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Troy Rohn about Alzheimer
http://theconversation.com/early-onset-alzheimers-should-you-worry-61845
What's about TOC-1 Mr. Maza?
Mr. Maza polished the ILNS website before the conference, IMO
Wax on Wax off
Iron is a catalyst in lipid peroxidation, IMO
Preventing this increase in lipid peroxidation, in neurons, protects against in cell death. This work describes the pathophysiological properties of the mitochondria in neurons from a FRDA mouse model and shows that lipid peroxidation could be an important target for novel therapeutic strategies in FRDA, which still lacks a cure.
http://www.ncbi.nlm.nih.gov/pubmed/27228352
..the fly pisst off and the sky was her limit?
Shire plc (LSE: SHP, NASDAQ: SHPG) announces that Jeff Poulton, Chief Financial Officer, will present at the Goldman Sachs 37th Annual Global Healthcare Conference on June 8, 2016 at 10:40 a.m. PDT (6:40 p.m. BST) and Perry Sternberg, Head of Neuroscience and Commercial Excellence will present at the Jefferies 2016 Healthcare Conference on June 9, 2016 at 11:30 a.m. EDT (4:30 p.m. BST).
http://finance.yahoo.com/news/shire-participate-two-upcoming-investor-120000556.html
Nice said, thanks
Thanks for that but much more interesting is Target Diseases and Shp622. I guess Shire will find the optimal pathway with Shp622 in FA and Wilson's disease :)
http://www.intellectns.com/pipeline/target-diseases
"Target Diseases
SHP622
Friedreich’s Ataxia
The following description of Friedreich’s ataxia (FA) may be found on the website of FARA, the Friedreich’s Ataxia Research Alliance, at wwww.curefa.org.
Friedreich’s ataxia (FA) is a debilitating, life-shortening, degenerative neuro-muscular disorder. Patients suffer progressive degeneration of the central and peripheral nervous systems, which causes impaired motion and gait; diminished vision, hearing and speech; loss of strength and coordination, leading to wheelchair use; increased risk of diabetes; and life-threatening heart complications. About one in 50,000 people in the United States have Friedreich's ataxia.
Most individuals have onset of symptoms of FA between the ages of 5 and 18 years. Adult or late onset FA is less common, <25% of diagnosed individuals, and can occur anytime during adulthood.
FA is an inherited or single gene disorder. Mutations or DNA changes in the FXN gene cause FA.
FA in inherited in an autosomal recessive manner, meaning that individuals with FA have two mutated or abnormal copies of the FXN gene, this means both biological parents must be a carrier of the disease for a child to be affected. It is estimated that 1 in 100 people are carriers, and carriers do not exhibit symptoms of FA. Each such carrier parent has one mutated gene (allele) and one normal gene (allele) in the FXN gene. Because each child gets one of the mother’s genes and one of the father’s genes in this location, there are four possible combinations of the genes passed down to the child or a 25% chance that the child will have FA.
The FA gene mutation limits the production of a protein called frataxin, which is known to be an important protein that functions in the mitochondria (the energy producing factories) of the cell. Frataxin helps to move iron and is involved with the formation of iron-sulfur clusters, which are necessary components in the function of the mitochondria and thus energy production. We also know that specific nerve cells (neurons) degenerate in people with FA, and this is directly manifested in the symptoms of the disease.
Shire is developing SHP622 as a treatment for FA on the basis that SHP622’s radical scavenging activity and metal chelation properties counteract the excess amount of iron in the mitochondria and free radicals in the bodies of FA patients.
There is no FDA approved treatment for FA; at typical orphan drug prices, FA represents a target market with worldwide peak year sales of ~ $1B ($440M-$770M in US and EU alone).
Penetration of the FA market should be rapid because of the significant unmet medical need and lack of competition.
Wilson’s Disease
Wilson’s Disease (WD) is a rare, hereditary, metabolic disorder that causes the body to retain copper, which can be toxic to bodily tissue. WD is caused by a defect in an enzyme that enables the liver to excrete ingested copper from the body. The liver fails to release copper into bile, leading to accumulation in the liver, brain and eyes. Left untreated, WD causes severe brain damage, liver failure and death.
Neurological symptoms typically begin in the second or third decade of life and include dystonia and Parkinsonism and hepatic damage, leading to inflammation, advancing fibrosis, cirrhosis, and liver failure.
Current treatment options for patients with WD include medical therapy and liver transplantation; metal chelators for copper and zinc have been shown to be effective in treating WD but tend to generate adverse effects.
WD affects an estimated 30,000 - 40,000 people worldwide with approximately 9,000 affected patients in the United States; at typical orphan drug prices, WDrepresents a target market with worldwide peak year sales of ~ $1B.
SHP622’s free radical scavenging activity and metal chelation properties counteract the excess amount of copper in the mitochondria and potential for oxidative stress in WD patients, thus suggesting that SHP622 would be an especially viable therapeutic agent for WD.
Anti-TauC3 Monoclonal Antibody
Progressive Supranuclear Palsy
Progressive Supranuclear Palsy (PSP) is a progressive brain disorder that resembles Parkinson’s disease. PSP affects movement, control of walking (gait) and balance, speech, swallowing, vision, mood and behavior, and thinking. Classic signs of the disease are an inability to aim and move the eyes properly and blurring of vision. Symptoms begin on average after age 60 and men are affected more often than women. It is estimated that PSP affects 6 in 100,000 Americans; Incidence 2.8 per 100,000.
The exact cause of PSP is unknown. The symptoms of PSP are caused by a gradual deterioration of brain cells in specific areas in the brain, mainly in the region called the brain stem. The hallmark of the disease, and a possible cause, is the accumulation of abnormal deposits of tau and eventual toxicity in nerve cells in the brain stem. These findings suggest that the use of tau antibody therapeutics, such as such as our anti-TauC3 monoclonal antibody, may be a viable treatment approach.
There is no FDA approved treatment for PSP. No medication is effective in halting the progression of the disease; however, several medications, including dopamine agonists, tricyclic antidepressants, and methysergide, may provide modest symptomatic improvement.
Drugs in development for PSP include: BMS-968168 (Bristol-Myers Squibb) and ABBV-8E12 (AbbVie) both of which are anti-tau antibodies in Phase 1; and several drugs in preclinical stage development.
Traumatic Brain Injury
Traumatic Brain Injury (TBI) is a form of acquired brain injury, which occurs when a sudden trauma causes damage to the brain. Sports-related concussion, which includes chronic traumatic encephalopathy (CTE) is caused by direct impact forces to the head; blast-induced TBI is caused by exposure to blast shock waves.
TBI results from secondary neuronal damage caused by the impact, which leads to progressive neuronal cell death, neural loss, and axonal degeneration in the brain. Symptoms of TBI can be mild, moderate, or severe, depending on the extent of the brain damage. Patients suffer headache, light-headedness, memory loss, confusion, attention deficits, difficulty balancing, aggression, anxiety, depression, etc.
The CDC estimates that TBI affects approximately 1.7 million Americans each year, including approximately 270,000 NFL players and 200,000 war veterans.
There is no FDA approved treatment for TBI; moderately to severely injured patients receive rehabilitation that involves treatment programs in physical therapy, occupational therapy, speech/language therapy, physical medicine, psychology/psychiatry, and social support.
A common feature of TBI related diseases is deposition of the tau protein around cerebral blood vessels in the frontal cortex of the brain. Studies have indicated that military personnel who reported three or more traumatic brain injuries showed high total tau protein concentrations in plasma, in some cases long after the injuries had occurred. These findings are consistent with reports for repetitive head injury in athletes linked to progressive tauopathy, axonal injury and post-concussive disorder symptoms. These findings suggest that the use of tau antibody therapeutics, such as our anti-TauC3 monoclonal antibody, may be a viable treatment approach.
CONJUMAB-A
Age-Related Macular Degeneration
Age-Related Macular Degeneration (AMD) is the leading cause of blindness in elderly people. The global market for AMD is estimated at $4 billion annually.
There are two types of AMD: Wet AMD, characterized by new blood vessel formation; and Dry AMD, with precursor characterized by drusen and atrophic loss of retinal pigment epithelium.
Dry AMD is a large potential market. Approximately 80 percent of patients with AMD have the dry form. Central loss of the macula and underlying retinal pigment epithelium, termed GA, is considered the most severe form of Dry AMD and is responsible for over 20 percent of all cases of legal blindness in North America. There is no approved treatment existing today for Dry AMD.
Evidence from preclinical studies on retinal degeneration demonstrate that combining treatments targeting different components of the amyloid beta formation and aggregation pathway is more effective than monotherapy, indicating that CONJUMAB-A may be an effective treatment agent for Dry AMD."
And there was and is a lot of interest from top tier pharmaceutical companies regarding CONJUMAB, what I know.
ALLIMO, if you think about CONJUMAB and their preclinical status you have to invest a lot of CHF to finish the R&D and go forward with LONZA which is the global leader in ADC business. I guess it is a double digit MM deal with LONZA to finish the program. For me that says it all, there must be a big deal behind the systematic course of action! ALLIMO again!
montanus
April 12, 2016 - Agreement replacement to use 82E1 (aka IN-N01, targets the N-terminus) as a antibody drug conjugate to treat AMD.
http://www.ibl-japan.co.jp/direct/topics/topics_pdf_download/topics_id=4604&disp=inline&_lang=en
From my perspective pps is a gift at the moment if you have the knowledge to understand where ILNS stands at the moment.
That's nonsense not more
Well, normally Mr. Maza is interested in cash only, it's not usual to hold a position in stock shares for him what I know and all insiders invested again. Something big will happen this time
I haven't seen any results and you didn't either, shp622 is save and the rest is strategy
I have to agree and it's insane to sell shares after what happened.
Can't spend a lot of time for a discussion today but the Ilns community is in good hands with you
There is no clinical difference based on primary outcome, that's positive!
The drug is save and no other results were published! Read the primary outcome of shp622 and you would know what Shire was trying to tell!
Pfizer bought Angiosyn a tiny Eye diseases firm for $527M with a preclinical drug in 2005
http://www.healio.com/ophthalmology/ophthalmic-business/news/print/ocular-surgery-news/%7B3a0fa140-b996-4f90-8099-dad1353fd068%7D/pfizer-to-buy-firm-developing-amd-product
http://www.prnewswire.com/news-releases/angiosyn-acquired-by-pfizer-54078897.html
I know about that and Blech was the Seed Investor and Chain is a genius, Maza is a talent in his bright wide business but it's about the preferred numbers, results and success in the real world!
Hey Deals
it's hard to say but there was a good reason to reinitialize conjumab program for AMD. I guess
there is some substantial interest from pharmaceutical industry, especially PFE, or ILNS has a partner, license agreement, or a possible buyer for ANTISENILIN and CONJUMAB in a package already. PFE spend billions based on ANTISENILIN, maybe I am wrong but they want the science and the patents.
ALLIMO
I want to show that there is a high interest regarding AMD and anti amiloyd technology.
Don't think there is an ilns gsk license agreement for gsk933776.
Pfe stopped ponezumab and rn6g and Ilns restarted conjumab for amd, all other is speculation at the moment.
GSK completed GSK933776 (anti Aß peptide, n-terminus ) AMD phase 2 trial last month.
Enrolment: 190
https://clinicaltrials.gov/ct2/show/NCT01342926?term=gsk933776&rank=4
RN6g phase 2 trial results have been removed from public view
https://www.clinicaltrialsregister.eu/ctr-search/search?query=rn6g
PFE/RINAT (RN6G) and AMD
"Pfizer is committed to developing novel therapies that improve the lives of patients with ophthalmic diseases. Our in-line medicines in this area include Xalatan® (latanoprost ophthalmic solution), Xalacom® (latanoprost and timolol), and Macugen® (pegaptanib injection). Within Pfizer an Ophthalmology forum exists to align several research units under WRD leadership. WRD established the Ophthalmology External Research Unit (OERU) to lead this effort. The OERU utilizes a virtual biotech model to build its portfolio through shared-risk partnerships leveraging the combined scientific, development, and commercial expertise of Pfizer and its partners. The OERU's alliance with Lpath, Inc. to develop and commercialize iSONEP®, which is being evaluated for the treatment of wet age-related macular degeneration and other ophthalmology disorders, is an excellent example of this innovative collaborative approach. The other units focusing on Ophthalmology within WRD are Rinat and Neusentis. Rinat focuses on a monoclonal antibody approach for the treatment of ophthalmic disease. Within this unit RN6G, a monoclonal antibody targeting amyloid beta peptides, is being tested in a clinical trial for use in dry AMD and Geographic Atrophy. The Neusentis unit within WRD is at the forefront of stem cell technology and is studying its use for wet AMD."
http://www.pfizer.com/partnering/areas_of_interest/ophthalmology
Last RN6G study was terminated in feb. 2016 and ILNS restarted (March 30, 2016) their CONJUMAB AMD programm after that, very interesting!
https://clinicaltrials.gov/ct2/show/NCT01577381?term=rn6g&rank=3
http://www.marketwired.com/press-release/intellect-neurosciences-inc-engages-benjamin-d-freilich-md-facs-as-senior-medical-affairs-otcqb-ilns-2110268.htm
About conjumab:
"Our lead program, CONJUMAB-A, offers an important advantage to the Aß antibodies currently in clinical development for both AD and AMD by several large pharmaceutical companies. This is because those antibodies (e.g. solanezumab, bapineuzumab, gantenerumab, crenzeumab, RN6G and GSK33766A) are designed for a single purpose, namely to clear Aß, while none act on the important secondary neurotoxic mechanisms, such as oxidative stress that causes most of the damage from Aß. By contrast, CONJUMAB-A is empowered with a potent antioxidant. An important step in establishing proof-of-principle was the initial data generated through our collaboration with iNovacia to evaluate compounds synthesized by Lonza for Intellect. The data demonstrated the conjugation of the antioxidant molecule to an amino acid does not reduce its antioxidant activity. Pending adequate financial resources, these studies, which are almost complete, will allow us to select a drug candidate to take into development, providing the trigger for us to move forward with LONZA into an expanded manufacturing project, bringing us closer to the submission of an Investigational New Drug application."
https://globenewswire.com/news-release/2013/02/13/523315/10021734/en/Intellect-Neurosciences-Issues-Letter-to-Shareholders.html
That's correct and we will get the results sooner or later, it's a waiting game.
About Disorders Caused by Oxidative Stress
http://www.oxidativestressresource.org/
SHP622 - trial outcome:
Primary Outcome Measures:
Incidence of adverse events and clinically relevant changes in safety laboratory testing, vital signs, and 12-lead electrocardiograms [ Time Frame: 10 days (single-dose groups) or 17 days (multiple-dose groups) ] [ Designated as safety issue: Yes ]
Secondary Outcome Measures:
Pharmacokinetic parameters (e.g., Cmax, Tmax, AUC, t1/2) [ Time Frame: 3 days (single-dose groups) or 10 days (multiple-dose groups) ] [ Designated as safety issue: No ]
Blood and urine samples will be collected to assess the pharmacokinetics of VP 20629 and a potential metabolite in plasma and urine after single and multiple doses of VP 20629.
Other Outcome Measures:
Pharmacodynamic parameters [ Time Frame: 10 days (multiple-dose groups only) ] [ Designated as safety issue: No ]
Blood and urine samples will be collected to measure biomarkers of oxidative stress and damage in the multiple-dose groups. These markers are plasma 8-isoprostane and malondialdehyde and urinary 8-hydroxydeoxyguanosine.
https://clinicaltrials.gov/ct2/show/NCT01898884?term=viropharma&rank=6
ILNS sponsered a phase Ia trial in healthy human and Shire a phase Ib in FA.
Phase 1:
the initial phase of testing of an investigational drug in humans. Usually a
Phase 1 clinical study is conducted in a small number of healthy volunteers or patients
with a disease for which the drug may be useful. Generally, the study is designed to
determine the side effects of the drug and its pharmacokinetics. Some information
regarding drug efficacy may be collected if patients with a disease participate. A phase
frequently encompasses more than one clinical trial. Phase 1 sometimes is sub-divided
into Phases 1a and 1b, for example when the first set of Phase 1 trials (Phase 1a) is
performed in healthy volunteers and a second set of Phase 1 trials (Phase 1b) is
performed in patients with a disease.
Phase 2:
the intermediate phase of testing of an investigational drug in humans. Usually
a Phase 2 clinical study conducted in patients with a disease for which the drug may be
useful. Generally, the study is designed to evaluate dosing, to obtain preliminary data on
the effectiveness of the drug, and to acquire more safety information. Phase 2 sometimes
is sub-divided into Phases 2a and 2b. Phase 2a studies typically are smaller and shorter
in duration and evaluate different drug doses to see how they affect certain tests that can
indicate whether the drug is working as expected. Phase 2b studies typically enroll more
patients, are of longer duration and evaluate whether the drug is offering clinical benefits
to patients. Phase 2b studies sometimes are considered pivotal or registration-directed.
Phase 3:
the final phase of testing an investigational drug in humans before regulatory
approval. Phase 3 studies are usually conducted in a large population of patients and are
generally designed to confirm the effectiveness of the drug and to evaluate the overall
risk-benefit ratio. Phase 3 studies usually test the investigational drug in comparison with
a standard treatment for the disease or a placebo.
Phase 4:
testing of a drug in humans after it has already been approved by regulatory
authorities and can be used in medical practice. Phase 4 studies may be conducted to
compare the drug to a similar type of drug, to explore whether it may help patients with
other diseases, to further study the long-term safety of the drug, or for other reasons.
You bore me to death, it's time to hit the ignore button
ILNS YAHOO PROFILE
Profile
Intellect Neurosciences, Inc.
550 Sylvan Avenue
Suite 101
Englewood Cliffs, NJ 07632
United States - Map
Phone: 201-608-5101
Fax: 212-448-9600
Website: http://www.intellectns.com
Details
Index Membership: N/A
Sector: Healthcare
Industry: Biotechnology
Full Time Employees: 1
Key Executives
Pay Exercised
350.00K 0.00
Dr. Elliot M. Maza J.D., CPA, 60
Chairman, Chief Exec. Officer and Chief Financial Officer
Dr. Troy Rohn Ph.D.,
Lead Scientific Advisor
N/A N/A
Amounts are as of Dec 31, 2015 and compensation values are for the last fiscal year ending on that date. Pay is salary, bonuses, etc.Exercised is the value of options exercised during the fiscal year.
Currency in USD.
Business Summary
Intellect Neurosciences, Inc., a biopharmaceutical company, discovers and develops therapeutic agents for the treatment and prevention of neurodegenerative conditions primrily proteinopathies. Its licensed programs include OX1 (SHP622), an orally-administered, brain-penetrating, and naturally-occurring copper-binding small molecule, which has tested in human Phase I safety clinical trials for the treatment of various neurodegenerative diseases, such as Friedreich?s Ataxia. The company?s internal pipeline, which are in preclincial comprise TauC3 for the treatment of Alzheimer?s disease; and CONJUMAB-A for the treatment of age related macular degeneration. The company has a research collaboration agreement with Medical Research Council Technology, as well as license agreements with the South Alabama Medical Science Foundation, New York University, AHP Manufacturing BV, and Northwestern University. Intellect Neurosciences, Inc. was founded in 2005 and is based in Englewood Cliffs, New Jersey.
http://finance.yahoo.com/q/pr?s=ILNS
INTELLECT NEUROSCIENCES INCORPORATED (OTCMKTS:ILNS) Shorted Shares Increased By 6.67%
by Franklin Staff — May 6, 2016
The stock of INTELLECT NEUROSCIENCES INCORPORATED (OTCMKTS:ILNS) registered an increase of 6.67% in short interest. ILNS’s total short interest was 4,800 shares in May as published by FINRA. Its up 6.67% from 4,500 shares, reported previously. With 21,800 shares average volume, it will take short sellers 0 days to cover their ILNS’s short positions. The stock is down 2.78% or $0.002 after the news, hitting $0.07 per share. About 218,235 shares traded hands or 1284.92% up from the average. Intellect Neurosciences, Inc. (OTCMKTS:ILNS) has risen 15.94% since October 8, 2015 and is uptrending. It has outperformed by 9.14% the S&P500.
Intellect Neurosciences, Inc. is a biopharmaceutical company. The company has a market cap of $339,757. The Company, together with its subsidiary, Intellect Neurosciences, USA, Inc., is engaged in the discovery and development of disease-modifying therapeutic agents for the treatment and prevention of neurodegenerative conditions especially proteinopathies, which include Alzheimer’s , Parkinson’s and Huntington disease. It currently has negative earnings. The Company’s internal drug discovery programs are focused on the therapeutic applications of monoclonal antibodies.
http://www.franklinindependent.com/intellect-neurosciences-incorporated-otcmktsilns-shorted-shares-increased-by-6-67/
We could see new partners and licence agreements too how knows
Shire is playing on time said my crystal ball, we will see
MA(200) 0,092 & MA(50) 0,091
I see a positiv end for the shareholders which invested at about $0.10, IMO.
I think Maza is great CEO regarding making a deal, IMO.
For himselve, LOL, IMO.