[aftermathman]

to enter phase 3. I know everything is supposed to have neuroprotective qualities, (Azilect, all dop ags, l-dopa etc, my brain will live forever!) however from memory this may be the first "neuroprotective only" drug to have got this far.

I'm probably wrong though

http://sev.prnewswire.com/health-car...5022007-1.html

"Avicena Completes Dose-Escalation Portion of Chronic Toxicology Study of Parkinson's Disease Drug Candidate PD-02
Results Pave Way for Phase III Study in Parkinson's Disease

PALO ALTO, Calif., Feb. 5 /PRNewswire-FirstCall/ -- Avicena Group, Inc. (OTC: AVGO) (BULLETIN BOARD: AVGO) , a biotechnology company focused on commercializing its proprietary cellular energy modulation technology, announced today the completion of the dose-escalating portion of a chronic toxicology study of PD- 02, its lead Parkinson's disease drug candidate. Results, which demonstrated that PD-02 is safe and well-tolerated, will allow Avicena to proceed with patient enrollment in a Phase III Parkinson's disease study.

"We are encouraged by the results to date, and our next step is to initiate patient enrollment for the Phase III trial," stated Belinda Tsao- Nivaggioli, Avicena's chief executive officer. "We are eager to pursue our clinical program to evaluate the potential of PD-02 as a treatment option for patients with Parkinson's disease."

The Food and Drug Administration (FDA) approved a Phase III study design for PD-02 in April 2006, and requested a dose-escalating chronic toxicology study of PD-02 prior to patient enrollment. This Phase III study is designed to evaluate PD-02's potential to slow the progression of Parkinson's disease and will be funded by the National Institute of Neurological Disorders and Stroke (NINDS) of the National Institute of Health. The trial's lead investigators are Karl Kieburtz, M.D., M.P.H., of the University of Rochester in New York, and Barbara C. Tilley, Ph.D., of the Medical University of South Carolina in Charleston.

ABOUT PD-02

PD-02 is Avicena's proprietary therapeutic that has demonstrated the potential to improve neurological function in patients with Parkinson's disease. In preclinical studies, PD-02 has demonstrated significant neuroprotective properties including protection of the dopaminergic cells which are affected in Parkinson's disease".

Aftermathman.

[ashleyk]

There is a good possibility that there is an FDA approved drug available now to slow or stop PD progression, it is LDN, naltrexone, used off-label for many neuro-degenerative, auto-immune diseases and even cancer. I have been taking 4.5mg LDN for 31 months. There have been few clinical trials because it cannot be patented by drug companies so they can not make money from it. Below is a university paper on the first LDN clinical trial used for Crohn's disease, an auto-immune disease.
Ashley

http://www.ncbi.nlm.nih.gov/entrez/q..._uids=17222320
http://www.lowdosenaltrexone.org/index.htm
Links
Low-Dose Naltrexone Therapy Improves Active Crohn's Disease.

* Smith JP,
* Stock H,
* Bingaman S,
* Mauger D,
* Rogosnitzky M,
* Zagon IS.

Department of Medicine, Pennsylvania State University College of Medicine, Hershey, Pennsylvania, USA.

OBJECTIVES: Endogenous opioids and opioid antagonists have been shown to play a role in healing and repair of tissues. In an open-labeled pilot prospective trial, the safety and efficacy of low-dose naltrexone (LDN), an opioid antagonist, were tested in patients with active Crohn's disease. METHODS: Eligible subjects with histologically and endoscopically confirmed active Crohn's disease activity index (CDAI) score of 220-450 were enrolled in a study using 4.5 mg naltrexone/day. Infliximab was not allowed for a minimum of 8 wk prior to study initiation. Other therapy for Crohn's disease that was at a stable dose for 4 wk prior to enrollment was continued at the same doses. Patients completed the inflammatory bowel disease questionnaire (IBDQ) and the short-form (SF-36) quality of life surveys and CDAI scores were assessed pretreatment, every 4 wk on therapy and 4 wk after completion of the study drug. Drug was administered by mouth each evening for a 12-wk period. RESULTS: Seventeen patients with a mean CDAI score of 356 +/- 27 were enrolled. CDAI scores decreased significantly (P= 0.01) with LDN, and remained lower than baseline 4 wk after completing therapy. Eighty-nine percent of patients exhibited a response to therapy and 67% achieved a remission (P < 0.001). Improvement was recorded in both quality of life surveys with LDN compared with baseline. No laboratory abnormalities were noted. The most common side effect was sleep disturbances, occurring in seven patients. CONCLUSIONS: LDN therapy appears effective and safe in subjects with active Crohn's disease. Further studies are needed to explore the use of this compound. (Am J Gastroenterol 2007;102:1-9).

PMID: 17222320 [PubMed - as supplied by publisher]

[jeanb]

Aftermathman,

This may not "count" as the first phase III study for neuroprotection, but from 2002-2005 Cephalon tested CEP-1347 for neuroprotection in a phase II/III trial on 806 people in the U.S. and Canada.

Although in tests on rats & monkeys CEP-1347 provided neuroprotection, it did NOT work on humans. The trial was cancelled in May 2005 because it did not work. In fact the placebo group did better than any of the groups on the trial drug...

I was on the lowest dose... and the people on the lowest dose found their parkinson's symptoms progressed the fastest ... go figure ...

[ZucchiniFlower]

MitoQ is a very exciting drug:

http://neurotalk.psychcentral.com/sh...t=mitochondria

IUBMB Life (International Union of Biochemistry and Molecular Biology: Life)
Publisher: Taylor & Francis
Issue: Volume 57, Number 4-5 / April-May 2005
Pages: 305 - 310
URL: Linking Options
DOI: 10.1080/15216540500092161

How to Clean the Dirtiest Place in the Cell: Cationic Antioxidants as Intramitochondrial ROS Scavengers

Vladimir P Skulachev

A School of Bioengineering and Bioinformatics, and Belozersky Institute of Physico-Chemical Biology, Moscow State University, Moscow, Russia

Abstract:

Membrane-penetrating triphenyl alkyl phosphonium cations have been suggested for many years in our group as having the ability to measure mitochondrial potential were recently used by Murphy as vehicles to specifically target CoQ to mitochondria.

As was shown in our group, the phosphonium derivative of CoQ (MitoQ) easily penetrates a planar bilayer phospholipid membrane as a cation, generating 60? mV electric potential (??) per a 10-fold MitoQ gradient. This means that MitoQ should be unequally distributed across the inner mitochondrial membrane, the intramitochondrial [MitoQ]?=?extramitochondrial [MitoQ]?×?103 at 180? mV ??. In line with such a calculation, Murphy and his colleagues reported that antioxidant efficiency of MitoQ added to mitochondria or cells appears to be very much higher than of CoQ.

It was found that H2O2-induced apoptosis (Murphy) and the H2O2-mediated bystander killing of the cultivated cells (our group) are completely arrested by pretreatement of the cells with 10-10?–?10-8 M MitoQ. These effects indicate that MitoQ and similar compounds may be promising in treatment of heart attack, stroke and other diseases accompanied by massive apoptosis in the injured tissue. The very fact that: (i) MitoQ is not only accumulated by mitochondria but also can be regenerated in its reduced form by mitochondrial respiratory chain, (ii) it is the mitochondrial interior that produces a large portion of reactive oxygen species (ROS) in our body, and (iii) the most sensitive ROS targets are localized in the mitochondrial matrix suggest the MitoQ-like compounds are promising tools of molecular therapy of aerobic cells. In line with this suggestion, we found that addition of MitoQ strongly improves structural and biochemical parameters of cultivated cells.

As to cationic tetrapeptides, recently advertised as mitochondrially-targeted ?? -independent antioxidants, their effect is most probably mediated by an opioid activity inherent in some of these substances.

IUBMB Life, 57: 305–310, 2005

[Ling2]

Jean B,

Could you elaborate further on your statement that "...and the people on the lowest dose found their parkinson's symptoms progressed the fastest..."

[jeanb]

Ling,

i was told that when they evaluated cep-1347 -- they found the people on placebo did the best, and the folks on the lowest dose did the worst. I believe this was determined by the time the participants went on standard pd meds, plus all the UPDRS tests you had to go through in the trial. (I don't know if the SPECT scans came into this finding)

It was not a huge difference. But if you read the data (and understand it ....) I've been told by my doctor (who was also a researcher) that this was the case.