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New non-invasive technology shows promise in shrinking liver tumors. Related?
http://www.uab.edu/news/latest/item/1538-new-non-invasive-technology-shows-promise-in-shrinking-liver-tumors
News is out. "Celsion has made tremendous progress since the beginning of the second quarter, having achieved some of our most important goals to date in the development of ThermoDox® and in our evolution as a biopharmaceutical company," said Michael H. Tardugno, Celsion's President and Chief Executive Officer. "Now that Celsion has reached its enrollment target for the Phase III HEAT Study, our sights are set on the next phases of the development strategy, including the development of a commercial manufacturing process for ThermoDox® in primary liver cancer and the expansion of our technology platform into additional indications. In support of these efforts, we have recently raised over $33 million in capital, expanded our intellectual property estate, added key members to the Celsion team and announced a relocation of the Company to an area that will support our anticipated growth. We look forward to continuing to build on the Company's momentum as the potential of ThermoDox® is revealed in the coming months."
Alzheimer's drug from Pfizer, J&J may prove safer
ReutersBy Julie Steenhuysen | Reuters – Wed, Jul 20, 2011
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PARIS (Reuters) - Experimental Alzheimer's drug bapineuzumab, from Pfizer and Johnson & Johnson , may be safer than originally thought, according to two studies by U.S. researchers released on Wednesday.
They said that a brain swelling condition called vasogenic edema, which caused a lot of worry over the drug's safety early on, may decrease over time.
"It looks like we can treat people for a number of years safely," Dr. Steven Salloway of Butler Hospital and Brown University in Providence, Rhode Island, told the Alzheimer's Association International Conference in Paris.
Salloway looked at the long-term safety of 194 patients in a mid-stage trial of the drug that stayed on treatment after the initial phase ended. Of those, 86 patients got the drug for at least 3 years and 43 were treated for at least 4 years.
About 24 percent of the patients had side effects possibly related to the drug, and some 85 percent of these were considered mild to moderate.
Cases of vasogenic edema, now called ARIA-E or Amyloid Related Imaging Abnormalities with Parenchymal Edema, appeared to lessen over time.
The risk of developing ARIA-E dropped from 6.7 percent in the first three infusions of the drug, to 2.7 percent for the fourth through the 10th treatment.
"That is very encouraging to me," Salloway said in an interview. "I think this is a transient condition."
"We've treated a lot of patients at our center. I think it is very well tolerated," he said.
Larger, late-stage clinical trials will be needed to determine whether the drug works. Those studies are expected to stop enrolling patients in mid-2012.
There is no current treatment for Alzheimer's, which affects nearly 36 million people worldwide.
SWELLING WITHOUT SYMPTOMS
In a separate study of the drug, a team led by Dr. Reisa Sperling of Brigham and Women's Hospital and Harvard Medical School in Boston reviewed more than 2,000 MRI scans from 262 patients who participated in mid-stage studies of bapineuzumab.
She looked for cases of amyloid-related abnormalities on the scans that might represent vasogenic edema or tiny leaks in blood vessels.
The radiologists in the study were specifically looking for amyloid abnormalities in the brain that might have gone undetected because patients had no symptoms.
The team found 36 cases thought to be linked to treatment with bapineuzumab, including 15 new cases. None of these patients had symptoms of ARIA-E, which can include headache, memory loss, loss of coordination and disorientation.
Since these cases were not identified, many of these patients continued to be treated with bapineuzumab.
"They were treated through their ARIA and remained asymptomatic," Sperling said in an interview.
"For me that was reassuring. You see these changes in the MRI and they look a little frightening. The fact that they can potentially be treated and remain OK is reassuring."
The team also found that people treated with higher doses of bapineuzumab who have an Alzheimer's risk gene called APOE-4 tend to have more ARIA-E side effects, confirming the companies' decision to lower the dose of the drug in these patients.
Salloway said the mid-stage study he looked at was not meant to show whether the drug helped improve clinical symptoms, but the researchers were encouraged to see it appears to be safe.
Many researchers think patients with mild to moderate Alzheimer's disease are too far gone to have any significant benefit from drugs like bapineuzumab.
Salloway says he is hopeful the drug will work, but he will not fret if the late-stage results do not improve symptoms.
"I don't think it would kill the drug or the amyloid hypothesis," he said. Drugs like bapineuzumab remove deposits of beta amyloid from the brain, on the theory that will help improve memory problems in people with Alzheimer's disease.
Despite several attempts, no anti-amyloid drug has shown a benefit, but all of them have been tried in people with more advanced disease.
Researchers are now looking for safe ways to test people in the earliest stages of Alzheimer's, in some cases even before symptoms appear.
J&J and Pfizer are developing bapineuzumab jointly. Elan Corp, one of the drug's original developers, still retains a financial stake.
A lot of info coming out of ICAD on Babi, read the ELN IV msg brd.
I am not n the wrong board.
Expecting good news out of ICAD? What about the big event you predicted this week?
Did you guys read the report on ELN by Jefferies yesterday. Go to the eln iv brd. Good stuff on babi.
For OX1 or the whole company? What is the guy on ymb talkng about the last 10k, saying 2b shares to get dumped?
I have a suspicion that solanezumab (LY2062430) from Eli Lilly and Co. is under ILNS's patent?? Any ideas?
.
Analysis: Cover Story - Ophthalmic disease
Osherovich, L. SciBX 4(26); doi:10.1038/scibx.2011.727
Published online June 30 2011
Aß's dry (AMD) humor
by Lev Osherovich, Senior Writer
A collaborative effort by Pfizer Inc. and U.S. academics has found that immunotherapy against ß-amyloid can reverse the retinal protein deposition that leads to dry age-related macular degeneration. The finding could open up a repurposing opportunity for mAbs in development for Alzheimer's disease.1
“We've established ß-amyloid as a therapeutic target for dry AMD,” a thus far untreatable form of the disease, said team leader Catherine Bowes Rickman, associate professor of ophthalmology and cell biology at Duke University.
Bowes Rickman's team built on prior observations by coauthor Lincoln Johnson that ß-amyloid (Aß) accumulated in drusen, the proteinaceous deposits that lead to age-related macular degeneration (AMD) over time.2 Johnson is associate director of the Center for the Study of Macular Degeneration at the University of California, Santa Barbara.
Previously, Johnson's team “looked at the components of drusen and found that there was amyloid there,” said Bowes Rickman. “Studies have found higher amounts of amyloid in the drusen of AMD patients than in controls” who had drusen but hadn't yet developed clinical AMD.
In the new study, Bowes Rickman's team extended those findings by introducing anti-Aß antibodies into a new mouse model of AMD. The result was a therapeutic effect on retinal pathology and visual acuity.
Top of page
Eyemyloid
Because good animal models for AMD are scarce, the team designed a mouse overexpressing the human form of the cholesterol transport protein apolipoprotein E4 (APOE4), which causes accumulation of Aß and increases AD risk. To speed up the disease process, the researchers overfed the animals a high-cholesterol diet.
Indeed, excess APOE4 caused retinal pathology that resembled AMD. Bowes Rickman's team found that the overfed APOE4 mice had retinal Aß deposits and abnormally large retinal cells, and had poorer visual function than wild-type controls.
The changes in cell size were similar to what is seen in the retinas of cadavers with dry AMD, thus corroborating the mouse model's validity.
Intraperitoneal injection of anti-Aß mAbs engineered to bind the C-terminal region of Aß decreased AMD-like pathology and increased visual acuity in mice compared with no treatment.
Among the antibodies the team tested was Pfizer's ponezumab (PF-04360365), which is in Phase II testing for AD.
Notably, anti-Aß mAbs do not penetrate the eye but remain in the periphery. Thus, Bowes Rickman thinks the mAbs work through the so-called sink effect, in which antibodies in the periphery soak up blood-borne Aß. Depleting peripheral Aß is thought to shift the misfolded protein's equilibrium and drive it out of immunologically privileged areas like the brain and retina.
“There is a blood eye barrier in the back of the eye, but we don't have to cross this barrier to get a therapeutic effect,” said Bowes Rickman.
Bowes Rickman suspects that keeping Aß out of the eye may lower the chronic activity of the complement system, an innate immune mechanism recently shown to contribute to dry AMD.3
“There is a blood eye barrier in the back of the eye, but we don't have to cross this barrier to get a therapeutic effect.”
Catherine Bowes Rickman
Duke University
Her team is now testing whether anti-Aß mAbs can alleviate disease in a mouse model of AMD caused by excessive complement activity.
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ADded value
At least seven companies have anti-Aß mAbs in preclinical through Phase III testing for AD. The Phase III compounds include bapineuzumab (AAB-001) from Johnson & Johnson and Pfizer and solanezumab (LY2062430) from Eli Lilly and Co.
Bowes Rickman thinks ponezumab may be especially suitable as an AMD therapeutic because, unlike other anti-Aß mAbs, it has been engineered to evade the complement system. Ordinary mAbs can activate complement and potentially exacerbate AMD.
The team has yet to test these other anti-Aß mAbs in its APOE4 model.
Ryo Kubota, chairman, president and CEO of ophthalmic company Acucela Inc., said that although Bowes Rickman's “data seem solid,” it may be better to go further upstream and prevent the conditions that lead to Aß deposition.
Acucela is developing compounds to block the formation of N-retinylidene-N-retinyl-ethanolamine (A2E), a toxic metabolite whose accumulation is associated with dry AMD. The company's ACU-4429 is in Phase II testing for the indication.
Kubota thinks A2E may act upstream of Aß. He said A2E, which prevents normal protein turnover by lysosomes, may lead to the deposition of Aß in the back of the eye, leading to AMD.
“Inhibition of lysosomal function by A2E is believed to be the cause of drusen formation,” said Kubota. “Drusen may be functioning like a magnet to attract Aß. Targeting the pathological event—A2E itself—earlier in the disease process is a logical approach, represents an ideal target and addresses the root cause of AMD.”
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References
Ding, J.-D. et al. Proc. Natl. Acad. Sci. USA; published online June 20, 2011; doi:10.1073/pnas.1100901108 | Article |
Contact: Catherine Bowes Rickman, Duke University, Durham, N.C.
e-mail: bowes007@duke.edu
Contact: John C. Lin, Pfizer Inc., South San Francisco, Calif.
e-mail: john.lin@pfizer.com
Johnson, L.V. et al. Proc. Natl. Acad. Sci. USA 99, 11830–11835 (2002) | Article | PubMed | ChemPort |
Bradley, D.T. et al. Eye (Lond.) 25, 683–693 (2011) | Article |
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Companies and institutions mentioned
Acucela Inc., Seattle, Wash.
Duke University, Durham, N.C.
Eli Lilly and Co. (NYSE:LLY), Indianapolis, Ind.
Johnson & Johnson (NYSE:JNJ), New Brunswick, N.J.
Pfizer Inc. (NYSE:PFE), New York, N.Y.
University of California, Santa Barbara, Calif.
Methodology to Assess the Disposition of Aß1-40–ponezumab Complexes in a Treated Cynomolgus Monkey
P2-494
Background: Ponezumab (PF-04360365) is a humanized anti-Aß40 monoclonal antibody in clinical development as a potential therapeutic to inhibit disease progression in subjects with mild-to-moderate Alzheimer's disease (AD). The goal of the present study was to evaluate the disposition of radiolabeled Aß1-40 and Aß1-40-ponezumab complexes in bile-duct cannulated cynomolgus monkeys. Methods: Non-human primates (NHP) were administered either an intravenous (IV) bolus of Aß1-40 I125 alone (NHP #1, n=1) or 10 mg/kg of IV ponezumab followed by Aß1-40 I125 (NHP #2, n=1). Plasma Aß1-40 I125 was measured using immunoprecipitation by ponezumab-Protein G for NHP #1, whereas the ponezumab-Aß complexes were precipitated by Protein G for NHP #2. Total radioactivity levels were measured in bile and urine as well as certain selected organs to assess the disposition in both NHP. Results: In NHP #1, plasma Aß I125 was below the lower limit of quantitation (LLOQ) by 4 hours and approximately 80% of Aß I125 radioequivalents were excreted into urine over 24 hours. In NHP #2, plasma Aß I125 did not reach LLOQ until 7 days post dose. Approximately 0.01%, 0.3% and 80% of radioequivalents from the Aß I125 dose were recovered in extracted organs (total from kidney, liver and small intestines), bile and urine, respectively, by 15 days post dose. Conclusions: The method described in this exploratory study allowed for evaluation of the disposition of plasma Aß1-40 I125 and Aß I125 radioequivalents in the presence and absence of ponezumab. This method could be further utilized in more definitive study designs for other anti-Aß biotherapeutic modalities.
Manoj Rajadhyaksha, Pfizer Inc.
Ellen Wang, Pfizer Inc.
Carol Cronenberger, Pfizer Inc.
James Kupiec, Pfizer Inc.
Susan Hurst, Pfizer Inc.
6-Month Chronic Study with Ponezumab (PF-04360365) Chinese Hamster Ovary (CHO)-derived Murine Surrogate in 18-Month-Old Tg2576 Mice
P3-013
Background: Cerebral vasogenic edema and microhemorrhages have been raised as potential safety concerns for compounds intended to treat Alzheimer's disease by targeting amyloid ß. Here, we describe the safety of an anti-amyloid ß monoclonal antibody chronically administered to amyloid ß-bearing mice. Methods: 18-month-old female Tg2576 (APP K670N;M671L) mice were selected for this study because at 12 and 24 months of age they have abundant cerebral parenchymal and vascular amyloid ß and are thus a relevant animal model. Mice (N=200) were injected intraperitoneally with a murine surrogate of the humanized anti-amyloid ß monoclonal antibody ponezumab (PF-04360365) once weekly for up to 26 weeks at doses of 10, 30, or 100 mg/kg. Mortality, clinical signs, body weight, food consumption, and anatomic pathology were evaluated. Brains were examined microscopically for microhemorrhages, and other tissues were evaluated from all animals dying prior to scheduled study termination to ascertain if such deaths were compound-related. All work was approved by an Institutional Animal Care and Use Committee and, for the most part, was conducted under Good Laboratory Practice conditions. Results: There were no compound-related changes in clinical signs, body weight, or food consumption. The numbers of surviving animals were generally similar in all groups. No compound-related anatomic macroscopic or microscopic findings were present. The incidence of Perl's iron-positive brain microhemorrhages was low and similar across all groups, and there was no increase in severity in mice given the test antibody, even at the highest dose. As expected, drug exposure and plasma amyloid ß levels increased with increasing dose of test article, and higher plasma drug levels were correlated with higher plasma amyloid ß levels. Most spontaneous deaths were attributed to age-related neoplasms typical of mice this age. Similar to other deglycosylated murine antibodies, this antibody demonstrated reduced binding against a panel of recombinant murine Fc gamma receptors, indicating a low potential to increase immune effector function. Conclusions: Within the limits of this study, administration of this CHO-derived surrogate of ponezumab to 18-month-old amyloid ß-bearing Tg2576 mice for up to 26 weeks did not result in an increase in microhemorrhages or other pathologies.
Gary Bruce Freeman, Pfizer Global Research and Development
Karin Wallace, Pfizer Global Research and Development
Thomas Brown, Pfizer Global Research and Development
Kelly Bales, Pfizer Global Research and Development
poster session ICAD 2011
http://icad.sclivelearningcenter.com/index.aspx
Unique brain PK properties of 3D6 and bapineuzumab depend on cerebral amyloid load in PDAPP transgenic mice
P4-406
Background: Passive immunization with anti-Aß antibodies leads to the reduction of AD-like neuropathology in transgenic mice. Previously we showed that anti Aß antibodies enter the brain and bind to amyloid plaques.
Methods: Now using 125I-labeled 3D6, the mouse form of the phase 3 clinical candidate bapineuzumab, we further characterized the specificity and the pharmacokinetics of this antibody in the brain and serum.
Results: The results of our studies demonstrate that 125I-labeled anti-Aß antibodies (3D6 and bapineuzumab) delivered intravenously accumulated over time in the brain. This accumulation was particularly evident in regions rich in amyloid plaques and was correlated with the overall level of plaque burden. The binding of 3D6 to brain amyloid plaques did not saturate at the doses tested since cold 3D6 dosed as high as 30 mg/kg did not compete with the binding of the 125I-labeled 3D6. Following one intravenous injection, serum levels of 125I-labeled 3D6 decreased exponentially over time while levels in the hippocampus increased to reach the maximal concentrations by day 14 (brain Tmax) and remained stable up to 27 days. Based on mean PK profile, the brain half-life (T1/2) of 3D6 was estimated to be 54 days whereas the serum T1/2 was 6 days.
Conclusions: In summary, we demonstrated that both 3D6 and bapineuzumab cross the blood brain barrier, that the CNS clearance is markedly slower than the serum clearance, and that this slower CNS clearance correlates with binding to amyloid in a transgenic model of Alzheimer’s disease.
Frederique Bard, Janssen Alzheimer Immunotherapy Research and Development
Gene Kinney, Janssen Alzheimer Immunotherapy R&D
Michael Fox, Elan Pharmaceuticals
Stuart Friedrich, Wyeth Biotech
Ted Yednock, Janssen Alzheimer Immunotherapy R&D
http://icad.sclivelearningcenter.com/index.aspx
Newt Gingrich thinks he can revive his debilitated campaign by talking about Alzheimer’s.
http://www.washingtonpost.com/politics/newt-gingrich-bets-on-alzheimers-as-key-to-a-2012-comeback/2011/06/29/AGR0JawH_story.html
Newt Gingrich thinks he can revive his debilitated campaign by talking about Alzheimer’s.
http://www.washingtonpost.com/politics/newt-gingrich-bets-on-alzheimers-as-key-to-a-2012-comeback/2011/06/29/AGR0JawH_story.html
Newt Gingrich thinks he can revive his debilitated campaign by talking about Alzheimer’s.
http://www.washingtonpost.com/politics/newt-gingrich-bets-on-alzheimers-as-key-to-a-2012-comeback/2011/06/29/AGR0JawH_story.html
Do you know if LLy's solanezumab is licensed from ILNS? Can you expand on next week?
Is solanezumab licensed from another company or is LLY the sole owner? Does LLY own patents on solanezumab?
Brendon Binneman, Pfizer
The monoclonal antibody, ponezumab, a phase 2 passive immunotherapy approach for Alzheimer’s disease
http://www-conference.slu.se/immunotherapyuppsala2011/programme.html
Brendon Binneman, Pfizer
The monoclonal antibody, ponezumab, a phase 2 passive immunotherapy approach for Alzheimer’s disease
http://www-conference.slu.se/immunotherapyuppsala2011/programme.html
Will data on this come out at ICAD 2011?
A Multiple Dose Study of PF-04360365 In Patients With Mild to Moderate Alzheimer's Disease
This study has been completed.
First Received on July 22, 2009. Last Updated on June 17, 2011 History of Changes
Sponsor: Pfizer
Information provided by: Pfizer
ClinicalTrials.gov Identifier: NCT00945672
Purpose
The purpose of this study is to determine whether multiple dose administration is safe and well tolerated in patients with mild to moderate Alzheimer's Disease.
Condition Intervention Phase
Alzheimer's Disease
Biological: PF-04360365 10 mg/kg
Biological: PF-04360365 7.5 mg/kg
Drug: placebo
Phase II
Study Type: Interventional
Study Design: Allocation: Randomized
Endpoint Classification: Safety Study
Intervention Model: Parallel Assignment
Masking: Double Blind (Subject, Caregiver, Investigator)
Primary Purpose: Treatment
Official Title: A Phase 2 Double-Blinded, Randomized, Placebo-Controlled, Multicenter Study Evaluating The Safety, Tolerability And Pharmacokinetics/ Pharmacodynamics Of PF-04360365 In Mild To Moderate Alzheimer's Disease Patients
Resource links provided by NLM:
Genetics Home Reference related topics: Alzheimer disease
MedlinePlus related topics: Alzheimer's Disease
U.S. FDA Resources
Further study details as provided by Pfizer:
Primary Outcome Measures:
Safety/tolerability/PK of multiple doses of PF-04360365 in subjects with mild to moderate Alzheimer's disease dosed for 1 year (adverse events, physical/neurological exams, vital signs, 12-lead ECG, clinical labs, brain MRI, cognitive assessments) [ Time Frame: 18 months ] [ Designated as safety issue: No ]
Brain amyloid burden [ Time Frame: 13 months ] [ Designated as safety issue: No ]
CSF abeta [ Time Frame: 13 months ] [ Designated as safety issue: No ]
Secondary Outcome Measures:
Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-cog); Disability Assessment for Dementia (DAD); plasma abeta, CSF tau and phosphotau; CSF protein, RBCs, WBCs and glucose; immunogenicity (anti-drug antibodies) [ Time Frame: 18 months ] [ Designated as safety issue: No ]
Enrollment: 36
Study Start Date: August 2009
Study Completion Date: June 2011
Primary Completion Date: June 2011 (Final data collection date for primary outcome measure)
Arms Assigned Interventions
PF-04360365 10 mg/kg: Experimental
Intervention: Biological: PF-04360365 10 mg/kg Biological: PF-04360365 10 mg/kg
10 mg/kg every 90 days (5 total doses)
PF-04360365 7.5 mg/kg: Experimental
Intervention: Biological: PF-04360365 7.5 mg/kg Biological: PF-04360365 7.5 mg/kg
10 mg/kg loading dose followed by 7.5 mg/kg monthly maintenance dosing (total of 13 doses)
placebo: Placebo Comparator
Intervention: Drug: placebo Drug: placebo
placebo administered every 90 days or monthly to match experimental treatment arms.
Voltaic has a new and cool solar charger that is made to protect and charge your iPad or similar tablet and a bunch of other devices. The case is called the Spark Tablet Case and it sells for a cool $299.
http://www.slashgear.com/voltaic-spark-tablet-cases-uses-the-sun-to-charge-your-ipad-and-more-24161289/
It's not this is it? Voltaic Spark Tablet Case powers your pad with the Sun's rays.
Voltaic makes tons of solar-charging gear, from laptop bags to backpacks, but what are those living in a post-PC world to do? Well, the company just unveiled its Spark Tablet Case -- a thin, padded tote designed for your iPad or other slate that can generate 8-watts of power in sunlight. In addition to directly charging your iPad in about 10 hours, it can also bank the Sun's rays in a universal battery pack, for use when those fluffy things in the sky don't cooperate with your outdoor computing schedule. Optionally, the included V39 USB Battery can be charged (as you may have guessed) via USB, for extra insurance. The Spark is available now for $299 and extra battery packs can be had for $99. Check out the gallery below and the PR after the break.
http://www.engadget.com/2011/06/23/voltaic-spark-tablet-case-powers-your-pad-with-the-suns-rays/
Can you post a link? I do not see anything new?
Alzheimer's drug hits two forms of toxic protein
http://www.reuters.com/article/2011/03/10/alzheimers-drug-idUSN107922920110310?feedType=RSS&feedName=companyNews&rpc=43
Will data on this come out at ICAD 2011?
A Multiple Dose Study of PF-04360365 In Patients With Mild to Moderate Alzheimer's Disease
This study has been completed.
First Received on July 22, 2009. Last Updated on June 17, 2011 History of Changes
Sponsor: Pfizer
Information provided by: Pfizer
ClinicalTrials.gov Identifier: NCT00945672
Purpose
The purpose of this study is to determine whether multiple dose administration is safe and well tolerated in patients with mild to moderate Alzheimer's Disease.
Condition Intervention Phase
Alzheimer's Disease
Biological: PF-04360365 10 mg/kg
Biological: PF-04360365 7.5 mg/kg
Drug: placebo
Phase II
Study Type: Interventional
Study Design: Allocation: Randomized
Endpoint Classification: Safety Study
Intervention Model: Parallel Assignment
Masking: Double Blind (Subject, Caregiver, Investigator)
Primary Purpose: Treatment
Official Title: A Phase 2 Double-Blinded, Randomized, Placebo-Controlled, Multicenter Study Evaluating The Safety, Tolerability And Pharmacokinetics/ Pharmacodynamics Of PF-04360365 In Mild To Moderate Alzheimer's Disease Patients
Resource links provided by NLM:
Genetics Home Reference related topics: Alzheimer disease
MedlinePlus related topics: Alzheimer's Disease
U.S. FDA Resources
Further study details as provided by Pfizer:
Primary Outcome Measures:
Safety/tolerability/PK of multiple doses of PF-04360365 in subjects with mild to moderate Alzheimer's disease dosed for 1 year (adverse events, physical/neurological exams, vital signs, 12-lead ECG, clinical labs, brain MRI, cognitive assessments) [ Time Frame: 18 months ] [ Designated as safety issue: No ]
Brain amyloid burden [ Time Frame: 13 months ] [ Designated as safety issue: No ]
CSF abeta [ Time Frame: 13 months ] [ Designated as safety issue: No ]
Secondary Outcome Measures:
Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-cog); Disability Assessment for Dementia (DAD); plasma abeta, CSF tau and phosphotau; CSF protein, RBCs, WBCs and glucose; immunogenicity (anti-drug antibodies) [ Time Frame: 18 months ] [ Designated as safety issue: No ]
Enrollment: 36
Study Start Date: August 2009
Study Completion Date: June 2011
Primary Completion Date: June 2011 (Final data collection date for primary outcome measure)
Arms Assigned Interventions
PF-04360365 10 mg/kg: Experimental
Intervention: Biological: PF-04360365 10 mg/kg Biological: PF-04360365 10 mg/kg
10 mg/kg every 90 days (5 total doses)
PF-04360365 7.5 mg/kg: Experimental
Intervention: Biological: PF-04360365 7.5 mg/kg Biological: PF-04360365 7.5 mg/kg
10 mg/kg loading dose followed by 7.5 mg/kg monthly maintenance dosing (total of 13 doses)
placebo: Placebo Comparator
Intervention: Drug: placebo Drug: placebo
placebo administered every 90 days or monthly to match experimental treatment arms.
PH 2 study just ended.
http://clinicaltrials.gov/ct2/show/NCT00945672?cond=
A Multiple Dose Study of PF-04360365 In Patients With Mild to Moderate Alzheimer's Disease
This study has been completed.
First Received on July 22, 2009. Last Updated on June 17, 2011 History of Changes
Sponsor: Pfizer
Information provided by: Pfizer
ClinicalTrials.gov Identifier: NCT00945672
Purpose
The purpose of this study is to determine whether multiple dose administration is safe and well tolerated in patients with mild to moderate Alzheimer's Disease.
Condition Intervention Phase
Alzheimer's Disease
Biological: PF-04360365 10 mg/kg
Biological: PF-04360365 7.5 mg/kg
Drug: placebo
Phase II
Study Type: Interventional
Study Design: Allocation: Randomized
Endpoint Classification: Safety Study
Intervention Model: Parallel Assignment
Masking: Double Blind (Subject, Caregiver, Investigator)
Primary Purpose: Treatment
Official Title: A Phase 2 Double-Blinded, Randomized, Placebo-Controlled, Multicenter Study Evaluating The Safety, Tolerability And Pharmacokinetics/ Pharmacodynamics Of PF-04360365 In Mild To Moderate Alzheimer's Disease Patients
Resource links provided by NLM:
Genetics Home Reference related topics: Alzheimer disease
MedlinePlus related topics: Alzheimer's Disease
U.S. FDA Resources
Further study details as provided by Pfizer:
Primary Outcome Measures:
Safety/tolerability/PK of multiple doses of PF-04360365 in subjects with mild to moderate Alzheimer's disease dosed for 1 year (adverse events, physical/neurological exams, vital signs, 12-lead ECG, clinical labs, brain MRI, cognitive assessments) [ Time Frame: 18 months ] [ Designated as safety issue: No ]
Brain amyloid burden [ Time Frame: 13 months ] [ Designated as safety issue: No ]
CSF abeta [ Time Frame: 13 months ] [ Designated as safety issue: No ]
Secondary Outcome Measures:
Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-cog); Disability Assessment for Dementia (DAD); plasma abeta, CSF tau and phosphotau; CSF protein, RBCs, WBCs and glucose; immunogenicity (anti-drug antibodies) [ Time Frame: 18 months ] [ Designated as safety issue: No ]
Enrollment: 36
Study Start Date: August 2009
Study Completion Date: June 2011
Primary Completion Date: June 2011 (Final data collection date for primary outcome measure)
Arms Assigned Interventions
PF-04360365 10 mg/kg: Experimental
Intervention: Biological: PF-04360365 10 mg/kg
Biological: PF-04360365 10 mg/kg
10 mg/kg every 90 days (5 total doses)
PF-04360365 7.5 mg/kg: Experimental
Intervention: Biological: PF-04360365 7.5 mg/kg
Biological: PF-04360365 7.5 mg/kg
10 mg/kg loading dose followed by 7.5 mg/kg monthly maintenance dosing (total of 13 doses)
placebo: Placebo Comparator
Intervention: Drug: placebo
Drug: placebo
placebo administered every 90 days or monthly to match experimental treatment arms.
Eligibility
Ages Eligible for Study: 50 Years and older
Genders Eligible for Study: Both
Accepts Healthy Volunteers: No
Criteria
Inclusion Criteria:
Males or females of non childbearing potential, age > or = 50.
Diagnosis of probable Alzheimer's disease, consistent with criteria from both:
National Institute of Neurological and Communicable Disease and Stroke and Alzheimer's Disease and Related Disorders Association (NINCDS-ADRDA).
Diagnostic and Statistical Manual of Mental Disorders (DSM IV).
Mini-mental status exam score of 16-26 inclusive.
Rosen-Modified Hachinski Ischemia Score of < or = 4.
Exclusion Criteria:
Diagnosis or history of other demential or neurodegenerative disorders.
Diagnosis or history of clinically significant cerebrovascular disease.
Specific findings on magnetic resonance imaging (MRI); cortical infarct, micro hemorrhage, multiple white matter lacunes, extensive white matter abnormalities.
History of autoimmune disorders.
History of allergic or anaphylactic reactions.
Contacts and Locations
Please refer to this study by its ClinicalTrials.gov identifier: NCT00945672
Locations
Sweden
Pfizer Investigational Site
Göteborg, Sweden, 413 45
Pfizer Investigational Site
Malmo, Sweden, 205 02
Pfizer Investigational Site
Molndal, Sweden, 431 41
Pfizer Investigational Site
Stockholm, Sweden, 141 86
Sponsors and Collaborators
Pfizer
Investigators
Study Director: Pfizer CT.gov Call Center Pfizer
More Information
Additional Information:
To obtain contact information for a study center near you, click here. This link exits the ClinicalTrials.gov site
No publications provided
Responsible Party: Pfizer, Inc. ( Director, Clinical Trial Disclosure Group )
ClinicalTrials.gov Identifier: NCT00945672 History of Changes
Other Study ID Numbers: A9951007
Study First Received: July 22, 2009
Last Updated: June 17, 2011
Health Authority: Sweden: Medical Products Agency
Keywords provided by Pfizer:
Alzheimer's disease amyloid imaging antibody
Additional relevant MeSH terms:
Alzheimer Disease
Dementia
Brain Diseases
Central Nervous System Diseases
Nervous System Diseases
Tauopathies
Neurodegenerative Diseases
Delirium, Dementia, Amnestic, Cognitive Disorders
Mental Disorders
ClinicalTrials.gov processed this record on June 21, 2011
This ph 2 study ends AUG 2011
Multiple IV Dose Study Of PF-04360365 In Patients With Mild To Moderate Alzheimer's Disease
This study is ongoing, but not recruiting participants.
First Received on July 23, 2008. Last Updated on June 2, 2011 History of Changes
Sponsor: Pfizer
Information provided by: Pfizer
ClinicalTrials.gov Identifier: NCT00722046
Purpose
Purpose of the study is to determine whether multiple dose administration of PF-04360365 is safe and well tolerated in patient with mild to moderate Alzheimer's disease.
Condition Intervention Phase
Alzheimer's Disease
Biological: PF-04360365 0.1 mg/kg
Biological: PF-04360365 0.5 mg/kg
Biological: PF-04360365 1 mg/kg
Drug: Placebo
Biological: PF-04360365 3 mg/kg
Biological: PF-04360365 8.5 mg/kg
Phase II
Study Type: Interventional
Study Design: Allocation: Randomized
Endpoint Classification: Safety Study
Intervention Model: Parallel Assignment
Masking: Double Blind (Subject, Caregiver, Investigator)
Primary Purpose: Treatment
Official Title: A Phase 2 Multicenter, Randomized, Double Blind, Placebo-Controlled Study Of The Safety, Tolerability, And Pharmacokinetics Of Multiple Doses Of PF-04360365 In Patients With Mild To Moderate Alzheimer's Disease
Resource links provided by NLM:
Genetics Home Reference related topics: Alzheimer disease
MedlinePlus related topics: Alzheimer's Disease
U.S. FDA Resources
Further study details as provided by Pfizer:
Primary Outcome Measures:
Safety/tolerability of PF-04360365 in subjects with mild to moderate Alzheimer's disease dosed for 18 months. (adverse events, physical/neurologic exams, vital signs, 12-lead ECG, clinical labs, brain MRI, cognitive assessments) [ Time Frame: 24 months ] [ Designated as safety issue: No ]
Pharmacokinetics of PF-04360365 following administration of multiple doses in subjects with mild to moderate Alzheimer's disease. (plasma and cerebrospinal fluid (as available) PF-04360365 concentrations) [ Time Frame: 24 months ] [ Designated as safety issue: No ]
Secondary Outcome Measures:
Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-cog); Disability Assessment for Dementia (DAD); plasma/CSF Abeta; CSF tau and phosphotau; CSF protein, RBCs, WBCs and glucose; Immunogenicity (anti-drug antibodies) [ Time Frame: 24 months ] [ Designated as safety issue: No ]
Estimated Enrollment: 175
Study Start Date: December 2008
Estimated Study Completion Date: August 2011
Estimated Primary Completion Date: August 2011 (Final data collection date for primary outcome measure)
Arms Assigned Interventions
PF-04360365 0.1 mg/kg: Experimental
Intervention: Biological: PF-04360365 0.1 mg/kg
Biological: PF-04360365 0.1 mg/kg
0.1 mg/kg every 60 days (10 doses total)
PF-04360365 0.5 mg/kg: Experimental
Intervention: Biological: PF-04360365 0.5 mg/kg
Biological: PF-04360365 0.5 mg/kg
0.5 mg/kg every 60 days (10 doses total)
PF-04360365 1 mg/kg: Experimental
Intervention: Biological: PF-04360365 1 mg/kg
Biological: PF-04360365 1 mg/kg
1 mg/kg every 60 days (10 doses total)
Placebo: Placebo Comparator
Intervention: Drug: Placebo
Drug: Placebo
Placebo every 60 days (10 doses total)
PF-04360365 3 mg/kg: Experimental
Intervention: Biological: PF-04360365 3 mg/kg
Biological: PF-04360365 3 mg/kg
3 mg/kg every 60 days (10 doses total)
PF-04360365 8.5 mg/kg: Experimental
Intervention: Biological: PF-04360365 8.5 mg/kg
Biological: PF-04360365 8.5 mg/kg
8.5 mg/kg every 60 days (10 doses total)
Eligibility
Ages Eligible for Study: 50 Years and older
Genders Eligible for Study: Both
Accepts Healthy Volunteers: No
Criteria
Inclusion Criteria:
Males or females of non childbearing potential, age > or = 50
Diagnosis of probable Alzheimer's disease, consistent with criterial from both:
National Institute of Neurological and Communicable Disease and Stroke and Alzheimer's Disease and Related Disorders Association (NINCDS-ADRDA)
Diagnostic and Statistical Manual of Mental Disorders (DSM IV)
Mini-mental status exam score of 16-26 inclusive
Rosen-Modified Hachinski Ischemia Score of < or = 4
Exclusion Criteria:
Diagnosis or history of other demential or neurodegenerative disorders
Diagnosis or history of clinically significant cerebrovascular disease
Specific findings on magnetic resonance imaging (MRI); cortical infarct, micro hemorrhage, multiple white matter lacunes, extensive white matter abnormalities
History of autoimmune disorders
History of allergic or anaphylactic reactions
Contacts and Locations
Please refer to this study by its ClinicalTrials.gov identifier: NCT00722046
Show 38 Study Locations
Sponsors and Collaborators
Pfizer
Investigators
Study Director: Pfizer CT.gov Call Center Pfizer
More Information
Additional Information:
To obtain contact information for a study center near you, click here. This link exits the ClinicalTrials.gov site
No publications provided
Responsible Party: Pfizer, Inc. ( Director, Clinical Trial Disclosure Group )
ClinicalTrials.gov Identifier: NCT00722046 History of Changes
Other Study ID Numbers: A9951002
Study First Received: July 23, 2008
Last Updated: June 2, 2011
Health Authority: United States: Food and Drug Administration
Keywords provided by Pfizer:
Alzheimer's disease
antibody
amyloid
Additional relevant MeSH terms:
Alzheimer Disease
Dementia
Brain Diseases
Central Nervous System Diseases
Nervous System Diseases
Tauopathies
Neurodegenerative Diseases
Delirium, Dementia, Amnestic, Cognitive Disorders
Mental Disorders
ClinicalTrials.gov processed this record on June 21, 2011
About one month ago.
SNRS? Samsung NC215S solar netbook will see the light of day in Russia
http://www.engadget.com/2011/06/20/samsung-nc215s-solar-netbook-will-see-the-light-of-day-in-russia/
Good video on Alzheimers was on HBO 55 min long
http://www.hbo.com/alzheimers/momentum-in-science.html
JNJ expects to file for Bapineuzumab
http://files.shareholder.com/downloads/JNJ/970343200x0x470990/69eca2f4-6abb-421c-96e3-05c9dcc85cfa/jnj_manji_neuro.pdf
Wow I did not know this. Traditional wired headsets act like an antenna and carry RF Energy and EMF’s emitted from a cell phone through the wire into the user’s ear/head, thus exposing the inner ear and brain to RF Energy and EMF’s.
TECHNOLOGY
AIRCOM TECHNOLOGY is a patented sound delivery process utilizing an airtube to produce “Live” sound with no interference.
Sound Quality: A natural and balanced “Live” effect delivering the true sound of the performer’s music. Traditional wired headsets lack the natural body of sound but Aircom headsets deliver music that you can feel,
not just hear. Although digital is the new technology, your music doesn’t have to be limited to it; with Aircom, music comes alive as if you’re front row at a concert.
Interference Free: Using air as the delivery mechanism Aircom technology protects the user’s ears, eyes, and brain from any direct contact with interferences such as RF Energy and EMF’s. Lab tests show the RF3 headsets have a SAR level of 0*. Many studies have shown that RF Energy and EMF’s are not completely safe and extended exposure to any one of them could be harmful, especially to younger people and children.
Traditional wired headsets act like an antenna and carry RF Energy and EMF’s emitted from a cell phone through the wire into the user’s ear/head, thus exposing the inner ear and brain to RF Energy and EMF’s. Bluetooth headsets constantly emit RF Energy and EMF’s, even when not in use because it must maintain a connection with the phone.
Only Aircom equipped headsets eliminate exposure to RF Energy, EMF’s and has a SAR level of 0*.
1000 to 1 would leave 34.5 million shares.
Who were those 17? Link please.
news out go to yahoo
I think this is GSK's drug lincenced from ILNS? 933776 beta amyloid monoclonal antibody Alzheimer’s disease.
http://clinicaltrials.gov/ct2/show/NCT00459550
http://clinicaltrials.gov/ct2/show/NCT01342926?term=GSK933776&rank=2
Costco is selling a solar charger. I hope SNRS is not too late to the party??
http://www.costco.com/Browse/Product.aspx?Prodid=11467546&whse=bc&Ne=4000000&eCat=bc|90607&N=4047282&Mo=35&No=5&Nr=P_CatalogName:BC&cat=82&Ns=P_Price|1||P_SignDesc1&lang=en-US&Sp=C
http://www.xpal.ru/prod2_1.htm