ACE 2 inhibitors and ARBs:
SARS-CoV-2 binds through ACE 2 receptors found predominantly in the lungs and enters the cells. In a case report, infecting Vero E6 cells with SARS and concomitantly giving human recombinant soluble ACE2 ( hrs ACE 2) to check the inhibitory effects of this drug on the viral entry into the cell. The infection is markedly reduced, and similar observations are obtained by infecting human capillary organoids and kidney organoids. In a prospective study, induced myocardial infarction in rats, which was chronically managed by ATR1 blockers, shows upregulation of cardiac ACE2 receptors. 13Also, kidney ACE 2 receptors were upregulated in rat studies after this treatment. In humans, this is confirmed by raised urinary ACE 2 levels. Viral entry is responsible for the downregulation of ACE 2 receptors, thereby increasing angiotensin responsible for lung injury. Although this seems paradoxical, ATR1 blockers are therapeutically exploited to prevent acute lung injury. [14]In another randomized clinical trial, confirmed COVID-19 patients (n=500) are treated with ACE 2 inhibitor and ATR1 blockers, and their hospital-stay and disease progression is assessed. This treatment is effective in decreasing the mortality rate as compared to those not taking these drugs.[37]
Colchicine:
In uncontrolled case series, COVID patients (n=9) are treated with colchicine, and the safety of the drug is assessed. Symptoms among most of the patients improved. Early administration of this drug is not beneficial as it impairs the immune response, and it is not effective in the later stages due to organ dysfunctioning by the cytokine storm[53]. There are four ongoing pieces of research on colchicine, which mainly address the topic of losing dose effectiveness in controlling myocardial complications, the response in patients with severe infection, efficacy in pneumonia, and reduction in death rate as a result of short-term treatment with this medicine.[36]