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10.1021/acsomega.1c01797 http://scihub22266oqcxt.onion/10.1021/acsomega.1c01797 34235330!8230949!34235330     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=34235330&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       ACS+Omega 2021 ; 6 (25): 16584-16591 Nephropedia Template TP {{tp|p=34235330|t=2021. Inhibition of the 3CL Protease and SARS-CoV-2 Replication by Dalcetrapib |pdf=|usr=}}{{34235330}} gab.com Text Inhibition of the 3CL Protease and SARS-CoV-2 Replication by Dalcetrapib JO: ACS Omega http://www.kidney.de/pget.php?&tw=1&pmid=34235330 #FOAvip The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) 3CL protease is a promising target for inhibition of viral replication by interaction with a cysteine residue (Cys145) at its catalytic site. Dalcetrapib exerts its lipid-modulating effect by binding covalently to cysteine 13 of a cholesteryl ester transfer protein. Because 12 free cysteine residues are present in the 3CL protease, we investigated the potential of dalcetrapib to inhibit 3CL protease activity and SARS-CoV-2 replication. Molecular docking investigations suggested that dalcetrapib-thiol binds to the catalytic site of the 3CL protease with a delta G value of -8.5 kcal/mol. Dalcetrapib inhibited both 3CL protease activity in vitro and viral replication in Vero E6 cells with IC(50) values of 14.4 +/- 3.3 muM and an EC(50) of 17.5 +/- 3.5 muM (mean +/- SD). Near-complete inhibition of protease activity persisted despite 1000-fold dilution after ultrafiltration with a nominal dalcetrapib-thiol concentration of approximately 100 times below the IC(50) of 14.4 muM, suggesting stable protease-drug interaction. The inhibitory effect of dalcetrapib on the SARS-CoV-2 3CL protease and viral replication warrants its clinical evaluation for the treatment of COVID-19. Twit Text FOAVip Inhibition of the 3CL Protease and SARS-CoV-2 Replication by Dalcetrapib ????ACS Omega http://www.kidney.de/pget.php?&tw=1&pmid=34235330 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34235330 #FOAvip English Wikipedia <ref>{{Cite pmid|34235330}}</ref> Inhibition of the 3CL Protease and SARS-CoV-2 Replication by Dalcetrapib #MMPMID34235330 Niesor EJ; Boivin G; Rheaume E; Shi R; Lavoie V; Goyette N; Picard ME; Perez A; Laghrissi-Thode F; Tardif JC ACS Omega 2021[Jun]; 6 (25): 16584-16591 PMID34235330show ga The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) 3CL protease is a promising target for inhibition of viral replication by interaction with a cysteine residue (Cys145) at its catalytic site. Dalcetrapib exerts its lipid-modulating effect by binding covalently to cysteine 13 of a cholesteryl ester transfer protein. Because 12 free cysteine residues are present in the 3CL protease, we investigated the potential of dalcetrapib to inhibit 3CL protease activity and SARS-CoV-2 replication. Molecular docking investigations suggested that dalcetrapib-thiol binds to the catalytic site of the 3CL protease with a delta G value of -8.5 kcal/mol. Dalcetrapib inhibited both 3CL protease activity in vitro and viral replication in Vero E6 cells with IC(50) values of 14.4 +/- 3.3 muM and an EC(50) of 17.5 +/- 3.5 muM (mean +/- SD). Near-complete inhibition of protease activity persisted despite 1000-fold dilution after ultrafiltration with a nominal dalcetrapib-thiol concentration of approximately 100 times below the IC(50) of 14.4 muM, suggesting stable protease-drug interaction. The inhibitory effect of dalcetrapib on the SARS-CoV-2 3CL protease and viral replication warrants its clinical evaluation for the treatment of COVID-19. äInhibition of the 3CL Protease and SARS-CoV-2 Replication by Dalcetrap(epmc).pdf DeepDyve Pubget Overpricing