Biomedical subjects
Publications and source records attributed to J Corbin.
A radiometric method has been established that permits evaluation of the potential of substances to act as modulators of arachidonate lipoxygenase activity. Using this method it has been found that human plasma and amniotic fluid contain substances that are inhibitory and stimulatory of arachidonate lipoxygenase activity.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Can PDE5 inhibitors inhibit fibrosis? Is this a direct effect of PDE5 inhibitors on the fibrotic cascade? If this hypothesis is found true, then an entire new algorithm for treatment of ED and other diseases may be realized. Three recent manuscripts this year discuss this question. Dr Jackie Corbin, a renowned PDE5 expert, offers a perspective in light of its potential clinical relevance.
Despite close structural similarity, vardenafil (Levitra) is 32-fold more potent than sildenafil (Viagra) to inhibit cGMP-binding cGMP-specific PDE (PDE5); this is due to differences between their heterocyclic rings. In co-crystals with PDE5, one of the rings of vardenafil or sildenafil interacts with Tyr(612), a catalytic site AA, via (1) a hydrogen bond with a water molecule and (2) hydrophobic bonds. For mutant PDE5(Y612F), which ablates hydrogen-bonding potential, vardenafil or sildenafil inhibition was strengthened (2.2- or 3.0-fold, respectively), implying that the Tyr(612) hydroxyl is a negative determinant for these inhibitors. For mutant PDE5(Y612A), which ablates both hydrogen bonding and hydrophobic-bonding potential, vardenafil inhibition was weakened much more than sildenafil inhibition (122- and 26-fold, respectively), suggesting that hydrophobic bonds involving Tyr(612) are stronger for vardenafil than for sildenafil.
Explore the source record for details and available documents.