Right, because that's not what clinical trials do.
As I understand it protease inhibitors are developed via molecular engineering. Compounds are designed to bind to specific viral enzymes which in turn disrupts viral replication.
They are synthetic compounds targeted at a specific enzyme.
These compounds are then evaluated in the lab to see if they do as intended, and if so they are probably tested in animals.
At some point there will be clinical trials but the fact that the compound is a protease inhibitor was established long ago.
Now just because something works in the lab (in vitro) doesn't mean it's going to be effective in humans in the real world. That's what clinical trials are for.
Pfizer knows whether a drug is a protease inhibitor or not without doing clinical trials.
A trial tells them that the drug is effective fighting a disease.
RE: Now just because something works in the lab (in vitro) doesn’t mean it’s going to be effective in humans in the real world. That’s what clinical trials are for.
Pfizer knows whether a drug is a protease inhibitor or not without doing clinical trials.
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And how does Pfizer know that?
Isn’t it because they evaluated these compounds in the lab IN ADVANCE and found out that they indeed showed Protease inhibition capabilities? Didn’t they also use computational modeling for this?
Then the next question arises — granted that Ivermectin was NOT originally developed for Covid, but was eventually found via lab observation to exploit protein targets from both virus and human ( as per the NIH study), which could be the reason behind its excellent in vitro efficacy against SARS-CoV-2, and also given that Ivermectin, in computational models, efficiently utilizes viral spike protein, main protease, replicase and human TMPRSS2 receptors as the most possible targets for executing its antiviral efficiency, why then is it appropriate to call Pfizer’s drug a Protease inhibitor but not Ivermectin?
This is especially so given that the NIH found (COPY AND PASTE FROM THEIR STUDY ) :
* The pharmacokinetic attributes of ivermectin were compared with other two anti-SARS-CoV-2 drugs and ivermectin was found to be a safe drug.
* Ivermectin was found to be an efficient inhibitor of Mpro, replicase and hTMPRSS2 and the study manifests a superior ground for the candidature of ivermectin to be an efficient anti-SARS-CoV-2 therapeutic option.
* IVM utilizes viral spike protein, main protease, replicase, and human TMPRSS2 receptors as the most possible targets for executing its antiviral efficiency by disrupting binding