I am a big user of oral inosine, but I think I have seen this paper before, and it involved injecting it directly, not oral administration....sustained delivery of inosine after injury to the caudal forelimb area in one hemisphere...
ummm.. me.mrbarlow wrote:Anyone else taking Inosine - if so what doses etc?
After posting the above, I thought it sounded a little high... I checked the pack, and its 500mg and the recommended dose is 1-3 tablets before a workout. No mention to be cautious of Gout.CureOrBust wrote:I take it twice a day, 4 capsules at 500mg (ie daily dose of 4g), and will continue until I get Gout, which after more than 4 years, still has not happened. Although my blood-work usually shows high uric acid, its not "off the charts". It was really low before I started.
http://biomed.brown.edu/Courses/BI108/BI108_2001_Groups/Nerve_Regeneration/Gene_Therapy/Gene_Therapy_Page_2.htmThe Master Switch
A whole set of genes is synchronically activated to produce proteins when neural cells engage in regenerative activity. What has eluded scientists for a long time is the answer to this question: Were these genes controlled by many distinct pathways activated by a plethora of growth factors? Or was there some 'master switch' to which many different signals converge to control the molecular program for growth?
Recently, a master switch has been discovered (3). Furthermore, a small, naturally occurring molecule, Inosine, has been shown to promote this molecular program and induce axon growth in the CNS. It seems that Inosine activates this program and activates genes important in neural regeneration. In the normal human brain this system is silent. It only needs to be targeted and turned on, and it appears Inosine serves this function quite well. Isolating the gene that encodes for the enzyme that Inosine works on is the next very important step in using gene therapy to activate this master switch for benefit in regenerating the central nervous system.
http://www.mult-sclerosis.org/news/Jun2000/CNSNerveRegeneration.html"Inosine, the Company's lead compound for nerve regeneration, easily appears to be the most effective compound ever identified (as documented in the scientific literature) in regenerating nerve connections in the CNS. Based on our previous results in stimulating nerve regeneration in the long motor tracts of the spinal cord (as published in the November 9, 1999 issue of the Proceedings of the National Academy of Sciences), we are very excited at the prospect that Inosine may eventually prove to be an effective regenerative therapy for stroke," added Dr. Lanser.
Inosine can be conveniently administered directly into the Cerebral Spinal Fluid (CSF) which bathes the brain, thereby exposing the specifically injured brain tissue to therapeutic amounts of Inosine while minimizing the potential for systemic toxicity. Inosine can potentially be administered via a widely-used delivery system for several months if necessary, in order to promote the optimal amount of regeneration. The Company's Inosine Development Program will concentrate on the optimization of dosage and duration of treatment, pharmacokinetic and toxicity studies, and cGMP production of Inosine for human use. If the preclinical development program is successful, the Company hopes to initiate human trials in 2001.
http://www.childrenshospital.org/dream/dream-fall01/circuits.htmlIn the meantime, Boston Life Sciences Inc., a company developing novel diagnostics and therapeutics for various diseases and disorders, plans to begin Phase I clinical trials using inosine with stroke patients this fall. Phase I trials target safety levels and toxicity of drugs. Since inosine is a naturally occurring molecule, and no toxicity has been detected in animal models, Benowitz and Boston Life Sciences have high hopes for its potential clinical uses.
Therapeutic value of serum uric acid levels increasing in the treatment of multiple sclerosis.
Clinical Center Kragujevac, Center of Neurology, Kragujevac, Srbija.
Uric acid was successfully used in both, prevention and treatment of the animal model of multiple sclerosis (MS). Recently it has been shown that inosine, a ribosylated precursor of uric acid, might be used to elevate serum uric acid levels in MS patients. The aim of this study was to evaluate the safety and efficacy of oral inosine as a single drug treatment in patients with MS.
We administered inosine orally to 32 MS patients from 2001-2004 year at doses from 1-2 g daily (given twice) depending on the pretreatment serum uric acid levels. The mean follow-up interval was 37.69+/-6.55 months. The other 32 MS patients, without any treatment except for a relapse period (matched by age, sex, duration of disease and functional disability), were used as controls. The follow-up interval of these patients was 36.39 +/- 2.68 months. The neurological disability was evaluated by the Expanded Disability Status Scale score (EDSS).
During the observed period the treated MS patients were found to have the lower relapses rate than the non-treated MS patients (Chi-square test, p = 0.001). None of the patients have showed any adverse effect of inosine treatment. The non-treated MS patients were found to have a higher increasing in the mean EDSS score than the treated ones (two-way ANOVA-repeated measures/factor times, p = 0.025).
Our results suggested that the treatment approaches based on the elevation of serum uric acid levels might prove beneficial for some MS patients.
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