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    A non sedating

    receptors mediate the sedative, amnestic, and to some extent the anticonvulsant actions of non-selective benzodiazepine (BZ) receptor ligands, such as diazepam (DZ).Anxiolytic and in part, anticonvulsant actions of BZ ligands are mediated by α2-, α3-, and α5-containing GABA receptors, including α2-, α3-, and α5-subunits, but devoid of efficacy at α1-containing receptors.Pain reduction of this magnitude in patients with diabetic neuropathy is quite significant and better than a lot of current treatments.Plus, this drug has a completely novel mechanism of action and actually treats the cause of the pain instead of masking symptoms." "We are very pleased to see that TV1001sr completely eliminated the headaches associated with the immediate release formulation and extremely excited to see that our second Phase II study once again demonstrated strong and consistent clinical results in the reduction of pain," added Thera Vasc founder and CEO Dr. "In addition to diabetic neuropathy, we believe that there are many other conditions associated with chronic pain that could be treated with TV1001sr." Over 300 million people worldwide suffer from diabetes—a number that is expected to grow by over 50 percent by 2035.Diazepam, the current anticonvulsant of choice in the management of OP poisoning, is associated with unwanted effects such as sedation, amnesia, cardio-respiratory depression, anticonvulsant tolerance, and dependence liabilities.In search for an efficacious and safer anticonvulsant benzodiazepine, we studied imidazenil, a potent anticonvulsant that is devoid of sedative action and has a low intrinsic efficacy at α1- but is a high efficacy positive allosteric modulator at α5-containing GABA receptors.We report here that the combination of atropine and imidazenil is at least 10-fold more potent and longer lasting than the combination with diazepam at protecting rats from DFP-induced seizures and the associated neuronal damage or ongoing degeneration in the anterior cingulate cortex, CA1 hippocampus, and dentate gyrus.While 0.5 mg/kg imidazenil effectively attenuated DFP-induced neuronal damage and the ongoing neuronal degeneration in the anterior cingulate cortex, dentate gyrus, and CA1 hippocampus, 5 mg/kg or a higher dose of diazepam is required to produce similar protective effects.

    No randomised trial has been conducted comparing sedation with no sedation, The non-sedation (NONSEDA) trial is an investigator-initiated, randomised, clinical, parallel-group, multinational trial designed to include 700 patients from at least six ICUs in Denmark, Norway and Sweden.

    Like DZ, the other IMD derivatives (enazenil, RO 25-2776, and RO 25-2847) not only elicit dose-dependent anticonflict, anti-proconflict, anti-BIC, anti-MES effects but also suppress locomotor activity.

    In contrast, none of the IMD derivatives studied shows any similarity to BTZ, which elicits anticonflict, anti-proconflict actions and suppresses locomotor activity but is virtually inactive against BIC-induced tonic–clonic convulsions.

    To define the pharmacological profile of IMD and its derivatives, we compared the anticonflict (anxiolytic), anti-proconflict (antipanic), anti-bicuculline (BIC), and maximal electroshock seizure (MES) effects, and the suppression of locomotor activity by imidazo-benzodiazepine carboxylic acid derivatives to those of DZ and bretazenil (BTZ).

    We report here that IMD and one of its derivatives (RO 25-2775) possess dose-dependent anticonflict, anti-proconflict, and anti-BIC actions but failed to suppress locomotor activity.

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