SARS-CoV-2 virus is responsible for the COVID-19 disease in patients. Only 15-20 % of COVID-19 patients have developed severe pulmonary symptoms and illness, which are fatal to patients. Hyper-immune response to the SARS-CoV-2 virus by the host’s immune system causes the release and over production of certain kinds of inflammatory mediators and cytokines. And it results in the cytokine storm. Cytokine storm produces the hyper inflammatory reaction, which deteriorates the cells and tissue. This type of immune response is host killing and suicidal response to the SARS-CoV-2 virus by the host. This suicidal response ultimately leads to lung damage, respiratory tract pneumonia, ARDS, multi-organ failure at a later stage and ultimately death. Hence, it needs to suppress the hyper-functioning of the immune system to inhibit the cytokine release and cytokine storm. Anti-inflammatory and immuno-modulatory drugs can be repurposed to manage the cytokine storm and hyper-immune response. Inhibition and management of the host’s suicidal immune response and cytokine storm, could be life-saving and reduce the mortality rate in COVID-19 patients.

Objective: Amide is one of the most important functional group presents in the chemicals, pharmaceuticals, and foods. Conventionally, it has been synthesized from the carboxylic acid and amines. This conventional reaction is lengthy and involves hazardous chemicals and solvents. Hence, it poses waste management, solvent removal, and environmental issues to the industries. To overcome this limitation, we have reported the green chemistry-based method for the synthesis of amide from carboxylic acid and urea. Methods: In this reaction, we have used boric acid as a catalyst, it is a simple and readily available compound. It is simple, efficient, and solvent-free procedure which involves the trituration of the reactant mixture and subsequent, direct heating of the triturated mixture. Results: The rate of reaction is very high and can synthesize the amide quickly. Conclusion: Various amides were prepared in good yield by this technique.

Cancer is a tumorous disease, which involves the unwanted cell growth and cell division. The imbalance or inactivity of the apoptosis in the body is responsible for the occurrence of tumour and cancer. This apoptosis is regulated by the p53 protein, which is tumour suppressor protein. In the cancer cells, this p53 has been inhibited by the MDM2 protein. MDM2 interact with the p53 and make it inactive. This p53-MDM2 interaction is responsible for the cancer genesis. If we target this interaction, then we can initiate the apoptosis in the cancer cells by making the free p53 protein. There are many strategies to inhibit this p53-MDM2 interaction. Among them non-peptidic small molecule inhibitors are the convenient approach. Small molecule inhibitors have a three pocket binding, so they bind with p53 binding pocket (Trp 23, Leu 26 and Phe 19), present in the MDM2 protein. That is how it spares the p53 protein and makes it available in the cancer cells. Hence, small molecule inhibitors successfully inhibit the p53-MDM2 interaction and can initiate the apoptosis in the cancer cells, which are having the un-mutated p53 protein. They can't inhibit this interaction in the cells which contains the mutated or deleted p53 protein.Hence, this limitation must be addressed. Many of the small molecular MDM2 inhibitors have been successfully entered into the clinical trials and they are performing well. The clinical data indicate that the small molecular MDM2 inhibitors are having very low toxicity to the normal cells. And they are non-genotoxic so they are near to nontoxic to the normal cells. But none of the any small molecule MDM2 inhibitor has been enters into the market yet. So till then, it has required advancement and research to make more selective and specific for the cancer cells over the normal cells.

Activation of the oncogenes and inhibition of the apoptotic function of the p53 protein is a gateway for the cancer genesis. Interaction of the MDM2 protein with p53 protein is responsible for the inhibition of the p53 function. Inhibiting the p53-MDM2 interaction by drug will lead to the p53 release in the cancer cells. And can restart the apoptosis in the cancer cell. Computational methods successfully used for the design and development of the new, potent MDM2 inhibitors. Researchers and pharma companies used rational approach like target-based drug design or ligand-based drug design to develop the novel MDM2 inhibitors. The number of MDM2 inhibitors, has been designed by the computer-aided drug design and in-silico studies. In clinical studies, MDM2 inhibitors are led by RG7112. RG7112 completed its phase-1 trials in 2016, and recently it is under phase-2 trials. Along with RG7112, the number of potent MDM2 inhibitors entered the clinical trials successfully. It indicates the successful development of this class (MDM2 inhibitors). MDM2 inhibitors were found very effective in various studies for the treatment of various kinds of cancers. They have good selectivity for the tumor cells over the normal cells. It induced the dose dependent cell cycle arrest only; in the normal cells. In studies, MDM2 inhibitors successfully detached the p53 protein from the MDM2 protein. And restart the cell-killing function of the p53 protein in the cancer cells. Hence, MDM2 inhibitors can selectively kill the cancer cells over the normal cells.

Tuberculosis is a disease caused by bacteria spread from person to person through air. TB usually affects the lungs, but it can also affect other parts of the body, such as brain or kidney. Global surveillance has shown that drug resistant TB is widespread and is now a treat to tuberculosis control programs in many countries. This review describes treatment of tuberculosis and the drug resistance problem in India.