Background and objective Due to the well-documented anti-proliferative activity of 2-thiohydantoin incorporated with pyrazole, oxadiazole, quinazoline, urea, β‑naphthyl carbamate and Schiff bases they are noteworthy in pharmaceutical chemistry. Methods An efficient approach for the synthesis of a novel series of 2-thiohydantoin derivatives incorporated with pyrazole and oxadiazole has proceeded via the reaction of the acyl hydrazide with chalcones and/or triethyl orthoformate. Schiff bases were synthesized by the reaction of the acyl hydrazide with different aromatic aldehydes. Also, Curtius rearrangement was applied to the acyl azide to obtain the urea derivative, quinazoline derivative, and carbamate derivative. Results The synthesized compounds structures were discussed and confirmed depending on their spectral data. The anticancer activity of these heterocyclic compounds was evaluated against the breast cancer cell line (MCF-7), where they showed variable activity. Compound 5d found to has a superior anticancer activity, where it has (IC50 = 2.07 ± 0.13 µg / mL) in comparison with the reference drug doxorubicin that has (IC50 = 2.79 ± 0.07 µg / mL). Then compound 5d subjected to further studies such as cell cycle analysis and apoptosis. Apoptosis was confirmed by the up-regulation of Bax, downregulation of Bcl-2, and the increase of the caspase 3/7percentage. Conclusion Insertion of pyrazole, oxadiazole and, quinazoline moieties with 2-thiohydantoin moiety led to the enhancement of its anti-proliferative activity. Hence they can be used as anticancer agents.As a unique and pleiotropic polymer, d-alpha-tocopheryl polyethylene glycol succinate (Tocophersolan) is a polymeric synthetic version of vitamin E. Tocophersolan has attracted enormous attention as a versatile excipient in different biomedical applications including drug delivery systems and nutraceuticals. The multiple inherent properties of Tocophersolan make it play flexible roles in drug delivery system design, including excipients with outstanding biocompatibility, solubilizer with the ability of promoting drug dissolution, drug permeation enhancer, P-glycoprotein inhibitor and anticancer compound. For these reasons, Tocophersolan has been widely used for improving the bioavailability of numerous pharmaceutical active ingredients. Tocophersolan has been approved by stringent regulatory authorities (such as US FDA, EMA, and PMDA) as a safe pharmaceutical excipient. In this review, we systematically curated current advances in nano-based delivery systems consisting of Tocophersolan with possibilities for futuristic applications in drug delivery, gene therapy, and nanotheranostic.Background Icariin has been shown to enhance bone formation. Objective The present study aimed to investigate whether icariin also promotes bone fracture healing and its mechanisms. Methods First, we isolated and cultured rat bone marrow stromal cells (rBMSCs) with icariin-containing serum at various concentrations (0%, 2.5%, 5% and 10%) and then measured alkaline phosphatase (ALP) activity and the expression of Corebinding factor, alpha 1 (Cbfα1), bone morphogenetic protein-2 (BMP-2) and bone morphogenetic protein-4 (BMP-4) in the rBMSCs. Second, we established a model of fracture healing in rats and performed gavage treatment for 20 days. Then, we detected bone biochemical markers (ELISA kits) in the serum, fracture healing (digital radiography, DR), and osteocalcin expression (immunohistochemistry). CDK inhibitor Results Icariin treatment increased ALP activity and induced the expression of Cbfα1, BMP-2 and BMP-4 in rBMSCs in a dose-dependent manner. In addition, Icariin increased the serum levels of osteocalcin (OC), bone-specific alkaline phosphatase (BAP), N-terminal telopeptides of type I collagen (NTX-1), C-terminal telopeptide of type I collagen (CTX-1) and tartrate-resistant acid phosphatase 5b (TRACP-5b); promoted osteocalcin secretion at the fracture site; and accelerated fracture healing. Conclusions Icariin can promote the levels of bone-formation markers, accelerate fracture healing, and activate the WNT1/β-catenin osteogenic signaling pathway.Background The re-emerging of targeting dihydroorotate dehydrogenase (DHODH) in cancer treatment particularly acute myelogenous leukemia (AML) have corroborated the substantial role of DHODH in cancer and fascinated the attention of many pharmaceutical industries. Objective The effects brequinar sodium (BQR) and 4SC-101 in lymphoblastoid cell lines were investigated. Method DHODH expression and cell proliferation inhibition of lymphoblastoid and lymphoma cell lines were analysed using Western blot analysis and XTT assay respectively. JC-1 probe and ATP biochemiluminescence kit was used to evaluate the mitochondrial membrane potential and ATP generation in these cell lines. Furthermore, we explored the cell cycle progression using Muse™ Cell Cycle Kit. Results Ramos, SUDHL-1 and RPMI-1788 cells are fast-growing cells with equal expression of DHODH enzyme and sensitivity to DHODH inhibitors that showed that the inhibition of DHODH was not cancer specific. In ATP depletion assay, the non-cancerous RPMI-1788 cells showed only a minor ATP reduction compared to Ramos and SUDHL-1 (cancer) cells. In the mechanistic impact of DHODH inhibitors on non-cancerous vs cancerous cells, the mitochondrial membrane potential assay revealed that significant depolarization and cytochrome c release occurred with DHODH inhibitors treatment in Ramos but not in the RPMI-1788 cells, indicating a different mechanism of proliferation inhibition in normal cells. Conclusion The findings in this study provide evidence that DHODH inhibitors perturb the proliferation of non-cancerous cells via a distinct mechanism compared to cancerous cells. These results may lead to strategies for overcoming the impact on non-cancerous cells during treatment with DHODH inhibitors, leading to better therapeutic window in patients.Background Atopic Dermatitis is one of the most common inflammatory skin diseases , with an estimated prevalence of 2.1-4.9% in adults. Recently, advances in Atopic Dermatitis understanding have highlighted the role of an inappropriate Th2 cells activation as principally involved in its pathogenesis. Other immune pathways seem to play a key role in the complex Atopic Dermatitis pathophysiology. The anti-IL-4/IL-13 was the first monoclonal antibody approved for the treatment of moderate to severe atopic dermatitis in adult patients whose disease is resistant to other therapies. Following its interesting results in terms of efficacy and safety new therapies are in development. Methods Monoclonal antibodies targeting IL-5, IL-13, IL-17, IL-22, IL-23, IL-31 and TSLP are currently under investigation on patients with moderate to severe Atopic Dermatitis patients. Moreover also small molecules like anti-PDE4 and JAK inhibitors may also represents other treatment possibilities. Results In this section, we present data available the efficacy and safety of newer molecules for the treatment of Atopic Dermatitis.