Publications by authors named "Luis E Sojo"

Rationale: Na 1.6 is a transmembrane voltage gated sodium channel implicated in various forms of epilepsy. Modulation of its activity in epilepsy animal models can be accomplished using inhibitors which may result in changes in its expression.

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Article Synopsis
  • - Researchers developed a new series of aryl sulfonamides that are very effective (nanomolar potency) and specifically target the human sodium channel hNaV1.7, which is important for pain signaling.
  • - They focused on enhancing the efficacy of these inhibitors while reducing potential safety issues, culminating in the creation of a promising compound (compound 3).
  • - This new compound showed strong pain-relieving effects in animal studies and works by binding to a specific part of the hNaV1.7 channel, highlighting its potential as a therapeutic target for pain management.
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Rationale: Catechols are an important class of analytes occurring in many natural and synthetic products. Electrospray ionization in negative mode is the preferred way of ion generation for these compounds; however, studies in positive ion mode can reveal their potential for in-source oxidation and further structural changes, some of which may also occur in the solution phase. Therefore in-source oxidation can provide a forward look into the potential for solution oxidation.

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The suppression of the internal standard by increasing concentrations of the co-eluting analyte in calibration series and plasma samples analysed by LC-ESI-MS was studied using the isotope dilution technique. A series of three analyte/deuterated analyte pairs including fexofenadine/d6-fexofenadine, dapsone/d4-dapsone and peudoephedrine/d3-ephedrine were investigated. Suppression of the internal standard signal was noticed in extracted plasma samples containing fexofenadine and d6-fexofenadine as internal standard, as well as in solvent based calibration solutions of the three pair of compounds noted above during LC-ESI-MS analysis at flow rates greater than 100 microL min(-1).

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