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A shorter bought the shares back that's the reason for the volume, IMO
I have to agree, that's so true! First, tencoin is a german and he know's nothing.... well I'm an Austrian but I am not interested to pump the stock.
I guess the trial will be encouraging and buying is a good choice - we will see. IMO, I see a big future for ILNS, all is possible!
GLTA
Estimated Primary Completion Date:July 2015 (Final data collection date for primary outcome measure)
Post must be < 48 hours old
Intellect Neurosciences Common Stock Approved for Trading on OTCQB
Company Initiates Collaboration With Harvard Medical School to Undertake Further Studies With TauC3 Monoclonal Antibody Targeting a Secreted Form of Tau Protein
ENGLEWOOOD CLIFFS, NJ--(Marketwired - April 15, 2015) - Intellect Neurosciences, Inc. (OTCQB: ILNS) a biopharmaceutical company engaged in the discovery and development of disease-modifying therapeutic and diagnostic agents for the treatment of Alzheimer's and other neurological diseases, today announced that its securities have been designated as trading on the OTCQB marketplace. Intellect has satisfactorily passed the requirements for eligibility, which include up to date reporting to the SEC, a minimum bid price test of one penny and an annual verification and management certification process providing additional information about the company's insiders, advisors and share count. As a result of the designation, among other things, Intellect investors will enjoy greater information availability through news and disclosure posted through the OTC Disclosure & News Service and transparent prices through full-depth of book with Real Time Level 2 quotes.
Recently, the Company announced that it has initiated a sponsored research collaboration with one of the foremost Alzheimer's disease research centers in the United States. The sponsored research collaboration is under the direction of Professor Bradley T. Hyman MD, PhD, Director, Massachusetts Alzheimer's Disease Research Center & Co-Director, Massachusetts General Hospital Memory Disorders Unit & John B. Penney Jr. Professor of Neurology, Harvard Medical School. The research is designed to examine the detailed molecular mechanism affecting propagation of tau pathology aimed at developing a novel treatment for Alzheimer's disease and other tauopathies.
Dr. Hyman is the Director of the Massachusetts Alzheimer's Disease Research Center. He directs the Alzheimer's disease research unit at the MassGeneral Institute for Neurodegenerative Disease (www.mghmind.org), with the goal of understanding the neuropathophysiologic and genetic factors that underlie dementia. His laboratory studies the anatomical and molecular basis of dementia in Alzheimer's disease and dementia with Lewy bodies. Dr. Hyman is the recipient of numerous awards in the field of Alzheimer's and related diseases, including the Metropolitan Life Award, the Potamkin Prize, a National Institute on Aging MERIT award, and an Alzheimer Association Pioneer Award.
"I am extremely proud that Intellect's common stock is trading on the OTCQB, a confirmation that our strategic plan of advancing our core programs and restructuring our capitalization is strengthening the company. The collaboration with Professor Hyman, the next step in development of our TauC3 program, should yield important new mechanistic insights that will attract interest from potential pharmaceutical partners," said Mr. Elliot Maza, Chairman and Chief Executive Officer of Intellect Neurosciences.
Safe Harbor Statements Regarding Forward Looking Statements
http://investorshub.advfn.com/boards/read_msg.aspx?message_id=112780626
post #17920
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post #17918
Tau-Associated MAPT Gene Increases Risk for Alzheimer’s Disease
17/02/2015 20:39:00
Finding could improve dementia diagnosis and treatment
Microscopic image depicting plaques and tangles characteristic of Alzheimer’s disease. Image courtesy of Tom Deerinck, NCMIR, UC San Diego.
An international team of scientists, led by researchers at the University of California, San Diego School of Medicine, has identified the microtubule-associated protein tau (MAPT) gene as increasing the risk for developing Alzheimer’s disease (AD). The MAPT gene encodes the tau protein, which is involved with a number of neurodegenerative disorders, including Parkinson’s disease (PD) and AD. These findings provide novel insight into Alzheimer’s neurodegeneration, possibly opening the door for improved clinical diagnosis and treatment.
The findings are published in the February 18 online issue of Molecular Psychiatry.
Alzheimer’s disease, which afflicts an estimated 5 million Americans, is typically characterized by progressive decline in cognitive skills, such as memory and language and behavioral changes. While some recent AD genome-wide association studies (GWAS), which search the entire human genome for small variations, have suggested that MAPT is associated with increased risk for AD, other studies have found no association. In comparison, a number of studies have found a strong association between MAPT and other neurodegenerative disorders, such as PD.
“Though a tremendous amount of work has been conducted showing the involvement of the tau protein in Alzheimer’s disease, the role of the tau-associated MAPT gene is still unclear,” said Rahul S. Desikan, MD, PhD, research fellow and radiology resident at the UC San Diego School of Medicine and the study’s first author.
In the new Molecular Psychiatry paper, conducted with collaborators across the country and world, Desikan and colleagues narrowed their search. Rather than looking at all possible loci (specific gene locations), the authors only focused on loci associated with PD and assessed whether these loci were also associated with AD, thus increasing their statistical power for AD gene discovery.
By using this approach, they found that carriers of the deleterious MAPT allele (an alternative form of the gene) are at increased risk for developing AD and more likely to experience increased brain atrophy than non-carriers.
"This study demonstrates that tau deposits in the brains of Alzheimer's disease subjects are not just a consequence of the disease, but actually contribute to development and progression of the disease," said Gerard Schellenberg, PhD, professor of pathology and laboratory medicine at the University of Pennsylvania, principal investigator of the Alzheimer’s Disease Genetics Consortium and a study co-author.
“An important aspect was the collaborative nature of this work. Thanks to our collaborators from the Consortium, the International Parkinson’s Disease Genetics Consortium, the Genetic and Environmental Risk in Alzheimer’s Disease, the Cohorts for Heart and Aging Research in Genomic Epidemiology, deCODE Genetics and the DemGene cohort, we had tremendous access to a large number of Alzheimer’s and Parkinson’s genetic datasets that we could use to identify and replicate our MAPT finding,” said Ole A. Andreassen, MD, PhD, professor of biological psychiatry at the University of Oslo and a senior co-author.
Sudha Seshadri, MD, professor of neurology at the Boston University School of Medicine, the principal investigator of the Neurology Working Group within the Cohorts for Heart and Aging Research in Genomic Epidemiology consortium and a study co-author added: “Although it has been known since Alois Alzheimer’s time that both plaques (with amyloid) and tangles (of tau) are key features of Alzheimer pathology, attempts to prevent or slow down clinical disease progression have focused on the amyloid pathway. Until this year no one had convincingly shown that the MAPT (tau) gene altered the risk of AD and this, combined with the greater ease of imaging amyloid in life, lead some researchers to postulate that tau changes were secondary to amyloid changes. The recent association of genetic variation in the MAPT gene with AD risk and the emerging availability of tau imaging are now leading to a recognition that perhaps tau changes are key in the pathophysiologic pathway of AD and this pathway should be more intensively targeted.”
These findings underscore the importance of using a multi-modal and multi-disciplinary approach to evaluating Alzheimer’s neurodegeneration.
“These findings suggest that the combination of genetic, molecular and neuroimaging measures may be additionally helpful for detecting and quantifying the biochemical effects of therapeutic interventions,” said Anders M. Dale, PhD, professor of neurosciences and radiology and director of the Center for Translational Imaging and Precision Medicine at UC San Diego and the study’s senior author.
Co-authors include Andrew J. Schork, Linda K. McEvoy, Dominic Holland, James B. Brewer, Chi-Hua Chen, Wesley K. Thompson, UCSD; Yunpeng Wang, UCSD and Oslo University Hospital; Aree Witoelar, Ingun Dina Ulstein, Srdjan Djurovic, Oslo University Hospital, Norway; Manu Sharma, Thomas Gasser, University of Tubingen, Germany; Denise Harold, Julie Williams, Michael J. Owen, Michael C. O’Donovan, Cardiff University School of Medicine, Wales; Margaret A. Pericak-Vance, University of Miami; Richard Mayeux, Columbia University; Jonathan L. Haines, Vanderbilt University; Lindsay A. Farrer, Boston University Schools of Medicine and Public Health; Peter Heutink, German Center for Neurodegenerative Diseases; Andrew B. Singleton, Lenore Launer, National Institute on Aging; Alexis Brice, Sorbonne University; Nicolas Wood, John Hardy, University College London; Maria Martinez, INSERM; Seung Hoi Choi, Anita DeStefano, Boston University; M. Arfan Ikram, Cornelia van Juijn, Erasmus MC University Medical Center; Joshua C. Bis, Annette L. Fitzpatrick, University of Washington; Albert Smith, Icelandic Heart Association; Dag Aarsland, Karolinska Institute, Sweden; Tormod Fladby, Akershus University Hospital, Norway; Bradley T. Hyman, Massachusetts General Hospital; Jon Snaedal, University Hospital Reykjavik, Iceland; and Hreinn Stefanson, Kari Stefanson, University of Iceland.
Funding for this research came, in part, the National Institutes of Health (grants R01AG031224, K01AG029218, K02NS067427, T32 EB005970, UO1AG032984, U24-AG041689, and R01 MH100351), the Research Council of Norway, the South East Norway Health Authority, the Norwegian Health Association and the KG Jebsen Foundation.
http://www.healthcanal.com/brain-nerves/brain-diseases/alzheimer%E2%80%99s/60322-tau-associated-mapt-gene-increases-risk-for-alzheimer%E2%80%99s-disease.html
Invenux -Xickle and Nicosan alias Xickle Rbc Plus alias SCD-101 in clinical trial
https://clinicaltrials.gov/ct2/show/NCT02380079
Estimated study completion date for OX1 is April
https://clinicaltrials.gov/ct2/show/NCT01898884?term=viropharma&rank=7
Good point, thanks for sharing
solanezumab back in trials
Yes, and clinicaltrials.gov was updated on the same day
Mr. Maza
Current Trademark Status: OXIGON
1/16/2015
CANCELLED - SECTION 8
http://www.trademarkia.com/oxigon-78108979.html
Section 8 Requirements
For Trademark Registrations
Any registrant who files in the Patent and Trademark Office, on or
after November 16, 1989, an affidavit or declaration under Section 8 of
the Trademark Act will be required to comply with the requirements of
the Trademark Law Revision Act of 1988 [Title 1 of Pub. L. 100-667, 102
Stat. 3935 (15 U. S. C. 1051)], which takes effect on November 16, 1989.
The Trademark Law Revision Act amends 15 U. S. C. 1058(a) by adding the
requirement that a registrant submit an affidavit "setting forth those
goods or services recited in the registration on or in connection with
which the mark is in use in commerce and attaching to the affidavit a
specimen or facsimile showing current use of the mark...."
For Section 8 affidavits or declarations filed on or after November
16, 1989, the Patent and Trademark Office will require registrants to
specify the goods and services to which the Section 8 affidavit or
declaration pertains. The registrant may comply with the requirement for
specification of its goods and services by listing each of the goods and
services to which the Section 8 affidavit or declaration pertains or by
making an all-encompassing reference to the goods and services recited
in the registration (e.g., "The mark is in use in connection with all
the goods and services recited in the registration." or The mark is in
use in connection with all the goods and services recited in the
registration, with the exception of ...". The Patent and Trademark
Office prefers that the registrant use an all-encompassing reference to
its goods and services as the method of specification, especiallly where
the mark is registered for numerous goods and services.
If the registrant fails to file, before the end of the sixth year
following registration, a Section 8 affidavit or declaration that sets
forth goods and services in connection with which the mark is in use,
the registration will be cancelled. Similarly, those goods or services
recited in the registration but not specified in a Section 8 affidavit
or declaration filed before the end of the sixth year following
registration will be deleted from the registration. After the end of the
sixth year following registration, the Patent and Trademark Office will
not accept a substitute Section 8 affidavit or declaration filed to
correct registrant's failure to specify, or to specify completely, the
goods and services on or in connection with which the mark is in use.
A Section 8 affidavit or declaration filed on or after November 16,
1989 must include a specimen or facsimile showing current use of the
registered mark. The registrant will be required to file one specimen or
facsimile for each class of goods or services to which the registration
pertains. For a single-class registration covering multiple goods or
services, only one specimen or facsimile showing current use of the mark
on one of the goods or services in that class will be required.
Similarly, for a multiple-class registration, the registrant will be
required to file, for each class of goods or services covered by the
multiple-class registration, one specimen or facsimile showing current
use of the mark on one of the goods or services in that class.
If the registrant fails to file, before the end of the sixth year
following registration, an affidavit or declaration that includes a
proper specimen or facsimile for each class of goods or services to
which the registration pertains, the registration will be cancelled as
to that class of goods or services. After the end of the sixth year
following registration, the Patent and Trademark Office will not accept
a substitute Section 8 affidavit or declaration filed to correct the
omission of a proper specimen or facsimile.
June 15, 1989 Jeffery M. Samuels
Assistant Commissioner for Trademarks
http://www.uspto.gov/web/offices/com/sol/og/con/files/cons166.htm
For example, I-3-PA has been shown to be involved in neuronal damage and oxidative stress in the brain.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3893491/?report=classic
I have no idea!
ASK $1.5
LoL, bought via prison I-phone
900% up from .50 to 5 bucks
http://finance.yahoo.com/q?s=ilnsd&ql=1
yes it is, the extraction process was modified by a different ph only
Explanation:
The first arm of shp622 was done in spring 2014. (1b from my perspective)
A letter to shareholders from Maza about OX1 in summer and a sec filling.
Shire went from a phase 1 to a phase 1/2.
And now a review....
Please read the dsmb procedure in positive and negative way
Thank you Jumpy, expecting positive news if your informations are correct.
About VP20629
VP 20629 (OX1 or indole-3-propionic acid (IPA)), is a naturally occurring, small molecule that has potentanti-oxidant properties that can protect against neurodegenerative disease. ViroPharma acquired this technology from Intellect Neurosciences, Inc. in September 2011.
About Friedreich’s Ataxia
Friedreich's Ataxia (FA) is a rare hereditary disease caused by a mutation in a gene which encodes frataxin, a protein essential for proper functioning of mitochondria, the energy pumps of the cell. In the absence of frataxin, iron in the cytoplasm builds up and causes free radical damage.
The disease causes progressive damage to the nervous system, resulting in symptoms ranging from gait disturbance to speech problems; it can also lead to heart disease and diabetes. Ataxia in general refers to the inability to coordinate voluntary muscular movements. The ataxia of Friedreich's ataxia results from the degeneration of nerve tissue in the spinal cord, in particular neurons essential for directing muscle movement of the arms and legs. The spinal cord becomes thinner and nerve cells lose some of their myelin sheath. The primary sites of pathology are the spinal cord and peripheral nerves. Symptoms typically begin sometime between the ages of 5 and 15 years, but may occur in patients between the ages of 20 to 30. The disease usually presents with progressive staggering or stumbling and frequent falling. The symptoms are slow and progressive with a median age of death at 37 years old. Friedreich’s Ataxia is the most common form of hereditary ataxia, and is thought to affect about 1 in every 50,000 people or approximately 6,000 patients in the United States. Currently there are no drugs approved in the United States for FA.
Status
ViroPharma has completed Phase 2-enabling toxicology studies with VP 20629, and has initiated Phase 1b testing in patients with Friedreich's ataxia.
http://www.viropharma.it/~/~/~/link.aspx?_id=0F8E81DC6AA34A079050C7C713FD3C21&_z=z
Where is our chart guru?
I am expecting
.... to the moon ....
f$$$ that's not enough!
Absolute true, that should be the strategy. imo
IMO, Maza is waiting for an update (milestone payment) from Shire.
Next step is the reverse split, fresh money and maybe a merger.
Immune is a company with an amazing pipeline, so it would make sense.
ALLIMO
Will we see a Imnp/Ilns merger after cocrystal/biozone?
http://m.seekingalpha.com/article/2836986-many-reasons-to-like-immune-pharma
Our CEO and Immune Pharmaceuticals:
"Additionally, the Board appointed Mr. Elliot Maza , JD, CPA (inactive) as an independent director and Chairman of the Audit Committee"
http://www.twst.com/update/95339-immune-pharmaceuticals-inc-immune-pharmaceuticals-appoints-gad-berdugo-as-chief-financial-officer-and-dr-cameron-durrant-as-lead-independent-director
http://immunepharmaceuticals.com/about-us/board-of-directors/
I guess if the shire trial result is encouraging then they will seek a fast track designation ASAP.
Expecting news in general soon.
GLTA
ILNS PIPELINE UPDATE
Our current focus is to establish proof of concept for TauC3, a therapeutic monoclonal antibody licensed by Intellect from Northwestern University on an exclusive basis, targeting a truncated form of tau protein. We believe that this truncated protein is a key driver of neurodegeneration in tauopathies, which causes irreversible damage to nerve cells and propagates pathology throughout the brain.
Several groups have observed that amyloid beta accumulation and tau itself, under certain circumstances, can activate enzymes known as “caspases” and that caspase-cleaved tau (TauC3, aka delta tau) may have biological properties that could compromise neurons (Guillozet-Bongaarts et al., 2005, Stoothoff et al., 2009, de Calignon et al., 2012, Plouffe et al., 2012; Lee et al.., 2012). For example, it has been demonstrated that TauC3 is a likely precursor for neurofibrillary tangles. More recently, it was suggested that tau (or potentially a misfolded or post-translationally modified tau) can be released from neurons, be taken up by other neurons, and act as a nidus for a new tangle – i.e. leading to “propagation” of tau species across neuronal pathways Fulga et al., 2007, Quintanillaet al., 2012, Yanamandra et al., 2013). Tau C3, along with hyperphosphorylated forms, appears to be preferentially secreted and to enhance misfolding and aggregation. Because misfolding and secretion are two prerequisites for uptake and propagation, we hypothesize that TauC3 may be a potent agent in terms of propagation of tau pathology from one neuron to the next.
In 2011, we filed a patent claiming therapeutic potential of antibodies targeting truncated forms of tau. In 2012, we licensed a TauC3 antibody from Northwestern University, acquiring exclusive global development and commercialization rights to the TauC3 antibody.
In January 2014, we announced top line data showing proof of concept in a preclinical Alzheimer's model indicating the antibody’s potential to be disease modifying. The study was conducted in collaboration with University of California, Irvine's Dr. Frank LaFerla, Chancellor's Professor and Chair, Neurobiology and Behavior School of Biological Sciences, Director, Institute for Memory Impairments and Neurological Disorders. The data showed that the TauC3 antibody effectively engaged the target and reduced certain phosphorylated pathological forms of Tau, indicating that the treatment with the peripherally administered antibody had an effect in the brain and is potentially disease modifying.
We have developed a detailed plan to corroborate these preliminary findings in additional models. This work will be outsourced to specialist contract research organizations and will involve collaboration with a leading AD investigator who has developed sophisticated models that are particularly well suited to test the TauC3 antibody.
http://www.intellectns.com/internal-pipeline
It is time for PR Mr. Maza!
Interresting, Cerespir expands its team and yes a merger with Cerespir would be nice
http://www.cerespir.com/cerespir-incorporated-appoints-eric-karran-ph-d-as-chairman-of-its-scientific-advisory-board/
A happy new year to all long term investors!
Greetings from Austria
I have to agree and it took about ten years of development to start a clinical trial