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Intellect Neurosciences, Inc. (ILNS)

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 Intellect Logo
 

                                             Targeting Rare, "Orphan", Diseases


  

http://www.intellectns.com


 




 

Licensed Programs

 

SHP622 – Licensed to Shire plc

In 2011, we granted an exclusive license to ViroPharma Inc. (now part of Shire plc) covering use of our drug candidate, “OX1” (renamed by Shire as SHP622), and certain of our licensed patents and patent applications related to OX1. Shire is developing SHP622 for the treatment of Friedreich’s Ataxia (“FA”). This drug candidate is a naturally occurring small molecular weight compound (indole-3-propionic acid) that prevents oxidative stress by a combination of hydroxyl radical scavenging activity and metal chelation.

Phase 1 studies in healthy adults were completed in 2010. The drug was found to be generally well tolerated, and the pharmacokinetics revealed that the drug was rapidly absorbed and distributed in the body after oral administration.

Recently, Shire completed a Phase 1b trial to evaluate the safety, tolerability, pharmacokinetics, and pharmacodynamics of SHP622 in 55 adults with FA. SHP622 was generally safe and well tolerated when administered as single and multiple ascending doses. There were no severe treatment emergent adverse events (“TEAEs”) or deaths reported in either the single or multiple dose groups, and the majority of TEAEs were of mild severity. Overall, there were no clinically meaningful differences between SHP622 and placebo or between the single and multiple dose groups. The mean terminal elimination half-life ranged between 7.36 and 10.33 hours across all dose groups. Inter-subject variability appeared to be low to moderate.

Shire has stated that it will continue to analyze the results from the recently completed study and determine an optimal path forward for this program.

SHP622 Phase 1b Study in FA Patients – Completed by Shire in June 2015

PHASE 1B SAFETY, TOLERABILITY, PK/PD STUDY OF SHP622 IN ADULTS WITH FA
TRIAL DESIGN Randomized, Double-blind, Placebo-controlled, Multicenter, Single and Multiple Ascending Dose Studies
ARM 1 Experimental: Single dose of SHP622 or placebo
  • Four groups of 8 subjects each will receive a single dose of SHP622 (150 mg, 450 mg, 900 mg, or 1200 mg) or placebo.
    Total of 32 patients
ARM 2 Experimental: Multiple doses of SHP622 or placebo
  • Three groups of 8 subjects each will receive multiple doses of SHP622 (300 mg, 600 mg, or 900 mg total daily dose) or placebo. SHP622 or placebo will be administered every 8 hours for 7 days with a single morning dose on Day 8.
    Total of 24 patients
ENROLLMENT 55
COMPLETION Last patient was enrolled in June 2015; Formal study report completed in April 2016
PRIMARY OBJECTIVE Evaluate the safety and tolerability of single and multiple oral doses of SHP622 in subjects with FA
SECONDARY OBJECTIVE Characterize the pharmacokinetics of SHP622 by investigation of the plasma concentration-time profile following single and multiple oral doses
EXPLORATORY OBJECTIVE Investigate the pharmacodynamic effects of SHP622 on plasma 8-isoprostane and malondialdehyde and urinary 8-hydroxydeoxyguanosine concentrations following multiple oral doses
RESULTS SHP622 was generally safe and well tolerated when administered as single and multiple PO doses. There were no severe treatment emergent adverse events (“TEAEs”) or deaths reported in either the single or multiple dose groups, and the majority of TEAEs were of mild severity.
NEXT STEPS Shire is determining the optimal path forward for this drug candidate.
 




SHP622/IPA/VP20629/OX1/OXIGON

The Strongest Naturally Occurring Antioxidant In Human Body



                                                                                                     IPA
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4840492/figure/Fig1/
 


 

IPA - Radical Scavenger Mechanism
 

                                                                                                                           IPA - radical scavenger mechanism
http://www1.biologie.uni-hamburg.de/b-online/chimes/molnews/ipa/dipa.htm



 

White Paper on Potential for SHP622 in Friedreich's Ataxia and Economic Implications for Intellect Neurosciences






 
Development Programs
 

Anti-TauC3 Monoclonal Antibody

In 2012, we obtained from Northwestern University an exclusive license to worldwide diagnostic and therapeutic applications of a novel monoclonal antibody targeted to caspase cleaved TauC3.

Scientific research and pre-clinical experiments have demonstrated that fragments of Tau protein are present in brains of patients suffering from various neurodegenerative diseases, commonly known as “tauopathies”, and that the truncated form of Tau, known as TauC3, is especially toxic.

We have conducted experiments to demonstrate that caspase cleaved TauC3 is present in models of various tauopathies at a level detectable by our anti-TauC3 antibody and that our anti-TauC3 antibody shows sufficient binding specificity to the target TauC3 protein to indicate that the antibody may be a viable treatment agent.

In 2014, we reported positive top line data from a pre-clinical study conducted on our behalf at UC Irvine showing proof of concept for the antibody in an Alzheimer's disease (AD) mouse model.

In April 2016, we obtained positive data from an in-vitro study conducted on our behalf at Harvard Medical School and the MassGeneral Institute for Neurodegenerative Disease. The experiments demonstrated that our anti-TauC3 antibody significantly blocks TauC3 fragment seeding, aggregation and toxicity, demonstrating that caspase cleaved TauC3 is a potential target for treatment in Progressive Supranuclear Palsy, Traumatic Brain Injury and other tauopathies and that our antibody may be a viable treatment agent.

We are initiating experimental treatment trials of our anti-TauC3 antibody in mouse models of progressive supranuclear palsy (PSP) and traumatic brain injury (TBI). These conditions are rare, “orphan”, neurological diseases of high unmet medical need with no approved therapies.

Presence of TauC3 in Tauopathies

Scientific evidence has proven that caspase cleaved TauC3 promotes formation of neurofibrillary tangles (NFTs), which are aggregates of hyper-phosphorylated tau found in numerous tauopathies.

Truncation of tau by caspases may occur relatively early in neurodegenerative disease, prior to the key folding steps that lead to the formation of phosphorylated pathological forms of tau. Also, it has been demonstrated that tau truncated at Asp421 (TauC3) aggregates more rapidly and to a greater degree than full-length tau.

Collectively, these studies suggest that the caspase cleavage of tau propagates the formation of NFTs and facilitates filament formation, which are disease- triggering events that are associated with various neurodegenerative conditions, such as Alzheimer’s disease, PSP and TBI.

Illustrative Diagram of Presence of TauC3 in Pick’s Disease, TBI and PSP





 

CONJUMAB ANTIBODY DRUG CONJUGATE PLATFORM AND CONJUMAB-A

We are conducting research into the use of antibody drug conjugates (ADCs), as a treatment of amyloidosis and other types of proteinopathies. ADCs chemically combine two different molecules - an antibody and a small molecule - into a single entity. We refer to this approach as “CONJUMAB”.

Our initial ADC candidate, CONJUMAB-A, is designed to combine an amyloid beta monoclonal antibody with a derivative of melatonin, thereby combining the amyloid clearing properties of the antibody with a potent neuroprotectant molecule. The rationale is that the antibody clears the amyloid peptide while the small molecule reduces the neurotoxicity caused by the peptide and provides additional neuroprotective effects to the retina.

CONJUMAB-A is an ideal compound to target amyloid beta in the eye, believed to be the leading cause of Age-Related Macular Degeneration (AMD). CONJUMAB-A would remove this toxic molecule and defend against the presence of free radicals.

We purchased the amyloid beta monoclonal antibody from Immuno-Biological Laboratories Ltd and collaborated with London-based Medical Research Council Technology to create a humanized form, which has the same properties as the original antibody.

CONJUMAB patents are pending worldwide.

 





 
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.


 

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.

 
 




 
ILNS Security Details
Share Structure
  Market Value1 $122,475 a/o Jul 05, 2016
  Authorized Shares 2,000,000,000 a/o Nov 04, 2015
  Outstanding Shares 5,567,037 a/o Nov 04, 2015
  -Restricted Not Available
  -Unrestricted Not Available
  Held at DTC Not Available
  Float 4,717,663 a/o Nov 04, 2015
  Par Value Not Available
 



 




 
Security Notes

Capital Change=shs decreased by 1 for 50 split Pay date=04/12/2011.
Capital Change=shs decreased by 1 for 250 split. Pay date=02/11/201
5.


http://www.otcmarkets.com/stock/ILNS/profile
 


                                                             

 


 


 

 


 


 

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ILNS News: Quarterly Report (10-q) 05/09/2016 02:41:14 PM
ILNS News: Current Report Filing (8-k) 04/28/2016 04:40:13 PM
ILNS News: Statement of Ownership (sc 13g) 02/05/2016 12:43:08 PM
PostSubject
#19716  Sticky Note Intellect Neurosciences, Inc. Engages Benjamin D. Freilich, MD, john1045 03/30/16 10:32:12 AM
#20214   WHITE PAPER SHP622 WAS UPDATED AGAIN TO A montanus 07/24/16 04:43:53 AM
#20213   OS is what 7 mil? Yeah, because the Jumpinjackas 07/23/16 07:29:14 PM
#20212   That's milestone payments to ilns from shire not dbing 07/23/16 06:33:11 PM
#20211   Been a while, so I thought I would AlaskaBushMan 07/22/16 03:56:04 PM
#20209   Science maybe real, but stock is scam Jumpinjackas 07/21/16 09:33:43 PM
#20208   what is real is shire is moving into mkaiz 07/21/16 09:19:47 PM
#20207   I feel for the guy. I think he Jumpinjackas 07/21/16 06:47:30 PM
#20206   I guess Deals is gone for good. TheSaint09 07/21/16 06:41:49 PM
#20205   Sorry to hear that. I took my losses Jumpinjackas 07/21/16 08:36:51 AM
#20204   I am down like 90%. I need it buckiii2 07/20/16 04:15:54 PM
#20203   pretty good artical about tau . would be mkaiz 07/20/16 04:01:59 PM
#20202   how much will ilns get if shp 622 mkaiz 07/20/16 03:59:53 PM
#20201   I am NOT buying. buckiii2 07/20/16 03:58:06 PM
#20200   why do you have the change of heart mkaiz 07/20/16 03:56:57 PM
#20199   I have a better location. buckiii2 07/20/16 02:19:18 PM
#20198   deals tried that already. He wishes he had Jumpinjackas 07/20/16 02:18:12 PM
#20197   I don't will have to go beg on buckiii2 07/20/16 02:16:51 PM
#20196   Surprised that you got anything left to do that. Jumpinjackas 07/20/16 02:15:38 PM
#20195   I am going to put mine in at. 0025. buckiii2 07/20/16 02:14:36 PM
#20194   Just placed a buy order for 1million shares Jumpinjackas 07/20/16 01:02:01 PM
#20193   so what does this have to do with akika 07/19/16 09:59:59 PM
#20192   TAU. buckiii2 07/19/16 04:41:39 PM
#20190   That's correct and SHP622 results are overdue! montanus 07/18/16 09:52:47 AM
#20189   That's potential milestone payments not share count. James salmon 07/18/16 08:48:21 AM
#20188   how did the share count get that big? akika 07/17/16 09:55:32 PM
#20187   138 million in potl milestones dbing 07/17/16 08:09:02 PM
#20186   70mil+ close to 100 Jumpinjackas 07/17/16 07:48:34 PM
#20185   how many shares are outstanding? akika 07/17/16 07:47:22 PM
#20184   Any info on the next RS ? Jumpinjackas 07/17/16 01:13:03 PM
#20183   Thanks James salmon 07/15/16 01:04:39 PM
#20182   ILNS IBOX LINK, or under publications - ILNS website montanus 07/15/16 12:00:48 PM
#20181   He is making stuff up. Jumpinjackas 07/15/16 10:21:23 AM
#20180   Where do you find this James salmon 07/15/16 09:55:58 AM
#20179   $ 38 million milestone payment, not so bad montanus 07/15/16 12:45:17 AM
#20178   IPA - CNS INFLAMMATION montanus 07/15/16 12:10:51 AM
#20177   IPA - neuronal damage & oxidative stress montanus 07/14/16 11:56:37 PM
#20176   Does that mean were going sub-penny in the morning? tyfoidhana 07/14/16 09:41:23 PM
#20175  Restored White paper out on shp622 and the implications dbing 07/14/16 05:17:13 PM
#20174   No, they are starting over on the stock. Jumpinjackas 07/13/16 04:20:58 PM
#20173   Are they starting the trial over? And Drs136 07/12/16 04:43:27 PM
#20172   http://friedreichsataxianews.com/2016/07/12/fruit-fly-model-of-friedreichs-ataxi montanus 07/12/16 10:31:18 AM
#20171   Indole derivatives and AMD montanus 07/12/16 09:20:26 AM
#20170   We should buy some shire Jumpinjackas 07/12/16 09:08:45 AM
#20169   SHIRE GOT FDA APPROVAL FOR DRY EYES... FLY HIGH NOW 07/12/16 09:06:02 AM
#20168   IPA http://www.ncbi.nlm.nih.gov/pubmed/27158906 montanus 07/12/16 04:40:27 AM
#20167   AD, Type 3 diabetes & Melatonin montanus 07/12/16 02:10:00 AM
#20166   $500 mil for RARE DISEASES? FLY HIGH NOW 07/12/16 01:21:28 AM
#20165   TOC1: a valuable tool in assessing disease progression montanus 07/07/16 08:18:39 AM
#20164   Thanks for that, Tauc3 and Troy Rohn montanus 07/06/16 03:56:02 PM
#20163   http://www.fiercebiotech.com/research/jhu-team-demystifies-one-two-punch-causes- buckiii2 07/06/16 03:02:00 PM
PostSubject