Purpose
Bupropion is an antidepressant drug that facilitates weight loss. It is a highly water-soluble drug that needs multiple dosing, so it is considered a potential candidate for oral controlled-release dosage form. The aim of this research was to formulate and evaluate satiety-inducing swellable floating bupropion tablets by direct compression targeting depression associated with eating disorders. Various combinations of natural and semi-synthetic hydrogels were selected to achieve maximum swelling and remaining buoyant in the stomach. This synergistically enhances weight loss by increasing satiety.
Methods
An I-optimal mixture design was conducted to establish the optimal quantitative composition of tablets. Friability, floating lag time, swelling index after 4 and 8 hours, along with the percent of bupropion released at 1 and 8 hours were selected as dependent variables. The optimized formulation was characterized by physicochemical properties, thermal stability, and chemical interaction. In vivo radiographic evaluation of gastric residence besides, the oral bioavailability relative to marketed Wellbutrin
®
sustained-release tablets were investigated using human volunteers.
Results
The optimized formulation (73.3 mg xanthan, 120 mg glucomannan, 8.4 mg tamarind kernel powder, 78.3 mg HPMC K15M) was achieved with the overall desirability equals 0.782. In vivo radiographic study showed that formulation was retained for >8 hours in the stomach. Compared with the marketed BUP tablets, the C
max
was almost the same with a significant increase (p =0.004) for T
max
.
Conclusion
Using combinations of these hydrogels would be promising gastroretentive delivery systems in the control of bupropion rate release with enhanced floating and swelling features.
Intellectual disability (ID) is a condition characterized by defective adaptive and cognitive attitude that can occur with various mental disorders, such as attention deficit/hyperactivity and autism spectrum disorder. It may also be associated with malformation syndromes affecting other organs. Genetic studies have linked several chromatin-modifying enzymes and epigenetic regulators to ID disorders (IDDs). This review explores how dysfunction in histone modifiers, chromatin remodelers, and methyl-DNA binding proteins can cause neurodevelopmental deformities and alter brain plasticity. The use of mouse models generated through human genetics has allowed researchers to uncover the molecular basis of ID and explore potential therapeutic strategies. Understanding the chromatin regulators associated with IDDs has broader implications for treating other IDDs, as they target common downstream genes and cellular functions. Investigating these disorders can also shed light on the function of chromatin regulators in brain growth, plasticity, and gene regulation, leading to new insights into fundamental questions in neurobiology.
Objective: Binge eating disorders (BED) recently become a global health care issue for clinicians with detrimental effects on all organ systems. A multidisciplinary strategy including pharmacotherapy is required for its management.
Methods: This review is intended to comparatively evaluate the relative efficacy of different pharmacological agents in BED treatment with new therapeutic approaches, focusing on the clinical evidence and on Phase III randomized controlled trials.
Results: Data suggest that certain treatments have advantages over placebos to reduce binge eating features; however, the small duration of such research with the lack of adequately sized trials was the major limitation in interpreting these findings. Furthermore, these medications are mostly not greatly efficient for BED associated with obesity except for topiramate, which markedly improves the features of binge episodes with weight loss. Till now, lisdexamfetamine is still the only drug with regulatory permission for BED therapy; however, its weight loss efficacy has not been established.
Conclusion: Drugs alone or in combination approaches may be useful pharmacotherapies to yield promising outcomes acutely and over longer-term follow-up in the treatment of BED.
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