Holy Cow! Do you realize you probably just put more time and effort into one post on this board than some reporters for major publications are putting into their news stories? I can't believe the amount of brain power on this board! Thanks for taking the time to share. What better protection against a stock market that might correct 20 or 30% than buying a stock that is undervalued by 100 or 200%.
I haven't forgotten about my promise to post more research that adds to the Prurisol picture. The problem is, it's much bigger than I expected.
Other projects, coupled with the explosive growth of nearly every stock I follow, has shifted my focus a bit these past few months so you'll have to forgive me.
One of the most surprising things about this compound is that it is very similar to Lanvis, yet lacks many of the adverse affects typically associated with this cancer drug -often used for psoriasis.
The only blemish in the drugs development, as some of TOB's research pointed out, is that the drugs efficacy was demonstrated in HIV/AIDS patients. As some of you know, SCID mice were used in the preclinical zenograft models. The fact that SCID mice are a great model for HIV/AIDS pathology, makes it hard to say difinitively that the drug works in humans not infected with HIV/AIDS.
I hope investors notice that this drug isn't like the psoriasis drugs of old. Even if the SCID issue causes less of an effect on humans and this isn't really a big 'IF'. I still think an efficacious dose can be found with some alterations.
After today's price movement, I feel most don't understand it's value.
I left off on some promising discoveries, but I'm not very well versed in genetics so that's about where I tapped out.
G1P3 (6-16)
"It is possible that the context of the combined motifs has a profound effect on their function or that small variations in the sequencescan modulate the response(interferon inducible) or even abolish it, as is the case for protein binding for the example of the single base change shown in Figure 6B. While everything is consistent with a major role for the 14 nucleotide sequence, flanking sequences and additional factors may well play an important role in modulating the response."
Overexpression of PRINS is associated with psoriasis susceptibility, with PRINS expression being elevated in the uninvolved epidermis of psoriatic patients compared with both psoriatic lesions and healthy epidermis (Sonkoly 2005).
Guanosine is required for an RNA splicing reaction in mRNA, when a "self-splicing" intron removes itself from the mRNA message by cutting at both ends, re-ligating, and leaving just the exons on either side to be translated into protein.
Nucleophosmin "Our data indicate that PRINS does not act alone, but forms a complex with the NPM protein and contributes to its stress-related intracellular trafficking." http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3565259/
cGMP-Dependent Protein Kinase Inhibitors in Health and Disease "Kinases are enzymes that transmit phosphate groups from a donor, usually a nucleoside triphosphate (e.g., ATP), to specific substrates. This phosphorylation results in a functional change of the substrate protein. A large group of kinases are protein kinases, which catalyze the transfer to a special amino acid in most cases with a free hydroxyl group."
"PRINS is strongly expressed in the uninvolved psoriatic epidermis and its expression is substantially down regulated in the hyper proliferative involved epidermis". This coupled with the use of SCID mice has the potential to skew the data. SCID mice are effective models for HIV/AIDS driven immunosuppression, so previous success in studies with Psoriasis and HIV maybe exclusive to this disease.
Menon could overlooked this in his study, but it's not really clear what methods were used to show PRINS reduction. He's much smarter than I, so I figure he tested the uninvolved tissue.
There are some dead ends in there, but from what I remember most of it is plausible. I whish I had more time to put it altogether concisely for you guys.
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