Diabetes mellitus, a very common and multifaceted metabolic disorder is considered as one of the fastest growing public health problems in the world. It is characterized by hyperglycemia, a condition with high glucose level in the blood plasma resulting from defects in insulin secretion or its action and in some cases both the impairment in secretion and also action of insulin coexist. Historically, animal models have played a critical role in exploring and describing malady pathophysiology and recognizable proof of targets and surveying new remedial specialists and in vivo medicines. In the present study, we reviewed the experimental models employed for diabetes and for its related complications. This paper reviews briefly the broad chemical induction of alloxan and streptozotocin and its mechanisms associated with type 1 and type 2 diabetes. Also we highlighted the different models in other species and other animals.

The alpha (α)-amylase is a calcium metalloenzyme that aids digestion by breaking down polysaccharide molecules into smaller ones such as glucose and maltose. In addition, the enzyme causes postprandial hyperglycaemia and blood glucose levels to rise. α-Amylase is a well-known therapeutic target for the treatment and maintenance of postprandial blood glucose elevations. Various enzymatic inhibitors, such as acarbose, miglitol and voglibose, have been found to be effective in targeting this enzyme, prompting researchers to express an interest in developing potent alpha-amylase inhibitor molecules. The review mainly focused on designing different derivatives of drug molecules such as benzofuran hydrazone, indole hydrazone, spiroindolone, benzotriazoles, 1,3-diaryl-3-(arylamino) propan-1-one, oxadiazole and flavonoids along with their target-receptor interactions, IC 50 values and other biological activities.

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According to the latest data, the cancer prevalence fraction has surged to the highest number. This is why cancer has become a prominent disease that must be seen as a serious issue. Inhibitory action and ideas become prominent and necessary because of the rising death incidence daily. The simplifying idea of inhibition of cancer is targeting the complex that forms between the tyrosine kinase and ATP, which ultimately provides a clear way. Tyrosine kinase is a proteinaceous enzyme responsible for various cellular events like cell development, growth, and division. But these functions are performed by the activated tyrosine kinase, and the activation occurs by phosphorylation using ATP. The transfer of the phosphate group from ATP to tyrosine is known as phosphorylation. The basic idea is to enhance the competitive inhibition of the ATP-Tyrosine complex is a promising target for treating cancer. Various molecules have a substantial effect on the above-said target. This review summarizes molecules currently in any drug development or clinical trial with the same effect. This review covers most inhibitory molecules from different categories, which either directly or indirectly inhibit the Tyrosin kinase-ATP complex by incorporating.

Recently released Globocan-2020 report has been disclosed an increase in new cancer cases, cancer deaths, and 5-year prevalence cases worldwide. The higher percent proportions of cancer deaths as compared to their incidence percentage in Asia and Africa. Cancer is a genetic but not inheritable disease that consists of various abnormal cells. Depending upon the nature and site of availability of cells cancer can spread all over the body. These abnormal cells can grow infinitely in which tyrosine kinases (TKs) play an important role as mediators for cellular signal transduction processes during migration, metabolism, proliferation and differentiation, apoptotic cell death, etc. TKs belong to a specific family of an enzyme that catalyses the transferring of phosphate groups from ATP to selected tyrosine residues of a target protein during the biological process to maintain the homeostasis. They work in various steps of development and progression pathways of cancer by affecting signal transduction. The aberrant and deregulated functioning of TKs results in a defective signal transduction pathway which leads to abnormality in cell transformation, proliferation, and differentiation, thus the development of cancer. Since their discovery in 1990 to date, more than 90 TKs have been reported and divided into two categories receptor and non-receptor TKs. Higher expression levels of TKs paved their status of oncoprotein and thus, they provide a potential target for the development of anti-cancer therapeutics. Here, we provided updated cancer demographic status, cancer types, and available therapeutic options targeted cancer therapeutic strategies and the role of different TKs in cancers along with recently identified molecules that target TKs. Moreover, we also included the binding interactions of chemical inhibitors with TKs.