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10.1038/s41598-021-84782-w http://scihub22266oqcxt.onion/10.1038/s41598-021-84782-w 33686143!7940615!33686143     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Sci+Rep 2021 ; 11 (1): 5433 Nephropedia Template TP {{tp|p=33686143|t=2021. The in-vitro effect of famotidine on sars-cov-2 proteases and virus replication |pdf=|usr=}}{{33686143}} gab.com Text The in-vitro effect of famotidine on sars-cov-2 proteases and virus replication JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=33686143 #FOAvip The lack of coronavirus-specific antiviral drugs has instigated multiple drug repurposing studies to redirect previously approved medicines for the treatment of SARS-CoV-2, the coronavirus behind the ongoing COVID-19 pandemic. A recent, large-scale, retrospective clinical study showed that famotidine, when administered at a high dose to hospitalized COVID-19 patients, reduced the rates of intubation and mortality. A separate, patient-reported study associated famotidine use with improvements in mild to moderate symptoms such as cough and shortness of breath. While a prospective, multi-center clinical study is ongoing, two parallel in silico studies have proposed one of the two SARS-CoV-2 proteases, 3CL(pro) or PL(pro), as potential molecular targets of famotidine activity; however, this remains to be experimentally validated. In this report, we systematically analyzed the effect of famotidine on viral proteases and virus replication. Leveraging a series of biophysical and enzymatic assays, we show that famotidine neither binds with nor inhibits the functions of 3CL(pro) and PL(pro). Similarly, no direct antiviral activity of famotidine was observed at concentrations of up to 200 microM, when tested against SARS-CoV-2 in two different cell lines, including a human cell line originating from lungs, a primary target of COVID-19. These results rule out famotidine as a direct-acting inhibitor of SARS-CoV-2 replication and warrant further investigation of its molecular mechanism of action in the context of COVID-19. Twit Text FOAVip The in-vitro effect of famotidine on sars-cov-2 proteases and virus replication ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=33686143 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33686143 #FOAvip English Wikipedia <ref>{{Cite pmid|33686143}}</ref> The in-vitro effect of famotidine on sars-cov-2 proteases and virus replication #MMPMID33686143 Loffredo M; Lucero H; Chen DY; O'Connell A; Bergqvist S; Munawar A; Bandara A; De Graef S; Weeks SD; Douam F; Saeed M; Munawar AH Sci Rep 2021[Mar]; 11 (1): 5433 PMID33686143show ga The lack of coronavirus-specific antiviral drugs has instigated multiple drug repurposing studies to redirect previously approved medicines for the treatment of SARS-CoV-2, the coronavirus behind the ongoing COVID-19 pandemic. A recent, large-scale, retrospective clinical study showed that famotidine, when administered at a high dose to hospitalized COVID-19 patients, reduced the rates of intubation and mortality. A separate, patient-reported study associated famotidine use with improvements in mild to moderate symptoms such as cough and shortness of breath. While a prospective, multi-center clinical study is ongoing, two parallel in silico studies have proposed one of the two SARS-CoV-2 proteases, 3CL(pro) or PL(pro), as potential molecular targets of famotidine activity; however, this remains to be experimentally validated. In this report, we systematically analyzed the effect of famotidine on viral proteases and virus replication. Leveraging a series of biophysical and enzymatic assays, we show that famotidine neither binds with nor inhibits the functions of 3CL(pro) and PL(pro). Similarly, no direct antiviral activity of famotidine was observed at concentrations of up to 200 microM, when tested against SARS-CoV-2 in two different cell lines, including a human cell line originating from lungs, a primary target of COVID-19. These results rule out famotidine as a direct-acting inhibitor of SARS-CoV-2 replication and warrant further investigation of its molecular mechanism of action in the context of COVID-19. |A549 Cells[MESH] |Animals[MESH] |COVID-19/virology[MESH] |Chlorocebus aethiops[MESH] |Famotidine/*pharmacology[MESH] |Humans[MESH] |Peptide Hydrolases/*metabolism[MESH] |SARS-CoV-2/drug effects/*enzymology[MESH] |Vero Cells[MESH]The in-vitro effect of famotidine on sars-cov-2 proteases and virus re(epmc).pdf DeepDyve Pubget Overpricing