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Re: PlentyParanoid post# 222181

Friday, 03/23/2018 4:19:33 PM

Friday, March 23, 2018 4:19:33 PM

Post# of 403147
Right, the company hasn't stated how prurisol (abacavir acetate or glycolate) might work, only that abacavir (and its metabolites? such as carbovir triphosphate - a nucleoside reverse transcriptase inhibitor antiviral drug) is NOT the active moiety.

Some here imply that prurisol directly inhibits IL-20, but I imagine the reduction in PRINS and IL-20 in psoriasis preclinical models is most likely some downstream effect of the causative mechanism of action of whatever is the "active moiety" (glycolic acid?) of prurisol in psoriasis - and not directly causative of reduced IL-20 in and of itself.

There are biologics in use or development for psoriasis that target some of these chemokines directly, such as anti-IL-17, anti-IL-23, and anti-IL-20 antibodies. Prurisol does something different.

A recent article on PRINS shows it to be anti-inflammatory in keratinocytes:

https://www.frontiersin.org/articles/10.3389/fimmu.2017.01053/full

So whatever prurisol does, the cell might respond by producing less of the PRINS stress response.

Molecular biology of many diseases is such a puzzle ...
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