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I have to agree
PFE invested billions to develop bapineuzumab and ponezumab and both are based on ANTSENILIN platform technology. CONJUMAB would be the next logical step for PFE with a huge project deep under water and a lot of indications that it could work, ALLIMO!
Sounds like a sensible plan to sell shp622 and tauC3 (for rare disease as pick's, huntington, morbus parkinson) to Shire and ANTISENILIN with CCONJUMAB to PFE, ALLIMO!
I guess it's the trial outcome to invest more money and a possible deal but we will see.
Mr. MAZA must update the shareholders regarding PONEZUMAB trial, the reason to restart CONJUMAB, SHP622 trial outcome and so on, ASAP!
It looks like someone is nervous out there and yes something will happen soon,IMO.
Stay tuned, regards from Austria
To go forward with CONJUMAB technology needs adequate financial resources that's clear, e.g. the next step with Lonza to develop and produce the molecules is possible with a partner or with non dilutive capital, approx. 10 to 20 million, ALLIMO.
montanus
About Age Related Macular Degeneration and CONJUMAB platform technology
AMD is the third most important cause of blindness in the world and the leading cause of blindness in higher income countries with ageing populations.
AMD is a disease affecting the central area of the retina (macula) at the back of the eye. In the early stages of the disease lipid material accumulates in deposits underneath the retinal pigment epithelium. These deposits are known as drusen, and can be seen as pale yellow spots on the retina. The pigment of the retinal pigment epithelium may become disturbed, with areas of hyperpigmentation and hypopigmentation. In the later stages of the disease, the retinal pigment epithelium may atrophy completely. This loss can occur in small focal areas or can be widespread (geographic atrophy). In some cases, new blood vessels grow under the retinal pigment epithelium and occasionally into the subretinal space (exudative or neovascular AMD). Haemorrhage can occur which often results in increased scarring of the retina. The early stages of the disease are in general asymptomatic. In the later stages there may be considerable distortion within the central visual field leading to a complete loss of central visual function.
Approximately 5% of blindness globally is due to AMD(1). It is estimated that globally 196 million (95% credible interval 140—261) people will have AMD in 2020, increasing to 288 million in 2040 (205—399)(2).
The major risk factors for AMD are age, genetic factors and tobacco smoking. Considerable research has focussed on the role of diet, light exposure and association with cardiovascular disease and its risk factors, however, the effects of these risk factors are less certain.
Treatment of AMD has been revolutionised by the use of anti-vascular endothelial growth factor agents that bind to vascular endothelial growth factor or their receptors and slow down the growth of new blood vessels. These interventions are delivered by injection into the eye. However, they are only applicable for the neovascular form of the disease. Currently there is no effective treatment for geographic atrophy. There is some evidence that antioxidant vitamin supplements may slow down the progression of AMD to late stage disease and visual loss.
---
1. Pascolini D, Mariotti SP. Global estimates of visual impairment: 2010. The British journal of ophthalmology. 2012 May;96(5):614-8. PubMed PMID: 22133988.
2. Wong WL, Su X, Li X, Cheung CMG, Klein R, Cheng C-Y, et al. Global prevalence of age-related macular degeneration and disease burden projection for 2020 and 2040: a systematic review and meta-analysis. The Lancet Global Health. 2014;2(2):e106-e16.
---
List of Cochrane reviews on AMD
Treatments that are effective
Antiangiogenic therapy with anti-vascular endothelial growth factor modalities for neovascular age-related macular degeneration
Photodynamic therapy for neovascular age-related macular degeneration
Laser photocoagulation for neovascular age-related macular degeneration (effective in slowing down progression of vision loss but no longer in general use)
Treatments that are probably not effective or where effectiveness is currently uncertain
Antiangiogenic therapy with interferon alfa for neovascular age-related macular degeneration
Macular translocation for neovascular age-related macular degeneration
Surgical implantation of steroids with antiangiogenic characteristics for treating neovascular age-related macular degeneration
Submacular surgery for choroidal neovascularisation secondary to age-related macular degeneration
Statins for age-related macular degeneration
Ginkgo biloba extract for age-related macular degeneration
Laser treatment of drusen to prevent progression to advanced age-related macular degeneration
Radiotherapy for neovascular age-related macular degeneration
Complement inhibitors for age-related macular degeneration
Nutritional interventions
Antioxidant vitamin and mineral supplements for preventing age-related macular degeneration
Antioxidant vitamin and mineral supplements for slowing the progression of age-related macular degeneration
Omega 3 fatty acids for preventing or slowing the progression of age-related macular degeneration
Related reviews
Reading aids for adults with low vision
Surgery for cataracts in people with age-related macular degeneration
Links to key websites
The Royal College of Ophthalmologists: http://www.rcophth.ac.uk
NICE website: http://www.nice.org.uk
National Eye Institute: http://www.nei.nih.gov
Journal of American Medical Association: http://jama.jamanetwork.com
AMD Alliance international www.amdalliance.org
Macular Society www.macularsociety.org
RNIB www.rnib.org.uk
Cochrane Eyes and Vision group www.cochraneeyes.org
(IAPB acknowledges Jennifer Evans, Co Coordinating Editor of the Cochrane Eyes and Vision Group and Tanya Moutray, January 2014)
http://www.iapb.org/vision-2020/what-is-avoidable-blindness/age-related
CONJUMAB:
I am excited about the potential of our CONJUMAB antibody drug conjugate platform and the therapeutic potential of the lead program, CONJUMAB-A, for treatment of age-related macular degeneration (AMD). CONJUMAB is designed to empower chaperone-like monoclonal antibodies with cytoprotective properties for treatment of various forms of amyloidosis and other types of proteinopathies in which irregular accumulation of abnormally folded proteins causes oxidative stress and inflammation, resulting in irreversible damage and death of cells. This relates to many different diseases, including diseases of the eye (AMD, glaucoma, diabetic retinopathy), brain diseases (Alzheimer's disease, Parkinson's disease (PD), Huntington's disease, motor neuron disease (ALS) and Creutzfeld Jacob disease (CJD)) and peripheral diseases (multiple myeloma, systemic amyloidosis, familial serum amyloid neuropathies and isolated atrial amyloidosis). Numerous proteins, including, amyloid beta (Aß), tau protein, huntingtin protein, superoxide dismutase, prion and transthryetin, become abnormally folded, making them potential targets for the CONJUMAB approach.
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.
In principle, our approach could be applied to improve many different types of antibodies, such as those that previously disappointed in clinical trials. However, currently we are focused on optimizing CONJUMAB-A using our own humanized antibody IN-N01, which targets the N-terminus of Aß. We believe IN-N01 to be superior to bapineuzumab because of its reduced potential to cause inflammation that results from our reengineering into an IgG4 class antibody.
Among several potential indications, we have decided to focus on AMD since both AMD and AD share several similarities, while the eye offers less challenge for delivering the drug. Indeed, physicians routinely perform injections into the eye cavity. Moreover, AMD is the leading cause of blindness in people over the age of 55, most of who respond poorly or not at all to existing therapies. While the relatively recent introduction of anti-vascular endothelial growth factor agents, such as intravitreal bevacizumab and ranibizumab, appear to have improved the prognosis for patients with wet AMD, preclinical studies have raised a potential red flag on anti-VEGF therapies, suggesting that increasingly aggressive use in eye disease could trigger side effects and potentially cause long-term damage. Moreover, no one has been able to develop an effective treatment for dry AMD, which is a significantly larger population, as it is the precursor to wet AMD.
Ample evidence has established oxidative stress as an important contributor in the pathogenesis of AMD and several studies have indicated antioxidant molecules can help reduce damage to the retina. Various Aß-lowering and Aß-neuroprotective strategies have demonstrated the ability to protect against damage in various models of retinal degeneration, including Aß-specific antibodies. Two such antibodies, GSK933766A and RN6Gare being tested in Phase 2 AMD trials having demonstrated an ability to reduce damage to RPE cells in animal models following systemic administration. These data lead us to believe CONJUMAB-A has the potential to become a strong leader in the field based on its combined properties to remove Aß and reduce oxidative stress when delivered in high concentrations directly to the eye.
https://globenewswire.com/news-release/2013/02/13/523315/10021734/en/Intellect-Neurosciences-Issues-Letter-to-Shareholders.html
Conjumab may increase the efficiency of solanezumab through linking with the melatonin (OX2) molecule (empower the mab to use the drug @ higher dose) or may help drugs like ponezumab with their anti inflammation properties which is a major issue in several potential drugs.
ALLIMO
GLTA
montanus
The last shareholder update was in October!
http://ir.stockpr.com/intellectns/press-releases/detail/996/intellect-neurosciences-inc-issues-letter-to-shareholders
You got it, oxidative stress and so on...will indicate if the drug works or not but for me it sounds like Shire want to go forward after evaluate their options. The drug is save.
IMO it was a positive statement to the primary trial outcome in general and not more or less, the rest is usual speculation.
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.
I have to agree, it's a total positive statement and they will go forward with SHP622. To find the optimal path could mean a lot but in a positive way again; other pharma co are testing their FA drug in several other diseases and OX1 was developed for AD, Parkingson, Huntington, FA and others.
https://clinicaltrials.gov/ct2/results?term=ACTIMMUNE&Search=Search
https://clinicaltrials.gov/ct2/results?term=EPI-743&Search=Search
https://clinicaltrials.gov/ct2/results?term=RTA+408&Search=Search
etc.
IPA AS A THERAPEUTIC AGENT, AS A PROTECTIVE AGENT, AND AS A BIOMARKER OF DISEASE RISK
The present disclosure relates to the use of indole-3-proprionic acid (IPA) as a therapeutic agent, as a protective agent against late onset of cardiovascular and neurodegenerative disease,, and as a biomarker for disease and health conditions. The disclosure has particular utility in connection with neurodegenerative diseases such as Huntington Disease (HD), A lzheimer Disease (AD), Mild Cognitive Impairment (MCI), Lower Motor Neuron Disease (MND) including but not limited to Amyotrophic Lateral Sclerosis (ALS), Parkingson's Disease (PD) as well as hypertension, stroke and ischemic heart disease and head injury, and will be described in connection with such utilities, although other utilities are contemplated.
http://www.google.com/patents/WO2013148709A1?cl=en
FA R&D:
Phase III
ACTIMMUNE ® (Interferon gamma-1b)
The phase II open label study of Interferon gamma in Philadelphia (12 children with Friedreich ataxia) showed significant improvement in FARS scores and a small increase in Frataxin levels, and there were no serious adverse effects (http://www.ncbi.nlm.nih.gov/pubmed/25335475). Based on these encouraging results, Horizon Pharma has initiated a Phase III clinical trial of ACTIMMUNE. (https://www.clinicaltrials.gov/ct2/show/NCT02415127)
Phase II
EPI-743
Edison Pharmaceuticals has completed recruitment for a phase II double blind, placebo controlled clinical trial of EPI-743 (a drug with close similarities to EPI-A0001, which aims to improve mitochondrial function) in Friedreich ataxia patients. The primary outcome measure is visual function. Results of the trial are expected in the third quarter of 2015. (https://www.clinicaltrials.gov/ct2/show/NCT01728064)
RTA 408 (Nrf2 activator)
Reata Pharmaceuticals has developed a compound, RTA 408, to target activation of the transcription factor Nrf2, a protein that is essential for protecting cells from oxidative stress and has reduced activity in frataxin deficient cells. Recruitment for a phase II clinical trial began recently in the United States and the estimated completion date is mid-2016. (https://www.clinicaltrials.gov/ct2/show/NCT02255435)
Nicotinamide
In an open label pilot study of nicotinamide (vitamin B3), an HDAC inhibitor, Frataxin levels increased in blood samples from participants but the neurological measures did not show significant improvement (http://www.ncbi.nlm.nih.gov/pubmed/24794816). While these results are of interest, further studies of longer duration are needed to determine if nicotinamide is safe and effective as a long-term treatment for Friedreich ataxia. Recruitment for a follow-up study is now underway in London, with an estimated completion date of September 2016. (http://www.clinicaltrials.gov/ct2/show/NCT01589809)
ALCAR (Acetyl-L-Carnitine)
Dr. Theresa Zesiewicz (University of South Florida) has initiated an open label study of ALCAR (Acetyl-L-Carnitine), a well-researched nutritional supplement that may be beneficial in cardiovascular disease and neurodegenerative disorders. ALCAR is a more bioavailable form of L-carnitine, a derivative of the amino acid lysine that is made naturally in the body. It functions as an antioxidant and has an important role in glucose metabolism. The 24-month study will examine cardiac and neurological measures in FRDA adults and is open for enrollment. (https://www.clinicaltrials.gov/ct2/show/NCT01921868)
EPO
Several reports have suggested that erythropoietin (EPO) can increase frataxin levels. A phase II clinical trial is being conducted by Dr. Francesco Saccà in Italy to test the effect of EPO on exercise capacity in FRDA patients. The treatment phase has been completed and results should be reported by the third quarter of 2015. (https://www.clinicaltrials.gov/ct2/show/NCT01493973)
Resveratrol
Resveratrol is found in the skin of red grapes and has been investigated as a compound that could improve mitochondrial function. Pre-clinical laboratory studies in Friedreich ataxia cell and mouse models indicated that resveratrol also increases Frataxin levels. Thus, Professor Martin Delatycki and his colleagues carried out an open label pilot study in Friedreich ataxia patients to evaluate the safety, tolerability and efficacy of two different doses of resveratrol (http://www.ncbi.nlm.nih.gov/pubmed/25845763). While Frataxin levels did not change at either dose, participants taking the higher dose showed improvement in FARS and speech measures, but they also had gastrointestinal side-effects. A placebo-controlled clinical trial is now being considered. (https://www.clinicaltrials.gov/ct2/show/NCT01339884)
Phase I
SHP622
ViroPharma (acquired by Shire in November 2013) initiated a phase I double blind, placebo controlled clinical trial of SHP622 / OX-1 (indole-3-propionic acid, a naturally occurring compound that has potent anti-oxidant properties) in adults with Friedreich ataxia. The results of this study should be available within the next few months. (https://www.clinicaltrials.gov/ct2/show/NCT01898884)
Incretin analogs
Incretins are gut hormones that stimulate insulin secretion to control blood sugar levels. Research on diabetes in Friedreich ataxia led Drs. Miriam Cnop, Mariana Igoillo-Esteve and Massimo Pandolfo to the discovery that incretin analogs induce frataxin expression in pancreatic b-cells and iPSC-derived neurons from Friedreich ataxia patients (http://www.ncbi.nlm.nih.gov/pubmed/25552656). Based on these findings, this team recently launched a small, short-term pilot clinical trial of incretin analogs in Friedreich ataxia patients in Belgium.
RT001
Polyunsaturated fatty acids (PUFAs) are needed by cells in the nervous system, but they are susceptible to oxidative damage, which may lead to mitochondrial dysfunction, particularly in individuals with neurological diseases. Retrotope evaluated chemical substitutes in which the hydrogen molecules in PUFAs are replaced with deuterium (a stable isotope of hydrogen) and found that dPUFAs had a protective effect in Friedreich ataxia cell models (http://www.ncbi.nlm.nih.gov/pubmed/25499576). Recruitment for a 28-day clinical trial to evaluate RT001, a dPUFA developed by Retrotope, was announced in August 2015. The trial is taking place at the University of South Florida and UCLA.
https://clinicaltrials.gov/ct2/show/NCT02445794
Pre-Clinical Studies
HDAC inhibitors
Repligen’s clinical trial in Italy to evaluate the safety and dosage of the HDAC inhibitor, RG2833, has been completed. The treatment was well tolerated and frataxin expression was increased in blood samples from participants, which is encouraging (http://www.ncbi.nlm.nih.gov/pubmed/25159818). However, it has been shown that metabolites formed when RG2833 is broken down in the body can be harmful over the long term. Thus, BioMarin, which acquired the HDAC inhibitor program from Repligen in January 2014, is now developing a follow-on compound with improved metabolic stability and better access to the central nervous system.
Gene Therapy
The Friedreich ataxia MCK mouse model develops a severe cardiac phenotype. Dr. Hélène Puccio’s group demonstrated the prevention and reversal of cardiomyopathy using AAV gene therapy (http://www.ncbi.nlm.nih.gov/pubmed/24705334). Following these exciting results, a new company, AAVLife, has been founded to move the development of gene therapy for FRDA cardiomyopathy forward as rapidly as possible. In April 2014 REGENX Biosciences, a leader in AAV gene therapy, announced that the company has entered into an agreement with AAVLife to develop and commercialize products to treat FRDA using a proprietary vector technology that includes novel AAV vectors. REGENX announced a similar agreement with the new gene therapy company, Voyager Therapeutics, in June 2014, and in February 2015 Voyager Therapeutics and Genzyme entered a major strategic collaboration, which is focused on developing and commercializing novel AAV gene therapies for patients with CNS diseases, including FRDA. Additionally, engineering innovative DNA-based therapeutics for FRDA is the lead program of Agilis Biotherapeutics, which has an exclusive collaboration agreement with Intrexon Corporation to provide promising new treatments for FRDA.
Frataxin replacement
Using a cell-penetrant peptide (TAT) to deliver human Frataxin protein to mitochondria in Friedreich ataxia cell and mouse models, Dr. Mark Payne reversed the disease phenotype, suggesting the potential of protein replacement therapy (http://www.ncbi.nlm.nih.gov/pubmed/22113996). Bioblast Pharma is pursuing a similar frataxin replacement approach, which they are testing in cell and animal models.
RNA-based approach
RaNA Therapeutics is focusing on identifying non-coding RNAs (ncRNAs) that may contribute to silencing the frataxin gene in Friedreich ataxia patients. Research by this company has shown that degrading specific ncRNAs results in increased expression of the frataxin gene. Thus, this may be a promising therapeutic approach.
Nrf2 activators
Dr. Gino Cortopassi (UC Davis and one of the founders of Ixchel Pharma) screened a library of approved drugs and identified several compounds that activate Nrf2. Together with Dr. Susan Perlman (UCLA), Dr. Cortopassi is doing further laboratory testing of these compounds, including dyclonine, a topical anesthetic, and dimethylfumarate, which has been approved for multiple sclerosis (http://www.ncbi.nlm.nih.gov/pubmed/25113747).
http://www.fara.org.au/promising-treatment/
ALLIMO
I love the optimal path forward for this program! ABSOLUTE POSITIVE!
SHP622:Shire will continue to analyze these results and determine an optimal path forward for this program.
"SHP622 for the treatment of FA
SHP622 is in development for the treatment of Friedreich’s Ataxia and was acquired as part of the acquisition of ViroPharma. This product is a
naturally occurring small molecular weight compound (indole-3-propionic acid) that prevents oxidative stress OX1 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. A Phase 1b
trial to evaluate the safety, tolerability, pharmacokinetics, and pharmacodynamics of SHP622 in adults with FA has been completed. 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. However, one subject in
the multiple dose group was discontinued due to a possibly related treatment emergent of angina pectoris. 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. Intersubject variability appeared to be low to moderate. Shire will continue to analyze
these results and determine an optimal path forward for this program.
"
Page 42:
http://api40.10kwizard.com/cgi/convert/pdf/Shireplc-20160504-10Q-20160331.pdf?ipage=10913903&xml=1&quest=1&rid=23§ion=1&sequence=-1&pdf=1&dn=1
They INSIDERS knew that about ponze and invested more money, restarted conjumab program....for a reason. Research was stopped in february - for me it smells like a deal. And Konrad Ackerman increased his position (junior lender?) in ILNS after that?
All imo
"These new criteria may help physicians managing ARIA-E in AD immunotherapy trials, once any such therapy is approved. “If AD immunotherapy is effective, then understanding how to predict, detect, and treat ARIA will be a major focus of putting that therapy into practice,” Greenberg told Alzforum. Iadecola agreed. “If CAA-ri is the basis of ARIA, immunosuppression may allow affected patients to continue immunotherapy.” He noted that ARIA is less serious than CAA-ri, so not all cases of ARIA may require treatment. “Nevertheless, having the opportunity to prevent or treat ARIA would expand the number of patients who could benefit from immunotherapy,” he said.—Gwyneth Dickey Zakaib"
http://www.alzforum.org/news/research-news/diagnosis-inflammation-cerebral-amyloid-angiopathy
Int. J. Mol. Sci. 2013, 14, 8638-8683; doi:10.3390/ijms14048638
International Journal of
Molecular Sciences
ISSN 1422-0067
www.mdpi.com/journal/ijms
Melatonin: Buffering the Immune System
Antonio Carrillo-Vico 1,†, Patricia J. Lardone 1,†, Nuria Álvarez-Sánchez 2
,
Ana Rodríguez-Rodríguez 2
and Juan M. Guerrero 1,2,*
1
Institute of Biomedicine of Seville (IBiS) and Department of Medical Biochemistry and Molecular
Biology, Virgen del Rocío University Hospital/CSIC/University of Seville, 41013 Sevilla, Spain;
E-Mails: vico@us.es (A.C.-V.); plardone@us.es (P.J.L.)
2
Institute of Biomedicine of Seville (IBiS) and Department of Clinical Biochemistry,
Virgen del Rocío University Hospital/CSIC/University of Seville, 41013 Sevilla, Spain;
E-Mails: nalvarez-ibis@us.es (N.Á.-S.); rodriguezana13m@gmail.com (A.R.-R.)
† These authors contributed equally to this work.
* Author to whom correspondence should be addressed; E-Mail: guerrero@us.es;
Tel.: +34-955-923-106; Fax: +34-954-907-048.
Received: 1 March 2013; in revised form: 6 April 2013 / Accepted: 7 April 2013 /
Published: 22 April 2013
Abstract:
Melatonin modulates a wide range of physiological functions with pleiotropic
effects on the immune system. Despite the large number of reports implicating melatonin
as an immunomodulatory compound, it still remains unclear how melatonin regulates
immunity. While some authors argue that melatonin is an immunostimulant, many studies
have also described anti-inflammatory properties. The data reviewed in this paper
support the idea of melatonin as an immune buffer, acting as a stimulant under basal or
immunosuppressive conditions or as an anti-inflammatory compound in the presence of
exacerbated immune responses, such as acute inflammation. The clinical relevance of the
multiple functions of melatonin under different immune conditions, such as infection,
autoimmunity, vaccination and immunosenescence, is also reviewed.
Well, understand, Ponezumab and inflammation might be the reason to restart the Conjumab-A platform?
Thanks for sharing to Stately
Sorry my bad!
Not true, ponezumab is on continued.
New study reveals: Propionic acid and its effects on autoimmune diseases (in german)
A FA treatment could be a blockbuster drug that's all I want to say,..
Personally, call or contact me when you or other investors are in europe, or want to make bussines... I will support you guys.. I am looking for good people and Investors always.
For example, the ROI of my private project are 6 month, it's a metal powder (nano)project...
It's snowing here man, what a $$$$
servus john, IPA was developed for AD, Parkinson, and I guess a few other deseases...
If IPA work for FA and it's not unlikely - we will see several other trials I guess.
Look at the competitors, Reata......
Okay, we will see...
Completely horse shit, boy! I know what I am talking about, have a english full blood and a arabian full blood.
Inflammation and CAA
http://www.alzforum.org/news/research-news/diagnosis-inflammation-cerebral-amyloid-angiopathy
Dr. Greenberg is director in ponezumab study.
Inflammation and antibodies, it could be one reason to restart the CONJUMAB-A program
I bet one Schilling, Shp622 will be a new generation in neurological treatment!
Mr. Maza, Mr. Rohn please read through the clinical trial below!
http://friedreichsataxianews.com/2016/04/05/clinical-experience-with-deferiprone-treatment-for-friedreich-ataxia/
THE ARTICLE IS MEGA!
It implements that the mechanisms how OX1 works is proofed to be a encouraging treatment in FA! A statement from Dr. Troy Rohn is necessary!
Very interesting - SHP622/VP20629/OXIGON/OX1/IPA should work in a same way but save and as a single drug
http://friedreichsataxianews.com/2016/04/05/clinical-experience-with-deferiprone-treatment-for-friedreich-ataxia/
KMVT-TV TROY ROHN - ALZHEIMER CONFERENCE
MAY 12, DR. TROY ROHN ALZHEIMER RESEARCH KEY NOTE SPEAKER
www.kmvt.com/content/news/Alzheimers-conference-set-for-May-12-at-CSI-371821792.html
MR. MAZA,
an update regarding the new findings in ponezumab preclinical and clinical trial is a must!
There is a license agreement with PFE and ILNS is a public company.
An interview with an expert, MARK LILLIE ponezumab director @PFE and Daniel Chain would make sense!
https://www.fightaging.org/archives/2016/03/recent-advances-in-anti-amyloid-passive-immunization.php
https://clinicaltrials.gov/ct2/show/NCT01821118?term=ponezumab&rank=5
You are right and I have to agree IMO Pfizer will go forward with ponezumab
Bull shit, that's a scientific paper, business as usual....but there are a lot of other hints for a positive ponezumab trial
A Chart analysis please!