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BACKGROUND In cancer chemotherapy, conventional drugs aim to target the rapidly growing and dividing cells at the early stages. However, at an advanced stage, cancer cells become less susceptible because of the multidrug resistance and the recruitment of alternative salvage pathways for their survival. Besides, owing to target non-selectivity, healthy proliferating cells also become vulnerable to the damage. The combination therapies offered using flavonoids to cure cancer not only exert an additive effect against cancer cells by targetting supplementary cell carnage pathways but also hampers the drug resistance mechanisms. Thus, the review aims to discuss the potential and pharmacokinetic limitations of flavonoids in cancer treatment. Further successful synergistic studies reported using flavonoids to treat cancer has been described along with potential drug delivery systems. METHODS A literature search was done by searching various online databases like Pubmed, Scopus, and Google Scholar with the specific ksuccessful methodologies employed to establish flavonoids as a safe and effective phytochemical class for cancer treatment. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.Kinases remain one of the major attractive therapeutic targets for a large number of indications such as cancer, rheumatoid arthritis, cardiac failure and many others. Design and development of kinase inhibitors (ATP-competitive, allosteric or covalent) is a clinically validated and successful strategy in the pharmaceutical industry. . The perks come with limitations, particularly development of resistance to highly potent and selective inhibitors. That's when the cycle needs to be repeated, i.e., design and development of kinase inhibitors active against the mutated forms. The complexity of tumor milieu makes it awfully difficult for these molecularly-targeted therapies to work. Every year newer and better versions of these agents are introduced in the clinic. Several computational approaches such as structure-, ligand-based or hybrid ones continue to live up to their potential in discovering novel kinase inhibitors. https://www.selleckchem.com/products/loxo-195.html Newer throught processes in this area continue to emerge, e.g., development of dual-target k epub@benthamscience.net.BACKGROUND Different parts of Psidium guajava are consumed as food and for medicinal purposes around the world, and studies have reported their antiproliferative effects via different biochemical mechanisms. Yet, the modulatory effects of compounds derived from this plant on epigenetic modification of DNA molecules via histone deacetylases (HDACs) are largely unknown. OBJECTIVE This in silico study was carried out to investigate the binding propensity of Psidium guajava-derived compounds on the activities of histone deacetylase 6 (HDAC6) and histone deacetylase 10 (HDAC10), for possible application as anticancer agents. METHODS 59 guava-derived compounds and apicidin, a standard HDAC inhibitor, were docked with HDAC6 and HDAC10 using AutodockVina after modeling (SWISS-MODEL server) and validating (ERRAT and VERIFY-3D) the structure of HDAC10, while their molecular interactions with the HDACs were viewed with Discovery Studio Visualizer. Binding sites, surface structural pockets, active sites, area, shape and volume of every pocket, and internal cavities of proteins were predicted using Computed Atlas of Surface Topography of proteins (CASTp) server, while Absorption, Distribution Metabolism and Excretion (ADME) study of notable compounds was done using Swiss online ADME web tool. RESULTS 2α-hydroxyursolic acid, asiatic acid, betulinic acid, crategolic acid, guajadial A and B, guavacoumaric acid, guavanoic acid, ilelatifol D, isoneriucoumaric acid, jacoumaric acid, oleanolic acid, psiguadial A, B and C demonstrated maximum interaction with the selected HDACs. ADME studies reveal that although isoneriucoumaric and jacoumaric acid ranked very high as HDAC inhibitors, they both violated the Lipinski’s rule of 5. CONCLUSION This study identified 13 drugable guava-derived compounds that can be enlisted for further studies as potential HDAC6 and HDAC10 inhibitors. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.INTRODUCTION The present study deals with the effect of Nectaroscordum koelzi fruit extract on acute and chronic inflammation. METHODS Totally, 84 NMRI mice were used in this study. The extract effect on acute inflammation was analyzed by increasing vascular permeability via acetic acid and xylene induced ear edema among mice. The extract was evaluated in terms of effects on chronic inflammation by means of the cotton pellet test among mice. For the assessment of inflammation degree, the mice paw edema volume was measured by the plethysmometric test. RESULTS The findings showed that the extract was effective on acute inflammation induced by acetic acid in mice. In the xylene ear edema, N. koelzi extract indicated the significant activity in mice. In the cotton pellet method, the methanol extract produced a significant reduction in comparison with the control and dexamethasone. Mice paw edema volume decreased with the extract. CONCLUSION In general, the data from the experiments indicated that the methanol extract of N. koelzi has an anti-inflammatory effect on acute and chronic inflammation. However, the exact contributing mechanisms have not been investigated for the pharmacological effects. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.Over the past decade, our increased understanding of the interactions between the immune system and cancer cells has led to paradigm shifts in the clinical management of solid and hematologic malignancies. The incorporation of immune-targeted strategies into the treatment landscape of acute myeloid leukemia (AML), however, has been challenging. While this is in part due to the inability of the immune system to mount an effective tumor-specific immunogenic response against the heterogeneous nature of AML, the decreased immunogenicity of AML cells also represents a major obstacle in the effort to design effective immunotherapeutic strategies. In fact, AML cells have been shown to employ sophisticated escape mechanisms to evade elimination, such as direct immunosuppression of natural killer cells and decreased surface receptor expression leading to impaired recognition by the immune system. Yet, cellular and humoral immune reactions against tumor associated antigens (TAA) of acute leukemia cells have been reported and the success of allogeneic stem cell transplantation and monoclonal antibodies in the treatment of AML clearly provides proof that an immunotherapeutic approach is feasible in the management of this disease.