This Is MS Multiple Sclerosis Community: Knowledge & Support

Hi,

Found this Drug which sounds very promising. Seems like it was on Phase II trail. Is this the same drug which is listed here on Phase II Trail

40. T-Cell Vaccination (Sheba Medical Center)

or is this a different one. If different, is it still in Phase II or was it discontinued.



http://www.usc.edu/hsc/info/pr/1vol5/526/ms.html

http://www.conquestgroup.org/research.htm#Continuing

This one actually was discussed a bit here at ThisISMS 2 years ago. It turns out that the article you posted is from 1999 (though that isn't made clear in the link) and the trial was terminated in 2004. I'm glad to see anybody digging stuff up though, thank you.



T Cell Vaccination Fails in Trial

http://www.mult-sclerosis.org

March 4, 2004
Paul Jones
All About Multiple Sclerosis

A four year trial of a potential multiple sclerosis treatment at the University of Southern California has been terminated.

The treatment involved vaccinating the body against the immune system cells, called T Cells. These T Cells were believed to be causing the damage to the brain and spinal cord that gives rise to the symptoms of MS.

The study compared the results of the vaccine against those of a placebo injection. It was headed up by Dr. Leslie Weiner and Dr. Norman Kachuck

The study's sponsors, the National Institute of Health and the National Multiple Sclerosis Society of America, decided to stop the clinical trial because it failed to show statistically significant results.

"Their conclusion was based on a failure to show any benefit to the patients who received the vaccine.", said Dr. Weiner. "The data showed that there was no difference between the group of patients treated with the T-cell vaccine and those on the placebo."

"The committee recommended that no more injections be administered to patients. As the principle investigator, I agree with this decision.", continued Dr. Weiner.

Dr. Weiner recommended that study volunteers switch either to Betaseron or to Novantrone.

http://www.mult-sclerosis.org/news/Mar2 ... Trial.html

Isn't that like Tovaxin?

Not sure if it is already added.


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Opsona gets research boost 03 February 2006


OPSONA Therapeutics is set to announce a major link-up with a multinational drugs company that will facilitate significant medical research in an area of auto-immune diseases.
Already the group, which is just over a year old, is close to clinically testing a new drug to combat multiple sclerosis. It is radical in terms of modern medicine, said Mark Heffernan, group chief executive, whose company was among the 75 start-ups announced yesterday by Enterprise Ireland.

“We are looking at a sub-set of immune cells called T-regulatory cells and we are working on how to turn those on,” he said.

These act as brakes to the immune system and when turned on halt the immune system. That could be a vital new way of preventing MS from taking hold because it is heightened immune systems that are most often the cause of such debilitating diseases as MS.

The attractiveness of the drug is that it tackles the cause rather than the effects of the disease, he said. The drug could be on the market within six years and human trials may start this time next year. The group has raised over €6.25 million to fund its research.

Opsona originated in Trinity College, Dublin. Kingston Mills, Luke O’Neill and Dermot Kelleher have put several years' work into the radical MS treatment.

Source: Irish examiner.com © Irish Examiner, 2005, Thomas Crosbie Media, TCH


http://www.msrc.co.uk/index.cfm?fuseact ... ageid=1076

Good find Gopi, I've never heard of it. Based on this:
http://www.opsona.com/aboutus.htm

I'll say it's OPN-101 and put it as "Pre-clinical".

Thanks.

Another preclinical treatment. This one sounds a bit different.



Successful Muscular Dystrophy Treatment Results Using AVI BioPharma Technology Published in Nature Medicine

BUSINESS WIRE - Feb. 9, 2006 - AVI BioPharma today announced that successful results from a new application of its proprietary NEUGENE(R) antisense technology, called ESPRIT (Exon Skipping Pre-RNA Interference Technology), were reported in the February issue of the prestigious scientific journal Nature Medicine by AVI collaborators at the Australian Neuromuscular Research Institute in Nedlands, Western Australia. The paper is titled "Systemic delivery of morpholino oligonucleotide restores dystrophin expression bodywide and improves dystrophic pathology," and relates to the treatment of Duchenne muscular dystrophy (DMD) in a mouse model of the disease.

ESPRIT therapeutics are designed to either delete disease-causing genetic sequences or skip functional sequences to redesign proteins that are overexpressed or harmful in certain diseases.

"This is a new approach to solving genetic disorders and diseases caused by overexpressed or harmful genes," said Denis R. Burger, Ph.D., chief executive officer of AVI. "ESPRIT therapeutics allow for fine genetic surgery at the RNA processing level, providing a new and very potent tool for altering many disease mechanisms. In addition to genetic disorders such as muscular dystrophy, AVI is now applying the ESPRIT therapeutic approach to diseases with an immunologic component, such as diabetes and multiple sclerosis."

In normal genetic function, gene transcription produces a full-length pre-RNA that is then processed to a much shorter and functional messenger RNA. The mRNA is the template for creating a protein. During pre-RNA processing, packets of useful genetic information, called exons, are snipped out of the full-length RNA and spliced together to make the functional mRNA template. AVI's proprietary third-generation NEUGENE chemistry can be used to target splice-joining sites in the pre-RNA, thus forcing the cell machinery to skip over targeted exons, providing altered mRNA, which in turn produces altered proteins.

Targeting the defective DMD dystrophin pre-RNA with an ESPRIT compound, Dr. Steve Wilton, associate professor and head of the Experimental Molecular Medicine Group at the Australian Neuromuscular Research Institute, forced the cell to snip out the disease-causing mutation region. Using this approach, a functional, but altered, dystrophin protein was made from a DMD gene that would previously have only made a nonfunctional protein.

"Antisense oligomers can alter gene expression by snipping out the disease-causing mutation of a gene transcript during the splicing step of gene expression to convert DMD to the much less disabling Becker muscular dystrophy," said Dr. Wilton. "Morpholino antisense oligomers appear to be the most efficient chemistry approach for exon-skipping, as they exhibit low toxicity, have been administered systemically, results persist for months in the body, and several compounds have already been used in human clinical trials."

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I made this post sticky (long overdue!). Again, thanks to dignan for the OUTSTANDING work in maintaining this listing.

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Disclaimer: Any information you find on this site should not be considered medical advice. All decisions should be made with the consent of your doctor, otherwise you are at your own risk.

I hate doing this, but based on this info from Active Biotech's website, I'm moving laquinimod back to phase II from phase III...



Clinical development of laquinimod proceeding according to plan

Teva’s additional Phase II multi-center study to establish the optimal dose for pivotal Phase III studies is progressing according to plan. This study started recruitment in the first half of 2005 and, comprises slightly more than 300 patients with relapsing MS, is a double-blind, placebo-controlled multi-center Phase IIb clinical study that is in progress in nine countries (Czech Republic, Germany, Hungary, Israel, Italy, Poland, Russia, Spain and the UK). The study measures the effect of laquinimod, administered once daily in tablet form at a dose of 0.3 mg/day and 0.6 mg/day during nine months versus placebo.

Based on the results of this Phase II study, the pivotal Phase III program will be initiated with the aim of confirming laquinimod’s efficacy and safety in the treatment of relapsing MS.

http://hugin.info/1002/R/1035142/167126.pdf

Damn...oh well, there are still other oral treatments further along in the trial process.



Effects of oral glatiramer acetate on clinical and MRI-monitored disease activity in patients with relapsing multiple sclerosis: a multicentre, double-blind, randomised, placebo-controlled study.

Lancet Neurol. 2006 Mar;5(3):213-20.
Filippi M, Wolinsky JS, Comi G; the CORAL Study Group.
Neuroimaging Research Unit, Institute of Experimental Neurology and University Ospedale San Raffaele, Milan, Italy; Department of Neurology, Institute of Experimental Neurology and University Ospedale San Raffaele, Milan, Italy.

BACKGROUND: Parenterally administered glatiramer acetate reduces the frequency of relapses and the formation of active brain lesions seen with MRI in multiple sclerosis. This study assessed whether two doses of glatiramer acetate given orally could improve clinical and MRI measures of inflammation and neurodegeneration in a large cohort of patients with relapsing-remitting multiple sclerosis.

METHODS: 1912 patients with relapsing-remitting multiple sclerosis were screened and 1651 were randomised to receive 50 mg or 5 mg of glatiramer acetate or placebo by daily oral administration over 14 months. The intention-to-treat cohort consisted of 1644 patients who took at least one dose of study medication (50 mg glatiramer acetate [n=543], 5 mg glatiramer acetate [n=553], placebo [n=548]). After baseline investigation, clinical assessments were done every 2 months and MRI was obtained for all patients at baseline and at study exit. Additionally, MRI was undertaken every 2 months for a cohort of 486 patients. The primary outcome was the total number of confirmed relapses observed during the study period. Several prespecified clinical and MRI secondary and tertiary outcomes assessed treatment efficacy on inflammation and neurodegeneration due to multiple sclerosis.

FINDINGS: The cumulative number of confirmed relapses did not differ between the two active treatment groups and the placebo group. Relative to placebo, the rate ratio for the 50 mg glatiramer acetate treated group was 0.92 (95% CI 0.77-1.08, p=0.30) and for the 5 mg glatiramer acetate treated group was 0.98 (0.83-1.15, p=0.76). No drug effect was seen for any of the secondary and tertiary endpoints. The study drug was safe and well tolerated.

INTERPRETATION: 5 mg and 50 mg glatiramer acetate administered orally on a daily basis do not affect relapse rate or other clinical and MRI parameters of disease activity and burden in patients with relapsing-remitting multiple sclerosis. Treatment with oral formulations of glatiramer acetate at the doses tested cannot be recommended.

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Dignan

Probably me but cant see this product Chaperonin10 * http://www.cbio.com.au/products_Cpn10.html from this company CBio, QL http://www.cbio.com.au in your list. It seems to be at Phase II with Prof Simon Broadley http://www.gu.edu.au/school/med/content_staffresearch.html at Griffith Uni, QL Medical School http://www.gu.edu.au/ which as usual seems to be very good for those long suffereing mice. Is it under another name?

* Also known as CPN10 - now wouldnt that be ironic

_________________
John
I am what I am

Nice find, thanks for the information. I added to phase II. I like it when there's a new entry at phase II and the company expects the trial to conclude very soon!

Hi Dignan,

I just observed that ciliary neurotrophic factor (aka CNTF) is listed in both Phase 1 & Pre clinical trails.

Since this is a remyelinating drug I am very interested in it. Is this drug in Phase 1 or pre clinical trail.


I hope this drug is really in Phase 1 trail & comes to market soon (i.e 5 to 6 years)

Good eye. I couldn't find any reference anywhere to a phase I trial of CNTF, so I just left it as "pre-clinical". If somebody knows of a trial, speak now or forever hold your peace.

Hi Dignan,

Is any remyelinating drug in Phase 1 trail ?

Hello, everyone.

I have a related question. I've read that inosine facilitates axonal repair (in mice, anyway), which sounds even more promising than remyelination. However, I can't find any current information about the Phase II inosine trial supposedly taking place at the U. of Penn. I believe they had the funding already in 2001, and the trial was supposed to start in 2002. The NIH web site says this trial is still recruiting patients, but could it be so difficult to find 30 people in a large city? I'm always dubious of conspiracy theories, but I couldn't help but notice that the lead scientist in this trial is a paid consultant at Biogen. Perhaps it would not be in his best interest to prove that an oral OTC product costing $8/bottle is an effective treatment. If anyone knows how this trial is progressing, I'd appreciate the information. Thanks!