior approvable letters for Vasovist.
In June 2007, EPIX announced that it received a response from the FDA regarding the company's appeal for immediate approval of Vasovist. The response from the FDA is a result of a formal appeal EPIX filed on February 28, 2007 to the director of the Center for Drug Evaluation and Research (CDER) at the FDA, asking the CDER director to approve Vasovist. In the response, the FDA, while denying the immediate approval of Vasovist, indicated that further clinical trials may not be necessary to gain approval. The FDA had previously indicated that one or two additional pivotal clinical trials would be required for approval. In its response, the FDA stated that a blinded re-read of the images obtained from the previously completed Phase 3 clinical trials of Vasovist could support approval of Vasovist if the results are positive. EPIX intends to work with the FDA's Division of Medical Imaging and Hematology Products to develop a jointly agreed-upon protocol for the blinded re-analysis of the Phase 3 images prior to conducting the re-read. After the re-reads are completed and an amended submission is provided by EPIX, the FDA will have up to 180 days to review the submission.
Vasovist reversibly binds to the human blood protein albumin, allowing imaging of the blood vessels for approximately an hour after administration. With a single injection, Vasovist enables clear three-dimensional images of arteries and veins throughout the body. Vasovist may make it possible for physicians to detect vascular disease earlier and less invasively than with X-ray angiography, and provide an improved evaluation of potential therapeutic options including percutaneous intervention and vascular surgery.
The NDA submitted for Vasovist was the culmination of an eight-year development program that included 18 clinical trials, 1,438 patients, and more than one million safety data points. In each pivotal trial, Vasovist met its primary endpoints. All four Phase 3 clinical trials demonstrated that Vasovist-enhanced MRA provided overall accuracy similar to X-ray angiography. In addition, it provides several important patient benefits:
No arterial catheterization; only a single intravenous injection is needed
No patient exposure to ionizing radiation
No nephrotoxic dyes
Complete vascular exam of multiple body regions for a more comprehensive diagnosis
Less invasive than X-ray angiography, reducing patient discomfort and recuperation time
Visualization of vessel wall structures (this is not part of the indication - it could be part of a follow-on indication however)
Research unveils new hope for deadly childhood disease
http://www.erbse.vm-elsig.de/form/base/YaBB.pl?num=1197521484/0
Have a nice day
Erbse
Targacept to Receive $6 Million from GlaxoSmithKline for Initiation of Phase I Trial of Neuropathic Pain Candidate
Winston-Salem, North Carolina
December 10, 2007
Targacept, Inc. (Nasdaq: TRGT), a clinical-stage biopharmaceutical company developing a new class of drugs known as NNR Therapeutics (TM), today announced that it has initiated a Phase I clinical trial of its product candidate TC-6499. The initiation of the trial triggers a $6.0 million milestone payment to Targacept under the terms of its alliance agreement with GlaxoSmithKline.
TC-6499 is a novel small molecule that Targacept plans to develop initially as a treatment for neuropathic pain. In preclinical studies, TC-6499 demonstrated analgesic activity in multiple models of neuropathic pain. TC-6499 was discovered using Targacept’s proprietary drug design technology known as Pentad (TM).
The Phase I study is designed to evaluate the safety, tolerability and pharmacokinetics of TC-6499. The trial is a double-blind, placebo-controlled study with escalating single doses of TC-6499 administered orally to healthy volunteers.
“TC-6499 represents the third Pentad-enabled product candidate that we have advanced into the clinic this year, demonstrating the strength of Pentad, our ability to execute our operating plans successfully and the breadth and pharmacological diversity of our pipeline of NNR Therapeutics,” said J. Donald deBethizy, Ph.D., Targacept’s President and Chief Executive Officer. “We are pleased to achieve this milestone in our GlaxoSmithKline alliance, which we entered into only a few months ago.”
“We are delighted to see TC-6499 enter clinical development,” said Hugh Cowley, M.D., Senior Vice President of GlaxoSmithKline and head of the Center of Excellence for External Drug Discovery (CEEDD). “There is a clear need for effective treatments for neuropathic pain and the preclinical profile of TC-6499 is very encouraging. We are pleased to be working with Targacept and excited by the potential of NNR-targeted therapeutics for pain, as well as the other four therapeutic focus areas of the alliance.”
Targacept anticipates that its Phase I program for TC-6499 will include, in addition to the ongoing single dose trial, a multiple rising dose trial. Under its agreement with GlaxoSmithKline, Targacept is eligible to receive an additional milestone payment if, following completion of its Phase I program, Targacept determines to advance TC-6499 into Phase II.
TC-6499 is subject to a contingent future option of GlaxoSmithKline for an exclusive license under the terms of the parties’ agreement. If licensed, Targacept retains an option to co-promote TC-6499 for pain to specialists and hospital-based physicians in the United States.
About Neuropathic Pain
Unlike nociceptive pain, which generally results from tissue damage, neuropathic pain results from damage to the nerves that transmit pain sensation. When this occurs, central nervous system (CNS) mechanisms that inhibit pain transmission do not function properly and pain signals continue to be sent to the brain. NNR-targeted treatments may have the potential to amplify the inhibitory CNS mechanisms directly, restoring their ability to shut off the pain signals. Neuropathic pain is characterized as severe, stabbing, burning or tingling and is most often associated with diabetes mellitus, chemotherapy, toxins, herpes, HIV infection or trauma. Neuropathic pain affects more than 15 million people in the United States alone, and the currently available treatments are often inadequate to relieve the pain effectively. Other options are needed to improve the outcomes for patients with neuropathic pain.
Schizophrenia And Smoking: Weighing The Role Of The Tobacco Industry
8 December 2007. The prevalence of cigarette smoking in the United States has declined precipitously over the past four decades to about 20 percent of the general adult population, half what it was when the Surgeon General released the landmark 1964 report on smoking and health (Centers for Disease Control and Prevention [CDC], 2007). However, cigarette smoking is twice as common among the mentally ill as in the general population (Lasser et al., 2000), which translates into $37 billion in annual sales for the tobacco industry. The prevalence of smoking among those diagnosed with schizophrenia is particularly striking, with some researchers proposing rates as high as 88 percent (Hughes et al., 1986).
A new report, published online November 5, 2007, in Schizophrenia Bulletin, by Judith Prochaska and colleagues at the University of California, San Francisco proposes that a concerted, multi-pronged effort by that industry has sustained the high rate of smoking among patients with schizophrenia, both by promoting their use of cigarettes and by discouraging smoking bans and smoking cessation programs in psychiatric hospitals.
Smoking is not hazardous to your health?
For their study, the UCSF team relied on word-searchable databases, such as the Legacy Tobacco Documents Library, of the nearly 40 million pages of internal tobacco industry documents that were made publicly available after a 1998 judgment against the industry by the State of Minnesota. Based on the information in documents retrieved by broad keyword searches (e.g., “psychosis”), the Prochaska group performed progressively restricted searches based on names of programs and individuals, dates, and reference numbers. The preliminary search yielded 280 documents, 130 of which were from the archive of the Council for Tobacco Research (CTR), an industry organization originally founded in the mid-1950s to fund research that could be used in public relations campaigns to counter the growing tide against cigarette smoking.
According to the UCSF team, the documents reveal that promotional tactics of the tobacco industry toward individuals with schizophrenia took two main forms. First, they funded research to corroborate the idea, largely based on anecdotal evidence, that individuals with schizophrenia have some psychosomatic or genetic profile that bestows resistance to tobacco-related diseases. They also backed studies of the hypothesis that the high rate of smoking among patients with schizophrenia represented a beneficial form of “self-medication,” presumably mediated by nicotinic acetylcholine receptors. Second, either directly or in collaboration with patient advocacy groups, the industry took steps to see that psychiatric patients had easy access to cigarettes and that smoking bans in psychiatric hospitals would either be lifted or substantially relaxed.
The authors found that as far back as the 1950s the industry was collecting correspondence and other material from medical journals proposing that patients with schizophrenia have low rates of cancer despite high rates of smoking. The CTR and other industry organizations funded studies—later discredited—asserting that patients with schizophrenia are less likely to develop cancer from smoking because they did not repress grief and other emotions as strongly as those in the general population.
Prochaska and colleagues cite a 1982 research grant proposal to the Canadian Tobacco Manufacturer’s Council (CTMC), wherein one investigator who planned to explore the self-medication hypothesis pointed out to the reviewers that positive findings would be a “significant bonus for the tobacco industry,” and indicated that patients who participated in the study would be paid in either cash or cigarettes. The Prochaska group found evidence that for both the disease-resistance and self-medication lines of inquiry, the industry denied funding to investigators whose grant requests entertained the possibility of negative findings, favoring researchers who approached these problems “from our point of view,” as Prochaska and colleages quote an internal company memo on a scientist who depended on CTMC money.
The documents reveal that only a fraction of industry-funded studies discussed in researchers’ progress reports were eventually published in peer-reviewed journals, a disparity that the Prochaska team takes as evidence that a great deal of unfavorable data may have been suppressed, a pattern they say has been paralleled in the industry’s research programs on harmfulness of secondhand smoke.
Forty years behind
Recent studies have revealed that individuals with schizophrenia have of higher risk of developing diseases associated with cigarette smoking, including lung cancer (Lichtermann et al., 2001), cardiovascular disease (Goff et al., 2005), and respiratory problems (Himelhoch et al., 2004), though the possible confounding effects of poor diet, lack of exercise, and side-effects of antipsychotic medications have not been fully sorted out (see related SRF news story).
Prochaska and colleagues suggest that the tobacco industry’s greatest damage to the health of patients with schizophrenia may be indirect: because the research enterprise has been skewed toward tobacco’s supposed harmlessness or beneficial effects, “astoundingly little” research has been published on smoking cessation among psychiatric patients. “Might it be,” the authors ask, “that the mentally ill are the largest remaining group of smokers, not because they need to smoke but rather because they are among the last to be treated?”—Peter Farley
Targacept Announces Results of Phase II Study of TC-2696 in Postoperative Dental Pain
TRGT 9.60, +0.12, +1.3%) , a clinical-stage biopharmaceutical company developing a new class of drugs known as NNR Therapeutics (TM), today announced results of a randomized, placebo controlled Phase II clinical trial of its product candidate TC-2696. In the trial, 181 patients received a single dose of one of three doses of TC-2696 or ibuprofen or placebo following third molar extraction surgery. TC-2696 did not meet the primary endpoints, superior pain relief four or six hours after dosing as compared to placebo. TC-2696 was generally well tolerated in the trial, as there were no clinically meaningful differences in the incidence of adverse events between the TC-2696 dose groups and the placebo group and no unexpected or serious adverse events. These results suggest that TC-2696 is not a viable therapeutic candidate for acute post-operative pain.
In Targacept's preclinical studies, TC-2696 demonstrated analgesic activity in a variety of models, including acute, chronic and inflammatory nociceptive pain and neuropathic pain. Targacept is continuing to analyze the data from the trial and plans to consider next steps with regard to the development of TC-2696 in conjunction with GlaxoSmithKline, with which it entered into a strategic alliance focused in five therapeutic areas, including pain, earlier this year.
EPIX New Patent with Bayer Schering
USE OF PERFLUORALKYL-CONTAINING METAL COMPLEXES AS CONTRAST AGENTS FOR DIAGNOSING ALZHEIMER'S DISEASE
http://v3.espacenet.com/textdoc?DB=EPODOC&IDX=WO2007128567&F=0
Behavioral and biological effects of chronic S18986, a positive AMPA receptor modulator, during aging.
Bloss EB, Hunter RG, Waters EM, Munoz C, Bernard K, McEwen BS.
The Laboratory of Neuroendocrinology, The Rockefeller University, New York, New York, USA.
AMPA receptors are a major subtype of ionotropic receptors that respond to glutamate. Positive allosteric modulators of AMPA receptors selectively enhance fast excitatory neurotransmission in the brain and increase overall neuronal excitability. In addition to enhancing cognitive performance, S18986 (Servier, France) and other AMPA receptor modulators have also been shown to be neuroprotective. A particularly relevant context for AMPAR modulator studies is during aging because of increased neuronal vulnerability. It is currently unknown if chronic AMPAR modulator treatment can alter the course of brain aging, a process characterized by impairment of cognitive function, reduced neuronal excitability, and increased inflammation in the brain. We examined the behavioral and some relevant CNS effects of chronic S18986 in rats from 14 to 18 months of age. Here we show that chronic, oral administration of S18986 increases locomotor activity and performance in a spatial memory task in aged rodents. In addition, chronic S18986 treatment retards the decline of forebrain cholinergic neurons by roughly 37% and midbrain dopaminergic neurons by as much as 43% during aging and attenuates the age-related increase in the expression of a microglial marker in the hippocampus. These results provide a framework for further studies of the potentially beneficial effects of AMPAR modulators on brain aging.
EPIX to Raise $16.3 Million through Private Financing
LEXINGTON, Mass.--(BUSINESS WIRE)--Nov. 12, 2007--EPIX Pharmaceuticals, Inc. (NASDAQ: EPIX) today announced it has entered into definitive agreements with institutional and accredited investors with respect to the private placement of approximately 5.2 million shares of its common stock at a purchase price of $3.10 per share for expected gross proceeds of approximately $16.3 million before payment of placement agent commissions and offering expenses. EPIX expects to utilize the proceeds to finance ongoing clinical trials, advance its research and development activities and fund general corporate operations. Closing is expected to occur on or about November 15, 2007, subject to customary closing conditions.
The shares of common stock sold in the private placement have not been registered under the Securities Act of 1933, as amended, or state securities laws and may not be offered or sold in the United States absent registration with the Securities and Exchange Commission (SEC) or an applicable exemption from the registration requirements. The shares were offered and sold only to institutional and accredited investors. EPIX has agreed to file a registration statement with the SEC covering the resale of the shares of common stock issued in the private placement. This press release shall not constitute an offer to sell or the solicitation of an offer to buy nor shall there be any sale of these securities in any jurisdiction in which such offer, solicitation or sale would be unlawful prior to the registration or qualification under the securities laws of any such jurisdiction. Any offer will be made only by means of a prospectus, forming a part of the effective registration statement. Copies of the final prospectus can be obtained at the SEC website at http://www.sec.gov or at the EPIX website at www.epixpharma.com.
EPIX Pharmaceuticals Announces Third Quarter Financial Results
Recent Achievements Include Positive Data in Obesity and PH with COPD, Milestones Reached with GSK and CFFT
LEXINGTON, Mass.--(BUSINESS WIRE)--Nov. 6, 2007--EPIX Pharmaceuticals, Inc. (NASDAQ:EPIX) today reported financial results for the third quarter ended September 30, 2007.
"This was a significant quarter for EPIX - one that was marked by clinical successes, pipeline progress and corporate growth," said Michael G. Kauffman, M.D., Ph.D., chief executive officer of EPIX. "We are excited by the results of our Phase 1b clinical trial of PRX-07034 in obesity and our Phase 2a clinical trial of PRX-08066 in patients with pulmonary hypertension (PH) associated with COPD. We've also achieved key milestones under our strategic collaborations with GlaxoSmithKline and Cystic Fibrosis Foundation Therapeutics, and have completed enrollment into both our Phase 2b trial of PRX-00023 in major depressive disorder and our Phase 2a trial of PRX-03140 in Alzheimer's disease. We are continuing to advance our programs on-schedule and deliver on key corporate goals."
EPIX Recent Corporate Highlights:
Positive Phase 1b Weight Loss Data for PRX-07034 in Obesity
In October, EPIX announced statistically significant results (p is less than 0.005) from its Phase 1b clinical trial of PRX-07034, the company's internally-discovered, novel 5-HT6 antagonist being developed for obesity, Alzheimer's disease and cognitive impairment associated with schizophrenia. Findings from the randomized, double-blind, placebo-controlled trial of 21 obese, but otherwise healthy, adults demonstrated that patients taking PRX-07034 (n=11) for 28 days lost an average of 0.45 kg, while patients on placebo (n=10) gained 1.37 kg during this period. An increase in corrected QT wave interval was apparent at the dose tested but, based on pre-clinical data, the company believes that this effect can be reduced by continuing the development of the compound in an isomeric (i.e., one enantiomer) form rather than the racemic form used in this trial.
Clinical Program Updates
In October, EPIX also provided key clinical program updates. EPIX announced the completion of patient enrollment in its Phase 2b trial of PRX-00023 in major depressive disorder (MDD). The company expects to announce study results in the first quarter of 2008. Further, EPIX announced that it completed patient enrollment and expects to report findings from its Phase 2a clinical trial of PRX-03140 in Alzheimer's disease by the end of 2007.
Final data from Phase 2a clinical trial of PRX-08066
In August, EPIX announced final results from its Phase 2a clinical trial of PRX-08066 in patients with pulmonary hypertension (PH) associated with chronic obstructive pulmonary disease (COPD). This randomized, double-blind, placebo-controlled trial of 71 patients resulted in statistically significant (p=0.043) reductions in systolic pulmonary artery pressure (SPAP). Responder (defined as greater than or equal to a 4mmHg drop in SPAP) rates were 45% on 400 mg once-daily vs. 14% on placebo. PRX-08066 also was well-tolerated and demonstrated the potential for co-administration with other therapies. Based on the top-line results from this trial, the company intends to continue the development of PRX-08066 as a first-in-class 5-HT2B antagonist in PH associated with COPD.
Expansion of Regulatory Affairs Management Team
In August, EPIX announced the expansion of the company's research and development team with the appointment of Margaret Uprichard, PharmD, to the position of senior vice president, regulatory affairs and quality. Dr. Uprichard is now responsible for leading all regulatory affairs activities for the company, including developing and maintaining effective regulatory strategies for EPIX's five lead product candidates currently in clinical trials.
Milestone Achievements with GlaxoSmithKline
Under its collaboration with GlaxoSmithKline (NYSE:GSK), EPIX announced in August and November that it reached initial milestones related to the first and second of three discovery stage programs. Using its proprietary, integrated computational-medicinal chemistry approach to drug discovery, EPIX identified three lead candidates to move forward into lead optimization in each of these first two collaborative G-protein coupled receptor (GPCR) discovery programs. In addition to the three joint discovery programs, EPIX and GSK maintain a joint focus on developing PRX-03140, EPIX's proprietary 5-HT4 agonist, for the treatment of Alzheimer's disease. The companies are continuing their efforts on the three discovery program targets, as well as on the achievement of key milestones across all collaborative programs.
Third Milestone Achievement with Cystic Fibrosis Foundation Therapeutics (CFFT)
As part of its collaboration with CFFT, EPIX announced in August that it had successfully identified a hit compound that corrects the functionality of the Cystic Fibrosis Transmembrane conductance Regulator (CFTR) ion channel in a cell-based model system. A mutation in the CFTR gene is one of the key factors that ultimately lead to the symptoms, complications and premature mortality in people with CF.
Approval of Vasovist in Turkey and Marketing Launch in CanadaEPIX is also announcing that its novel blood pool imaging agent Vasovist has been approved for marketing in Turkey and that marketing of Vasovist has been launched by its partner Bayer HealthCare Pharmaceuticals in Canada. Vasovist is now approved for marketing in more than 30 countries worldwide, including all 27 member states of the European Union, Norway, Iceland, Switzerland, Australia and Canada. EPIX is making progress in its discussions with the FDA regarding its NDA for Vasovist and expects to initiate its re-read protocol and analysis in early 2008.
Financial Results
Net loss for the third quarter of 2007 was $12.9 million, or $0.39 per share, versus $133.1 million, or $6.00 per share, for the same period in 2006. The decrease in the net loss was primarily due to a non-recurring charge of $123.5 million recorded for in-process research and development in the third quarter of 2006.
Total revenues in the third quarter of 2007 were $5.3 million, compared to $1.3 million in the third quarter of 2006. Research and development expenses totaled $14.9 million in the third quarter of 2007, compared to $7.9 million in the third quarter of 2006. The increase in research and development expenses was primarily attributable to expenses associated with the company's five ongoing clinical development programs, as well as preclinical programs and internal costs, which began after the acquisition of Predix Pharmaceuticals Holdings, Inc. was completed on August 16, 2006.
General and administrative expense was $3.6 million in the third quarter of 2007 compared to $3.1 million in the third quarter of 2006. The increase in general and administrative expense was primarily due to costs associated with the increase in personnel and infrastructure relating to the Predix acquisition. Additionally, EPIX incurred greater legal expenses, including for patent-related matters, due to the increased complexity of the post-merger company.
As of September 30, 2007, EPIX had cash, cash equivalents and short-term investments of $66.1 million compared to $109.5 million on December 31, 2006. Management estimates that cash, cash equivalents and marketable securities on hand as of September 30, 2007, together with anticipated revenue earned in 2007 and 2008, will fund operations through 2008.
EPIX currently has $100.0 million of convertible debt outstanding. Approximately 32.9 million shares of common stock were outstanding at September 30, 2007. On October 29, 2007, EPIX issued 3,167,000 common shares and paid approximately $5.8 million in cash in full satisfaction of the second and final milestone payment to the former Predix shareholders.
Dr. Kauffman added, "We are looking forward to continuing our progress and delivering on additional corporate milestones. By the end of the year, we expect to announce the results of our Phase 2a trial of PRX-03140 in Alzheimer's disease. Moving into 2008, we anticipate continued achievements and are on-schedule to report our Phase 2b trial results of PRX-00023 in depression in the first quarter of that year."
Upcoming Milestones
-- Results from Phase 2a trial of PRX-03140 in Alzheimer's
disease expected 4Q07
-- Initiation of Phase 2b right-heart catheter study in PRX-08066
program expected 1Q08
-- Results from Phase 2b trial of PRX-00023 in major depressive
disorder expected 1Q08
-- Initiation of Phase 2b trial of PRX-03140 in combination with
Aricept(R) in Alzheimer's disease expected 1H08
EPIX Pharmaceuticals Achieves Milestone For Second Discovery Program in Collaboration with GlaxoSmithKline
Three Lead Candidates Identified
LEXINGTON, Mass.--(BUSINESS WIRE)--Nov. 5, 2007--EPIX Pharmaceuticals, Inc. (NASDAQ:EPIX) today announced that it has achieved a key milestone related to the second of three discovery programs under its collaboration with GlaxoSmithKline (NYSE:GSK). Using its proprietary, integrated computational-medicinal chemistry approach to drug discovery, EPIX has identified three lead candidates to move forward into lead optimization in this second G-protein coupled receptor (GPCR) discovery program. Under the collaboration, EPIX is entitled to receive a $3 million milestone payment from GSK in the next 30 days. In August, EPIX announced that it had identified three lead candidates for the first discovery program, which entitled the company to a $3 million milestone payment.
"We continue to be pleased by the ongoing progress of our collaboration with GSK and our ability to move these discovery programs forward," said Michael G. Kauffman, M.D., Ph.D., chief executive officer of EPIX. "Our ability to deliver lead candidates for two discovery programs further validates our approach and the productivity of our partnership with GSK. We look forward to continuing our efforts to deliver on our joint goals and achieve key milestones."
"We're very happy that the EPIX in silico approach to drug discovery continues to deliver promising results, in this case three more lead candidates that we will move forward into lead optimization as part of our collaboration with GSK," said Yael Marantz, Ph.D., executive director of computational drug discovery at EPIX. "We are extremely proud of our group and our joint work with GSK - together, we are delivering on joint timelines and goals for our collaborative GPCR discovery programs."
In December 2006, EPIX and GSK announced a worldwide multi-target strategic collaboration to discover, develop and market novel medicines targeting four G-protein coupled receptors (GPCRs) for the treatment of a variety of diseases, including EPIX's novel 5-HT4 partial agonist program, PRX-03140, which is in early-stage clinical development for the treatment of Alzheimer's disease. As part of the collaboration, EPIX received total initial payments of $35 million, including $17.5 million through the purchase of its common stock, and may be eligible to earn up to $1.2 billion in milestones across the four GPCR programs. Under the collaboration, EPIX is also entitled to receive tiered double-digit royalties of sales by GSK on all collaboration-developed product sales. The alliance is conducted through GSK's Center of Excellence for External Drug Discovery (CEEDD).
"We continue to be impressed by the quality and efficiency of the lead identification process for this collaborative effort between EPIX and GSK," said Hugh Cowley, M.D., head of GSK's Center of Excellence for External Drug Discovery (CEEDD). "We are moving forward on-schedule and this achievement marks an additional milestone in what we hope will be a long and productive collaboration."
Milestones Cortex