Glucose monitoring is essential for managing diabetes, and continuous glucose monitoring biosensors can offer real-time monitoring with little invasiveness. However, challenges remain in improving sensor accuracy, selectivity, and overall performance. This article aims to review current trends and recent advancements in glucose-monitoring biosensors while evaluating their benefits and limitations for diabetes monitoring. An analysis of current literature on transdermal glucose sensors was conducted, focusing on detection techniques, novel nanomaterials, and integrated sensor systems. Recent research has led to advancements in electrochemical, optical, electromagnetic, and sonochemical sensors for transdermal glucose detection. The use of novel nanomaterials and integrated sensor designs has improved sensitivity, selectivity, and accuracy. However, issues like calibration requirements, motion artifacts, and skin irritation persist. Transdermal glucose sensors show promise for non-invasive, convenient diabetes monitoring but require further enhancements to address limitations in accuracy, reliability, and biocompatibility. Continued research and innovation focusing on sensor materials, designs, and surface chemistry is needed to optimize biosensor performance and utility. The study offers a comprehensive analysis of the present status of technological advancement and highlights areas that need more research.

Background: Multiple myeloma (MM) is a hematological malignancy of plasma cells that produce a monoclonal immunoglobulin protein. Despite significant advances in the treatment of MM, currently available therapies are associated with toxicity and resistance. As a result, there is an increasing demand for novel, effective therapeutics. Inhibition of histone deacetylases (HDACs) is emerging as a potential method for treating cancer. HDAC6 is one of 18 different HDAC isoforms that regulate tubulin lysine 40 and function in the microtubule network. HDAC6 participates in tumorigenesis and metastasis through protein ubiquitination, tubulin, and Hsp90. Several studies have found that inhibiting HDAC6 causes AKT and ERK dephosphorylation, which leads to decreased cell proliferation and promotes cancer cell death via the PI3K/AKT and MAPK/ERK signaling pathways. Objective: The objective of this study is to target HDAC6 and identify potent inhibitors for the treatment of multiple myeloma by employing computer-aided drug design. Materials and Methods: A total of 199,611,439 molecules from five different chemical databases, such as CHEMBL25, ChemSpace, Mcule, MolPort, and ZINC, have been screened against HDAC6 by structure- based virtual screening, followed by filtering for various drug-likeness, ADME, toxicity, consensus molecular docking, and 100 ns MD simulation. Results: Our research work resulted in three molecules that have shown strong binding affinity (CHEMBL2425964 -9.99 kcal/mol, CHEMBL2425966 -9.89 kcal/mol, and CSC067477144 -9.86 kcal/mol) at the active site HDAC6, along with effective ADME properties, low toxicity, and high stability. Inhibiting HDAC6 with these identified molecules will induce AKT and ERK dephosphorylation linked to reduced cell proliferation and promote cancer cell death. Conclusion: CHEMBL2425964, CHEMBL2425966, and CSC067477144 could be effective against multiple myeloma.

The discovery of effective breast cancer therapy is both urgent and daunting, beset by a myriad of challenges that range from the disease's inherent heterogeneity to its complex molecular underpinnings. Drug resistance, the intricacies of the tumor microenvironment, and patient-specific variables further complicate this landscape. The stakes are even higher when dealing with subtypes like triple-negative breast cancer, which eludes targeted hormonal therapies due to its lack of estrogen, progesterone, and HER2 receptors. Strategies to overcome such challenges include combinations of drugs and identifying new drug targets. Developing new drugs based on such targets could be a better solution than relying on costly immunotherapy or combinational therapies. In this review, we have endeavored to comprehensively examine the proven therapeutic drug targets associated with breast cancer and elucidate their respective molecular mechanisms and current clinical status. This study aims to facilitate researchers in conducting a comparative analysis of different targets to select single and multi-targeted drug discovery approaches for breast cancer.

Background: Even with the massive increase in financial investments in pharmaceutical research over the last decade, the number of new drugs approved has plummeted. As a result, finding new uses for approved pharmaceuticals has become a prominent alternative approach for the pharmaceutical industry. Objective: Drug repurposing or repositioning is a game-changing development in the field of drug research that entails discovering additional uses for previously approved drugs. Methods: In comparison to traditional drug discovery methods, drug repositioning enhances the preclinical steps of creating innovative medications by reducing the cost and time of the process. Drug repositioning depends heavily on available drug-disease data, so the fast development of available data as well as developed computing skills has resulted in the boosting of various new drug repositioning methods. The main goal of this article is to describe these different methods and approaches for drug repurposing. Results: The article describes the basic concept of drug repurposing, its significance in discovering new medications for various disorders, drug repurposing approaches such as computational and experimental approaches, and previous as well as recent applications of drug repurposing in diseases such as cancer, COVID-19, and orphan diseases. Conclusion: The review also addresses obstacles in drug development using drug repurposing strategies, such as a lack of financing and regulatory concerns and concludes with outlining recommendations for overcoming these challenges.

The field of drug discovery has long been challenged by the existence of "undruggable" proteins - targets that have resisted traditional small molecule approaches due to their structural or functional characteristics. This review explores the revolutionary potential of small interfering RNA (siRNA) technology in addressing these elusive targets, marking a paradigm shift in therapeutic development. We discuss the historical development of siRNA technology and its unique mechanism of action, which allows for the silencing of virtually any gene, including those coding for proteins previously deemed undruggable. The review provides a comprehensive analysis of the challenges in targeting undruggable proteins and how siRNA approaches are overcoming these obstacles. We examine several case studies of undruggable targets being successfully addressed by siRNA, including oncogenic proteins like KRAS and c-Myc, transcription factors such as NF-κB and STAT3, and proteins involved in complex protein-protein interactions. The article delves into the latest advances in siRNA design, delivery systems, and targeting strategies, highlighting innovations that enhance specificity and reduce off-target effects. We also discuss the challenges facing siRNA therapeutics, including delivery obstacles, potential immune responses, and regulatory considerations. The review concludes with an exploration of future directions, including combination therapies, personalized medicine approaches, and emerging technologies that complement siRNA strategies. By providing a thorough examination of the advances, challenges, and prospects of using siRNA to target undruggable proteins, this review underscores the transformative potential of this technology in expanding the landscape of therapeutic targets and ushering in a new era of precision medicine.

Background: CDK4/6 plays a crucial role in regulating cell proliferation, and inhibiting this kinase can effectively prevent the initiation of cell growth and division. However, current FDAapproved CDK4/6 inhibitors have limitations such as poor bioavailability, adverse effects, high cost, and limited accessibility. Thus, this research aimed to discover novel CDK4/6 inhibitors to overcome the challenges associated with FDA-approved inhibitors. Methods: To identify potential CDK4/6 inhibitors, we have performed structure-based virtual screening. Chem-space and Mcule databases have been screened, followed by a series of filtering steps. These steps included assessing drug-likeness, PAINS alert, synthetic accessibility scores, ADMET properties, consensus molecular docking, and performing molecular dynamics simulations. Results: Four new compounds (CSC089414133, CSC091186116, CSC096023304, CSC101755872) have been identified as potential CDK4/6 inhibitors. These compounds exhibited strong binding affinity with CDK4/6, possessed drug-like features, showed no PAINS alert, had a low synthetic accessibility score, demonstrated effective ADMET properties, were non-toxic, and exhibited high stability. Conclusion: Inhibiting CDK4/6 with the identified compounds may lead to reduced cell proliferation and the promotion of cancer cell death.