Coronavirus COVID-19

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Re: Coronavirus COVID-19

Post by JohnStOnge »

I'm surprised I just noticed this today: https://www.ama-assn.org/press-center/p ... t-covid-19.
The American Medical Association (AMA), American Pharmacists Association (APhA), and American Society of Health-System Pharmacists (ASHP) strongly oppose the ordering, prescribing, or dispensing of ivermectin to prevent or treat COVID-19 outside of a clinical trial.
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Re: Coronavirus COVID-19

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JohnStOnge wrote: Thu Nov 18, 2021 4:26 pm I'm surprised I just noticed this today: https://www.ama-assn.org/press-center/p ... t-covid-19.
The American Medical Association (AMA), American Pharmacists Association (APhA), and American Society of Health-System Pharmacists (ASHP) strongly oppose the ordering, prescribing, or dispensing of ivermectin to prevent or treat COVID-19 outside of a clinical trial.
You and many on this message board are too focused on political bickering to notice any medical stuff.
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Re: Coronavirus COVID-19

Post by JohnStOnge »

Gil Dobie wrote: Thu Nov 18, 2021 6:17 pm
JohnStOnge wrote: Thu Nov 18, 2021 4:26 pm I'm surprised I just noticed this today: https://www.ama-assn.org/press-center/p ... t-covid-19.

You and many on this message board are too focused on political bickering to notice any medical stuff.
Not at all. I AM focused on medical stuff. This should not be political. But it is. My position has always been to listen to the credible sources. It's not "political bickering" to say that ivermectin has not been shown to be effective according to the recognized standards. That's completely consistent with being "medical"

Same with the vaccine stuff. It's not "political bickering" to say that the vaccines are safe and effective. That's the mainstream medical outlook.

Same with the idea that COVID-19 is indeed a serious problem. That's a mainstream medical outlook.
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Re: Coronavirus COVID-19

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JohnStOnge wrote: Thu Nov 18, 2021 4:01 pm
SeattleGriz wrote: Wed Nov 17, 2021 7:57 pm

Dude. Please. Within the first 60 words of your article:



I said right in my post (which one can see above) this drug and Ivermectin were both protease inhibitors. :ohno: CL3 Protease inhibitors no less.

This is serious. Stop wasting time trolling.
I should have provided some quotes in the article. There is discussion of the protease inhibitor angle later on. Here are some quotes from the article:
Some iterations of the claim incorrectly posit that Pfizer’s drug is “based on” ivermectin and that the two are essentially the same because both are protease inhibitors — something that has not been established, and even if true, doesn’t mean the drugs are similar, as we’ll explain.
The supposed connection, according to a computational modeling paper published by some Indian scientists in March, is that ivermectin might act as a protease inhibitor, among other potential mechanisms. This alleged connection is made explicit in social media posts with a graphic juxtaposing a Pfizer press release and the abstract of the Indian paper.That paper, however, does not show that ivermectin acts as a protease inhibitor against SARS-CoV-2 through any sort of biological experiment — it only proposes the possibility based on computer simulations.

The data so far do not support using ivermectin to treat COVID-19, although clinical trials are underway to find out for sure. But if the drug does work, it is likely not through protease inhibition or any other antiviral mechanism, as the dose needed to see antiviral effects in the test tube is much higher than the amount prescribed to people.
“Pfizer’s 3CL protease inhibitor is nothing like ivermectin,” Dr. David Boulware, an infectious disease specialist at the University of Minnesota, told us in an email.
Several mechanisms have been proposed for how ivermectin limits coronavirus replication in cells in the lab, but protease inhibition, as is claimed in social media posts, is not generally one of them.

More often, scientists — including the Australians who first published on the drug — cite the drug’s potential ability to prevent a host protein from importing viral proteins into the nucleus, or, more rarely, to interfere with SARS-CoV-2’s ability to use its spike protein to enter human cells.
“While one could debate the exact mechanism of ivermectin, the biggest difference is that pfizer’s protease inhibitor inhibits coronavirus at concentrations that are achievable in the human body,” said Boulware, who is an investigator on a clinical trial at the University of Minnesota evaluating ivermectin as an outpatient COVID-19 treatment. “In the initial lab experiments, ivermectin required 50-100x the achievable concentrations in humans.”
You can find more by doing a find on the word "protease" in the article.
So much wrong in your quote mining. I'll just say, "no". Weak sauce.
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Re: Coronavirus COVID-19

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SeattleGriz wrote: Fri Nov 19, 2021 11:02 pm
JohnStOnge wrote: Thu Nov 18, 2021 4:01 pm

I should have provided some quotes in the article. There is discussion of the protease inhibitor angle later on. Here are some quotes from the article:











You can find more by doing a find on the word "protease" in the article.
So much wrong in your quote mining. I'll just say, "no". Weak sauce.
I did the quotes because it looked like you didn't read far enough down in the article to see all the stuff contradicting the idea the ivermectin and the Pfizer drug are equivalent in that they are both protease inhibitors. There's language saying it hasn't even been shown that ivermectin acts as a protease inhibitor against SARS-CoV-2 through biological experiments. It's one possible mechanism proposed during a modeling exercise. There are quotes from a guy who is an investigator in an ivermectin clinical trial saying Pfizer’s 3CL protease inhibitor is nothing like ivermectin. There's a quote from the same guy saying that Pfizer's medication is different from ivermectin in that Pfizer’s protease inhibitor inhibits coronavirus at concentrations that are achievable in the human body. I think it's fair to interpret that as him saying that ivermectin does not, as a protease inhibitor, inhibit coronavirus at concentrations that are achievable in the human body. There's a statement that researchers who do think ivermectin may be effective don't think that it's effective because it is a protease inhibitor. They point to other mechanisms.

You have the link to the piece. Read the whole thing. I'm not misrepresenting the content. There's no way to interpret it as saying anything other than that the idea that ivermectin is similar to the Pfizer drug or the Merck drug is false. It also clearly makes the argument that the attempt to draw a "protease inhibitor" parallel is bogus.
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Re: Coronavirus COVID-19

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JohnStOnge wrote: Sat Nov 20, 2021 12:18 pm
SeattleGriz wrote: Fri Nov 19, 2021 11:02 pm

So much wrong in your quote mining. I'll just say, "no". Weak sauce.
I did the quotes because it looked like you didn't read far enough down in the article to see all the stuff contradicting the idea the ivermectin and the Pfizer drug are equivalent in that they are both protease inhibitors. There's language saying it hasn't even been shown that ivermectin acts as a protease inhibitor against SARS-CoV-2 through biological experiments. It's one possible mechanism proposed during a modeling exercise. There are quotes from a guy who is an investigator in an ivermectin clinical trial saying Pfizer’s 3CL protease inhibitor is nothing like ivermectin. There's a quote from the same guy saying that Pfizer's medication is different from ivermectin in that Pfizer’s protease inhibitor inhibits coronavirus at concentrations that are achievable in the human body. I think it's fair to interpret that as him saying that ivermectin does not, as a protease inhibitor, inhibit coronavirus at concentrations that are achievable in the human body. There's a statement that researchers who do think ivermectin may be effective don't think that it's effective because it is a protease inhibitor. They point to other mechanisms.

You have the link to the piece. Read the whole thing. I'm not misrepresenting the content. There's no way to interpret it as saying anything other than that the idea that ivermectin is similar to the Pfizer drug or the Merck drug is false. It also clearly makes the argument that the attempt to draw a "protease inhibitor" parallel is bogus.
The whole premise of your article is that the new Pfizer drug isn't the same as Ivermectin, which is pretty obvious from the chemical structure. I said nothing of the sort. I said Ivermectin was a 3CL Protease Inhibitor, just like the Pfizer drug, which is true. They don't even have to have the same mechanism of action and they can still be Protease Inhibitors. Do you know the difference between competitive and non-competitive inhibition? You've created this straw man type argument that has not refuted what I said in any way, shape or form.

As you don't seem to grasp what an actual protease inhibitor in this case means, let me give you a quick overview of what is happening. After the virus "invades" your cell, it then uses your cells machinery to make a polypeptide. This polypeptide has something like 12 proteins in one long string that 3CL needs to cut free. If you can prevent the 3CL protease from cutting the proteins free, you "inhibit" the protease from doing its job.

This can be done by two main options. One is to jam up the "cutting" portion and the other is to prevent the Protease from joining, as it requires two units to join together to become functional (dimerization).

From the journal in which you erroneously claim it is only in a computer simulation: (https://www.nature.com/articles/s42003-020-01577-x)
The protein structure-based drug design using computational methods is an alternative for screening of currently approved drugs to rapidly identify potential drug candidates for the treatment of emerging infectious diseases such as COVID-1915,16,17. However, the potential for false positives with computational modeling is one of the most common limitation of docking studies18. Therefore, we have established SARS-CoV-2 3CLpro enzymatic assays for selected drugs using commercially available 3CLpro protease inhibitor screening assay kits to evaluate the in vitro inhibitory activity of the drugs and investigated whether any correlation exist between the computational binding score and the in vitro inhibitory activity.
In other words, they used computational methods (in silico) to narrow down 3987 approved drugs to 47 so they COULD RUN STUDIES IN VITRO. Do you know what In Vitro means?

Lastly,
We observed that, boceprevir, ombitasvir, paritaprevir, tipranavir, and micafungin exhibited partial inhibitory effect whereas, ivermectin blocked more than 85% of 3CLpro activity of SARS-CoV-2. Although the anti-viral activity of ivermectin mediated through the blocking of α/β1 importin19,20,21,22,23 is established, herein we report the inhibitory effects of ivermectin on 3CLpro enzyme of SARS-CoV-2, suggesting additional anti-viral mechanism of ivermectin towards SARS-CoV-2
Interestingly, one of the OTD, ivermectin was able to inhibit more than 85% (almost completely) of 3CLpro activity in our in vitro enzymatic assay with an IC50 value of 21 µM. These findings suggest the potential of ivermectin to inhibit the SARS-CoV-2 replication. In support of this, a recent finding suggested that ivermectin (5 µM) inhibited the replication of live SARS-CoV-2 isolated from Australia (VIo1/2020) in Vero/hSLAM cells23. They found that >5000-fold viral counts were reduced in 48 hr in both culture supernatant (release of new virion: 93%) as well as inside the cells (unreleased and unassembled virion: 99.8%) when compared to DMSO treated infected cells. Interestingly, this study reported the IC50 value of ivermectin as 2.5 µM23, whereas, we observed an IC50 value of 21 µM (10-fold increase). The variability in the IC50 values reported could be attributed towards the differences in the assay conditions such as the use of live virus vs enzymatic assay with purified 3CLpro protein. Further, preclinical studies need to be established to validate the in vivo inhibitory activity and IC50 values of ivermectin.

Ivermectin is known to be effective against many positive-sense, single stranded RNA viruses such as Zika, Dengue, Yellow fever, West nile, Venezuelan equine encephalitis, Chikungunya, Semliki forest, Sindbis, Rorcine Reproductive and Respiratory Syndrome, and Human immunodeficiency-1 viruses38. The list of anti-viral effects of ivermectin against other RNA and DNA viruses were summarized in a recent review38. Earlier studies have demonstrated that the possible anti-viral mechanism of ivermectin was through the blockage of viral-protein transportation to the nucleus by inhibiting the interaction between viral protein and α/β1 importin heterodimer, a known transporter of viral proteins to the nucleus especially for RNA viruses19,20,21,22,23. However, in this study, we have reported that ivermectin inhibits the enzymatic activity of SARS-CoV-2 3CLpro and thus may potentially inhibit the replication of RNA viruses including SARS-CoV-2. These studies suggest that ivermectin could be a potential drug candidate to inhibit the SARS-CoV-2 replication and the proposed anti-viral mechanism of ivermectin presented in Fig. 8 and in vivo efficacy of ivermectin towards COVID-19 is currently been evaluated in clinical trials (ClinicalTrials.gov Identifier: NCT04438850).
If you want to read some real science, this gal does a great job of explaining what is happening with the Pfizer drug.

https://thebumblingbiochemist.com/365-d ... inhibitor/
For now, just know that if this peptide gets cut by the protease, the fluorophore and the quencher will be separated so you won’t see light – and this tells you that the protease is active. If you add an inhibitor that works, you should keep seeing light. ⠀

PF-07321332 passed this test. How does it work?

That nitrile nitrogen is really negative – atoms (like those individual carbons and oxygens) join together to form molecules by sharing pairs of negatively-charged subatomic particles called electrons, but some don’t share fairly. Nitrogen is a major electron hog (it’s highly electronegative) so, in the carbonyl, it draws the shared electrons closer to it, making it partly negative and the carbon partly positive. The carbon thus “wants” more electrons so it’s called electrophilic.

The active site’s catalytic Cysteine has a sulfur that wants to share electrons (is electrophilic) thanks to the Histidine pulling off its proton, so the sulfur attacks the electrophilic carbon, leading the compound to get stuck on.

It gets covalently stuck through a thioimidite adduct, as you can see in the structure of it bound to MPro, PDB 7si9 https://www.rcsb.org/structure/7si9

but it’s reversible inhibition. So it’s strongly stuck but it can still come off since enzymes can catalyze reactions in both directions and you literally have it stuck in the active site, where enzymes do their biochemical magic. But the forward direction is greatly favored, so it stays stuck pretty well.

It also passed additional tests for bioavailibilty and stuff.

But it wasn’t lasting long enough once the liver had a say. Instead, it was being modified by CYP enzymes, leading to them being excreted quickly. So that’s why they added ritonavir – it inhibits a CYP enzyme in our body that they show to be responsible.
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Re: Coronavirus COVID-19

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Is it possible for 2 protease inhibitors to exist and be used in different applications/different types of patients?

In other words, they all aren't created and used equally.
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Re: Coronavirus COVID-19

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Ibanez wrote: Mon Nov 22, 2021 6:50 am Is it possible for 2 protease inhibitors to exist and be used in different applications/different types of patients?

In other words, they all aren't created and used equally.
Im sure you can use multiple applications, I just can't think of a good example.

Correct! Not all inhibitors are created equal. Here are just a couple of factors to consider:

What is the concentration level of the inhibitor? If you have more, it obviously has more opportunity to bind and inhibit. If you remember any Chemistry, concentration drives reactions

Is it competitive or noncompetitive inhibition? The easiest way to understand this would be to think of a pair of scissors. In competitive inhibition, we are blocking the scissors from cutting by jamming up the actual blades. The inhibitor is competing with the protein for a space on the scissor blades. In noncompetitive, we simply tape the scissor handles together so you can't open the scissors to cut. It's noncompetitive, because you aren't competing with the protein for the active spot.

Simple effectiveness of how strongly the inhibitor binds to it's spot. If it can be knocked off easily, it obviously won't be as good as one that's binds hardcore.
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Re: Coronavirus COVID-19

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SeattleGriz wrote: Mon Nov 22, 2021 7:07 am
Ibanez wrote: Mon Nov 22, 2021 6:50 am Is it possible for 2 protease inhibitors to exist and be used in different applications/different types of patients?

In other words, they all aren't created and used equally.
Im sure you can use multiple applications, I just can't think of a good example.

Correct! Not all inhibitors are created equal. Here are just a couple of factors to consider:

What is the concentration level of the inhibitor? If you have more, it obviously has more opportunity to bind and inhibit. If you remember any Chemistry, concentration drives reactions

Is it competitive or noncompetitive inhibition? The easiest way to understand this would be to think of a pair of scissors. In competitive inhibition, we are blocking the scissors from cutting by jamming up the actual blades. The inhibitor is competing with the protein for a space on the scissor blades. In noncompetitive, we simply tape the scissor handles together so you can't open the scissors to cut. It's noncompetitive, because you aren't competing with the protein for the active spot.

Simple effectiveness of how strongly the inhibitor binds to it's spot. If it can be knocked off easily, it obviously won't be as good as one that's binds hardcore.
Right - there's more than 1 application for a drug (but is that additional application the BEST drug for that problem?)

All this is beyond me. I have to rely on what the people that actually created the medicine say the best use of it is for. I understand there's a liability issue but that also has to do with a drug might HELP with symptoms of Virus X but that doesn't mean it should be used to treat Virus X.
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Re: Coronavirus COVID-19

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:lol: :lol: :lol:

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Re: Coronavirus COVID-19

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Re: Coronavirus COVID-19

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Australia has been ahead of the curve the whole time...and not in a good way. Once a penal colony, always a penal colony.



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Re: Coronavirus COVID-19

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SDHornet wrote: Mon Nov 22, 2021 10:50 pm Australia has been ahead of the curve the whole time...and not in a good way. Once a penal colony, always a penal colony.



If we didn't have the 2nd amendment, can you imagine where we would be?
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Re: Coronavirus COVID-19

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SDHornet wrote: Mon Nov 22, 2021 10:40 pm :lol: :lol: :lol:

The CDC and the IOC seem to be run by some of the same people. :ohno:
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Re: Coronavirus COVID-19

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SeattleGriz wrote: Sun Nov 21, 2021 8:49 pm
JohnStOnge wrote: Sat Nov 20, 2021 12:18 pm

I did the quotes because it looked like you didn't read far enough down in the article to see all the stuff contradicting the idea the ivermectin and the Pfizer drug are equivalent in that they are both protease inhibitors. There's language saying it hasn't even been shown that ivermectin acts as a protease inhibitor against SARS-CoV-2 through biological experiments. It's one possible mechanism proposed during a modeling exercise. There are quotes from a guy who is an investigator in an ivermectin clinical trial saying Pfizer’s 3CL protease inhibitor is nothing like ivermectin. There's a quote from the same guy saying that Pfizer's medication is different from ivermectin in that Pfizer’s protease inhibitor inhibits coronavirus at concentrations that are achievable in the human body. I think it's fair to interpret that as him saying that ivermectin does not, as a protease inhibitor, inhibit coronavirus at concentrations that are achievable in the human body. There's a statement that researchers who do think ivermectin may be effective don't think that it's effective because it is a protease inhibitor. They point to other mechanisms.

You have the link to the piece. Read the whole thing. I'm not misrepresenting the content. There's no way to interpret it as saying anything other than that the idea that ivermectin is similar to the Pfizer drug or the Merck drug is false. It also clearly makes the argument that the attempt to draw a "protease inhibitor" parallel is bogus.
The whole premise of your article is that the new Pfizer drug isn't the same as Ivermectin, which is pretty obvious from the chemical structure. I said nothing of the sort. I said Ivermectin was a 3CL Protease Inhibitor, just like the Pfizer drug, which is true. They don't even have to have the same mechanism of action and they can still be Protease Inhibitors. Do you know the difference between competitive and non-competitive inhibition? You've created this straw man type argument that has not refuted what I said in any way, shape or form.

As you don't seem to grasp what an actual protease inhibitor in this case means, let me give you a quick overview of what is happening. After the virus "invades" your cell, it then uses your cells machinery to make a polypeptide. This polypeptide has something like 12 proteins in one long string that 3CL needs to cut free. If you can prevent the 3CL protease from cutting the proteins free, you "inhibit" the protease from doing its job.

This can be done by two main options. One is to jam up the "cutting" portion and the other is to prevent the Protease from joining, as it requires two units to join together to become functional (dimerization).

From the journal in which you erroneously claim it is only in a computer simulation: (https://www.nature.com/articles/s42003-020-01577-x)
The protein structure-based drug design using computational methods is an alternative for screening of currently approved drugs to rapidly identify potential drug candidates for the treatment of emerging infectious diseases such as COVID-1915,16,17. However, the potential for false positives with computational modeling is one of the most common limitation of docking studies18. Therefore, we have established SARS-CoV-2 3CLpro enzymatic assays for selected drugs using commercially available 3CLpro protease inhibitor screening assay kits to evaluate the in vitro inhibitory activity of the drugs and investigated whether any correlation exist between the computational binding score and the in vitro inhibitory activity.
In other words, they used computational methods (in silico) to narrow down 3987 approved drugs to 47 so they COULD RUN STUDIES IN VITRO. Do you know what In Vitro means?

Lastly,
We observed that, boceprevir, ombitasvir, paritaprevir, tipranavir, and micafungin exhibited partial inhibitory effect whereas, ivermectin blocked more than 85% of 3CLpro activity of SARS-CoV-2. Although the anti-viral activity of ivermectin mediated through the blocking of α/β1 importin19,20,21,22,23 is established, herein we report the inhibitory effects of ivermectin on 3CLpro enzyme of SARS-CoV-2, suggesting additional anti-viral mechanism of ivermectin towards SARS-CoV-2
Interestingly, one of the OTD, ivermectin was able to inhibit more than 85% (almost completely) of 3CLpro activity in our in vitro enzymatic assay with an IC50 value of 21 µM. These findings suggest the potential of ivermectin to inhibit the SARS-CoV-2 replication. In support of this, a recent finding suggested that ivermectin (5 µM) inhibited the replication of live SARS-CoV-2 isolated from Australia (VIo1/2020) in Vero/hSLAM cells23. They found that >5000-fold viral counts were reduced in 48 hr in both culture supernatant (release of new virion: 93%) as well as inside the cells (unreleased and unassembled virion: 99.8%) when compared to DMSO treated infected cells. Interestingly, this study reported the IC50 value of ivermectin as 2.5 µM23, whereas, we observed an IC50 value of 21 µM (10-fold increase). The variability in the IC50 values reported could be attributed towards the differences in the assay conditions such as the use of live virus vs enzymatic assay with purified 3CLpro protein. Further, preclinical studies need to be established to validate the in vivo inhibitory activity and IC50 values of ivermectin.

Ivermectin is known to be effective against many positive-sense, single stranded RNA viruses such as Zika, Dengue, Yellow fever, West nile, Venezuelan equine encephalitis, Chikungunya, Semliki forest, Sindbis, Rorcine Reproductive and Respiratory Syndrome, and Human immunodeficiency-1 viruses38. The list of anti-viral effects of ivermectin against other RNA and DNA viruses were summarized in a recent review38. Earlier studies have demonstrated that the possible anti-viral mechanism of ivermectin was through the blockage of viral-protein transportation to the nucleus by inhibiting the interaction between viral protein and α/β1 importin heterodimer, a known transporter of viral proteins to the nucleus especially for RNA viruses19,20,21,22,23. However, in this study, we have reported that ivermectin inhibits the enzymatic activity of SARS-CoV-2 3CLpro and thus may potentially inhibit the replication of RNA viruses including SARS-CoV-2. These studies suggest that ivermectin could be a potential drug candidate to inhibit the SARS-CoV-2 replication and the proposed anti-viral mechanism of ivermectin presented in Fig. 8 and in vivo efficacy of ivermectin towards COVID-19 is currently been evaluated in clinical trials (ClinicalTrials.gov Identifier: NCT04438850).
If you want to read some real science, this gal does a great job of explaining what is happening with the Pfizer drug.

https://thebumblingbiochemist.com/365-d ... inhibitor/
For now, just know that if this peptide gets cut by the protease, the fluorophore and the quencher will be separated so you won’t see light – and this tells you that the protease is active. If you add an inhibitor that works, you should keep seeing light. ⠀

PF-07321332 passed this test. How does it work?

That nitrile nitrogen is really negative – atoms (like those individual carbons and oxygens) join together to form molecules by sharing pairs of negatively-charged subatomic particles called electrons, but some don’t share fairly. Nitrogen is a major electron hog (it’s highly electronegative) so, in the carbonyl, it draws the shared electrons closer to it, making it partly negative and the carbon partly positive. The carbon thus “wants” more electrons so it’s called electrophilic.

The active site’s catalytic Cysteine has a sulfur that wants to share electrons (is electrophilic) thanks to the Histidine pulling off its proton, so the sulfur attacks the electrophilic carbon, leading the compound to get stuck on.

It gets covalently stuck through a thioimidite adduct, as you can see in the structure of it bound to MPro, PDB 7si9 https://www.rcsb.org/structure/7si9

but it’s reversible inhibition. So it’s strongly stuck but it can still come off since enzymes can catalyze reactions in both directions and you literally have it stuck in the active site, where enzymes do their biochemical magic. But the forward direction is greatly favored, so it stays stuck pretty well.

It also passed additional tests for bioavailibilty and stuff.

But it wasn’t lasting long enough once the liver had a say. Instead, it was being modified by CYP enzymes, leading to them being excreted quickly. So that’s why they added ritonavir – it inhibits a CYP enzyme in our body that they show to be responsible.
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Re: Coronavirus COVID-19

Post by Gil Dobie »

Local schools going back to remote learning. Grade school with 30 students and 10 faculty out with Covid.
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Re: Coronavirus COVID-19

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Gil Dobie wrote: Tue Nov 23, 2021 9:21 am Local schools going back to remote learning. Grade school with 30 students and 10 faculty out with Covid.
By out, do you happen to know if it includes symptoms or just a positive test?

The school district here has been allowing those that don't exhibit symptoms to go back pretty quickly.
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Re: Coronavirus COVID-19

Post by GannonFan »

Gil Dobie wrote: Tue Nov 23, 2021 9:21 am Local schools going back to remote learning. Grade school with 30 students and 10 faculty out with Covid.
The middle school where my youngest goes has had a rash of COVID cases recently - basically 2-3 new positive tests per day for a good 2 week stretch. Coming out of Thanksgiving they are going to move to a "test-to-stay" policy, where they will offer close contacts of a positive case the option to test for COVID. If negative, they don't need to quarantine. I think they also don't need to quarantine if they were vaccinated and/or masked (students can opt out of mask wearing if they have a signed note from the parent - my kid (who wears a mask) said probably a good 1/3 of the school are opt outs). I don't see any way that they go back virtual - my district was all in person, 5 days a week, since last September, and they touted that.
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Re: Coronavirus COVID-19

Post by Gil Dobie »

SeattleGriz wrote: Tue Nov 23, 2021 9:26 am
Gil Dobie wrote: Tue Nov 23, 2021 9:21 am Local schools going back to remote learning. Grade school with 30 students and 10 faculty out with Covid.
By out, do you happen to know if it includes symptoms or just a positive test?

The school district here has been allowing those that don't exhibit symptoms to go back pretty quickly.
That information wasn't given. They do have to test negative or quarantine for 14 days, to return.
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Re: Coronavirus COVID-19

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Watched an interesting YouTube video last night in regards to the sudden collapse of COVID cases in Japan. Looking at the genetic code, it's looks as if the "error correcting" protein in the virus mutated and was unable to perform its job, therefore the virus died out.

It's just speculation at this point, but the guy talking about it also mentioned the rapid disappearance of SARS 1 and was wondering if that's what happened when it quickly dropped off the scene.
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Re: Coronavirus COVID-19

Post by SeattleGriz »

Don Surber hits it out of the park again.

https://donsurber.blogspot.com/2021/11/ ... m.html?m=1
Deaths this year now outstrip last year's because his plan was political, not medical, in nature. Just because some bureaucrat has an MD does not mean his advice is medical.

The purpose of the vax mandate is not to protect anyone, but rather to create a class of scapegoats for Biden's failure called the unvaccinated.
Been saying it from the start. You cannot vaccinate your way out of a pandemic with leaky vaccines.

Instead of being happy the vaccines are offering 4-6 months of protection against hospitalizations and death, Biden has to blame someone for his failure to stop COVID, when in reality, this was always going to be the end game with leaky vaccines and there was little he could really do. COVID gonna COVID.
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Re: Coronavirus COVID-19

Post by kalm »

SeattleGriz wrote: Wed Nov 24, 2021 10:35 am Don Surber hits it out of the park again.

https://donsurber.blogspot.com/2021/11/ ... m.html?m=1
Deaths this year now outstrip last year's because his plan was political, not medical, in nature. Just because some bureaucrat has an MD does not mean his advice is medical.

The purpose of the vax mandate is not to protect anyone, but rather to create a class of scapegoats for Biden's failure called the unvaccinated.
Been saying it from the start. You cannot vaccinate your way out of a pandemic with leaky vaccines.

Instead of being happy the vaccines are offering 4-6 months of protection against hospitalizations and death, Biden has to blame someone for his failure to stop COVID, when in reality, this was always going to be the end game with leaky vaccines and there was little he could really do. COVID gonna COVID.
How many deaths occurred Jan-March? What percentage are from the unvaxxed?
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Re: Coronavirus COVID-19

Post by SeattleGriz »

kalm wrote: Wed Nov 24, 2021 11:03 am
SeattleGriz wrote: Wed Nov 24, 2021 10:35 am Don Surber hits it out of the park again.

https://donsurber.blogspot.com/2021/11/ ... m.html?m=1



Been saying it from the start. You cannot vaccinate your way out of a pandemic with leaky vaccines.

Instead of being happy the vaccines are offering 4-6 months of protection against hospitalizations and death, Biden has to blame someone for his failure to stop COVID, when in reality, this was always going to be the end game with leaky vaccines and there was little he could really do. COVID gonna COVID.
How many deaths occurred Jan-March? What percentage are from the unvaxxed?
What is your definition of unvaxxed? Is it someone who had zero shots, one or before 14 days after their second?

Regardless, with an efficacy of 95%, we shouldn't be ANYWHERE close to the same amount of deaths. Vaccines were going to end this pandemic, right?
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Re: Coronavirus COVID-19

Post by GannonFan »

SeattleGriz wrote: Wed Nov 24, 2021 11:16 am
kalm wrote: Wed Nov 24, 2021 11:03 am

How many deaths occurred Jan-March? What percentage are from the unvaxxed?
What is your definition of unvaxxed? Is it someone who had zero shots, one or before 14 days after their second?

Regardless, with an efficacy of 95%, we shouldn't be ANYWHERE close to the same amount of deaths. Vaccines were going to end this pandemic, right?
But we already know the efficacy isn't that high. Maybe it is at the point of getting the shot, but I think the data's been pretty clear that the efficacy is far lower than that the further you get away from the shot.

I got my booster the first week in November. I wouldn't be shocked if we're looking at a second booster (a 4th shot) 6 months after that. These aren't vaccines like we're used to think of vaccines (polio is always the comparison people like to trot out) - these may be like flu shots - sometimes they work, but sometimes you still get the flu. That could be what endemic looks like for COVID.
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Re: Coronavirus COVID-19

Post by JohnStOnge »

AZGrizFan wrote: Tue Nov 23, 2021 8:42 am
SeattleGriz wrote: Sun Nov 21, 2021 8:49 pm

The whole premise of your article is that the new Pfizer drug isn't the same as Ivermectin, which is pretty obvious from the chemical structure. I said nothing of the sort. I said Ivermectin was a 3CL Protease Inhibitor, just like the Pfizer drug, which is true. They don't even have to have the same mechanism of action and they can still be Protease Inhibitors. Do you know the difference between competitive and non-competitive inhibition? You've created this straw man type argument that has not refuted what I said in any way, shape or form.

As you don't seem to grasp what an actual protease inhibitor in this case means, let me give you a quick overview of what is happening. After the virus "invades" your cell, it then uses your cells machinery to make a polypeptide. This polypeptide has something like 12 proteins in one long string that 3CL needs to cut free. If you can prevent the 3CL protease from cutting the proteins free, you "inhibit" the protease from doing its job.

This can be done by two main options. One is to jam up the "cutting" portion and the other is to prevent the Protease from joining, as it requires two units to join together to become functional (dimerization).

From the journal in which you erroneously claim it is only in a computer simulation: (https://www.nature.com/articles/s42003-020-01577-x)



In other words, they used computational methods (in silico) to narrow down 3987 approved drugs to 47 so they COULD RUN STUDIES IN VITRO. Do you know what In Vitro means?

Lastly,





If you want to read some real science, this gal does a great job of explaining what is happening with the Pfizer drug.

https://thebumblingbiochemist.com/365-d ... inhibitor/

JSO is a medical expert just like he's an economics expert. That is to say, he is neither. :rofl: :rofl: :rofl:
I am not going to post what I do until after I retire. But it's highly likely that I am more of an expert with respect to the things we are talking about now than SG is. Besides, all I did was refer to quotes and reports on what people who clearly ARE experts have to say that Ivermectin is a protease inhibitor like the Pfizer drug is.
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