Adrenergic β-blockers are used to treat many conditions, including hypertension, cardiac arrhythmias, heart failure, angina pectoris, migraine, and tremors. The majority of the β-blockers including Propranolol, Metoprolol, Acebutolol, Alprenolol, Betaxolol, Carvedilol, Nebivolol and Oxprenolol are metabolised majorly by CYP2D6, and Bisoprolol is primarily metabolised by CYP3A4 enzymes. The drugs inhibiting or inducing them may alter the pharmacokinetics of those β-blockers. The plasma concentrations of Propranolol might be elevated by the concomitant use of drugs, such as SSRIs (Fluoxetine, Paroxetine), SNRIs (Duloxetine) and Cimetidine, while the plasma concentrations of Metoprolol increased by the concurrent use of SSRIs (Fluoxetine, Paroxetine), Amiodarone, Celecoxib, Cimetidine, Terbinafine, and Diphenhydramine. β-blockers can also interact pharmacodynamically with drugs, including fluoroquinolones, antidiabetic agents and NSAIDs. In addition, β-blockers may interact with herbs, such as curcumin, Ginkgo biloba, Schisandra chinensis, green tea, guggul, hawthorn, St. John’s wort and Yohimbine. This article focuses on clinically relevant drug interactions of β-blockers with commonly prescribed medications. In addition to Pharmacokinetics and Pharmacodynamics of the drug interactions, recommendations for clinical practice are highlighted. The prescribers and the pharmacists are needed to be aware of the drugs interacting with β-blockers to prevent possible adverse drug interactions.

Alzheimer's disease is an age-associated, irreversible, progressive neurodegenerative disease that is characterized by severe memory loss, unusual behavior, personality changes and a decline in memory function. It is the most common form of dementia and affects an estimated 10 million people worldwide. Alzheimer’s disease demolishes the vital brain cells, causing trouble with memory, thinking and behavior, brutal enough to affect work, lifelong hobbies and social life. Recognized factors in Alzheimer's disease include acetylcholine deficiency, free radicals and inflammation of the brain tissue. There is no cure for Alzheimer's disease, but drugs designed to slow down the disease progression are available. Some herbs may help to improve brain function, but scientific evidence to prove that they can treat Alzheimer's disease. Medicinal plants have been the single most productive source of leads for the development of drugs, and over a hundred new products are already in clinical development. Indeed, several scientific studies have described the use of various medicinal plants and their constituents for treatment of Alzheimer's disease. This review gathers research on various medicinal plants that have shown promise in reversing the Alzheimer's disease pathology. The report summarizes information concerning applications of these various plants in order to provide sufficient baseline information that could be used in drug discovery campaigns and development process, thereby providing new functional leads for Alzheimer's disease.

Since last two decades the work on oleogels is being exploited in pharmaceutical, cosmetics, and nutraceutical industries for their desired rheological, physical, and chemical stabilities in semisolid formulations. Recently, we had developed a

stable and efficacious oleogel containing diclofenac diethylamine for topical application.The present review article deals with the literature of oleogels including its application in various fields from last few decades till date. The literature reveals that the oleogels have simplicity in manufacturing, high physical, chemical, and mechanical stability and better invivo efficacy,which make them appropriate to employ as bases for topical formulations.

Tiagabine (TGB) is an antiepileptic agent enhancing the activity of GABA at neuronal and glial region. It has recently been shown that enhancement of TGB chemical stability was improved by complexation with 2-hydroxypropyl-beta-cyclodextrin (2-HPβCD). The aim of this project is to explain the improvement of the chemical stability of complexed TGB by studying the inclusion properties and factors affecting the complexation selectivity between 2-HPβCD and TGB. Analysis of the interaction between 2-HPβCD and TGB and the effect of 2-HPβCD on TGB solubility was performed by phase solubility method described by Higuchi and Connors; the complexation was followed by characterization using DSC, FTIR and NMR spectroscopy. In aqueous media, the analysis of NMR proton shift change continuous variation method (Job’s plot) and the NMR diffusion-ordered spectroscopy (DOSY) measurements clearly show that TGB form 1:1 inclusion complex with 2-HPβCD with an association constant (K a) of 3396 M⁻¹. More detailed information about the inclusion mode and the geometry of the complex was obtained by the analysis of 2D NMR NOESY experiment and molecular modelling calculations. The inclusion process indicates that A-ring, C10–C11 double bond and the half of the B-ring of TGB molecule were located inside the cavity while the nipecotic acid part of TGB (Ring C) was exposed towards the outside of the 2-HPβCD cavity. These results suggest that the inclusion of the C10–C11 double bond in the 2-HPβCD cavity may possibly the reason of improvement of TGB chemical stability.

The aim of this paper was to describe the use of a 2-hydroxypropyl beta-cyclodextrin (2-HPβCD) as a tool to improve the chemical stability of tiagabine hydrochloride (TGB). HPLC method was used to quantify TGB. The correlation coefficient of the linearity (r2) of HPLC method was more than 0.999 whilst the limit of detection and the limit of quantification of TGB were 0.6494 μg ml-1 and 1.765μg ml-1 respectively. The effect of 2-HPβCD on the chemical stability of TGB was compared with α-tocopherol and ascorbic acid, the most recognized antioxidants used to enhance the stability of TGB. The stability was expressed by (% w/w) of the total related substances (TRS) of TGB. When TGB was exposed for 24 h to 50°C, the TRS were 3.264% (SD ±0.077) and 3.125% (SD ±0.053) in the presence of α-tocopherol and ascorbic acid, respectively. The TRS of TGB complexed with 2-HPβCD was 2.142% (SD ±0.045). This study demonstrates that 2-HPβCD exhibits an obvious enhancement of TGB chemical stability with a different mechanism compared with the usual antioxidants.