http://www.ipharminc.com/brilacidin-1
heres the citation...https://bmcmedicine.biomedcentral.com/articles/10.1186/1741-7015-11-96
this intrigues me about BRILs potential as an anti-PDE4 agent along w/ its other notable properties,ie;highly viracidal, etc.
PDEs are a family of enzymes responsible for the hydrolysis and subsequent inactivation of cyclic nucleotides, and have been organized into at least 11 families based on sequence homogeneity, inhibitor sensitivity, and biochemical properties [12].
Each enzyme within the PDE4 family specifically targets cAMP for degradation and consists of four subtypes (PDE4A to PDE4D). These enzymes are located within brain and immunocompetent cells such as neutrophils, T lymphocytes, macrophages and eosinophils [13].
PDE4 inhibition results in the accumulation of the intracellular second messenger cAMP, downstream activation of protein kinase A (PKA), and subsequent phosphorylation of the transcription factor cAMP-response element binding protein (CREB). Activation of this pathway modulates gene transcription of numerous cytokines, and results in suppression of TNFα production and eventual inhibition of their proinflammatory and destructive properties [14].
so we also know that antiPDE4 can act CENTRALLY and becomes a AE..likle Nausea and vomiting....this does NOT appear to be the case w/ BRIL as AEs are di minimus in all the clin studies Ive reviewed!
GLTA longs!
RP
heres the citation...https://bmcmedicine.biomedcentral.com/articles/10.1186/1741-7015-11-96
this intrigues me about BRILs potential as an anti-PDE4 agent along w/ its other notable properties,ie;highly viracidal, etc.
PDEs are a family of enzymes responsible for the hydrolysis and subsequent inactivation of cyclic nucleotides, and have been organized into at least 11 families based on sequence homogeneity, inhibitor sensitivity, and biochemical properties [12].
Each enzyme within the PDE4 family specifically targets cAMP for degradation and consists of four subtypes (PDE4A to PDE4D). These enzymes are located within brain and immunocompetent cells such as neutrophils, T lymphocytes, macrophages and eosinophils [13].
PDE4 inhibition results in the accumulation of the intracellular second messenger cAMP, downstream activation of protein kinase A (PKA), and subsequent phosphorylation of the transcription factor cAMP-response element binding protein (CREB). Activation of this pathway modulates gene transcription of numerous cytokines, and results in suppression of TNFα production and eventual inhibition of their proinflammatory and destructive properties [14].
so we also know that antiPDE4 can act CENTRALLY and becomes a AE..likle Nausea and vomiting....this does NOT appear to be the case w/ BRIL as AEs are di minimus in all the clin studies Ive reviewed!
GLTA longs!
RP
