Why would you ever take Paxlovid?

In a lengthy response to my post titled “New Austrian Study shows Paxlovid causing resistant Covid strains”, a reader sent a catalog of readings. You can see all the links in the comment section of that post.

To abbreviate, here are the pertinent headlines:

HIV-1 protease inhibitors (-navir) have their best efficacy against retroviruses.

NS3/4A protease inhibitors (-previr) have their best efficacy against hepatitis C.

Papain-like protease (PLpro) inhibitors have had efficacy in vitro but never in vivo.

3C-like protease (3CLpro) inhibitors (-trelvir) are also known as nonstructural protein 5 (NSP5) inhibitors or main protease (Mpro) inhibitors.

Pfizer’s PF-07321332 (nirmatrelvir) is a 3CL protease inhibitor that breaks down too rapidly in the human bloodstream without the addition of ritonavir.

Pfizer’s PF-07304814 (intravenous nirmatrelvir) is a 3CL protease inhibitor that was halted prematurely in the ACTIV-3 trial because of both bad side effects and lack of efficacy:

Enanta’s EDP-235 is a 3CL protease inhibitor that does not require the addition of ritonavir:

Todos Medical’s Tollovir is, like vitamin B12, a “natural” 3CL protease inhibitor:

Ascletis’ ASC-11 (requires ritonavir), Everest Medicines’ EDDC-2214 (no ritonavir), Pardes Bio’s PBI-0451 (no ritonavir), Sorrento’s STI-1558 (no ritonavir), and Sohei Heptares’ SH-879 (no ritonavir) have now all been tested in lab animals:

China’s Y180, which has about the same EC50 (in vitro efficacy) as Pfizer’s nirmatrelvir, is a 3CL protease inhibitor that does not require the addition of ritonavir:

Zhongsheng Pharma’s RAY1216, which has about the same EC50 (in vitro efficacy) as Pfizer’s nirmatrelvir, is a 3CL protease inhibitor that does not require the addition of ritonavir:

Simcere Pharma’s SIM0417, which has about the same EC50 (in vitro efficacy) as Pfizer’s nirmatrelvir, is a 3CL protease inhibitor that does not require the addition of ritonavir:

Shionogi’s S-217622, which has now been named, Xocova (ensitrelvir), is a 3CL protease inhibitor that does not require the addition of ritonavir and has an excellent EC50 (in vitro efficacy) of 0.29μM to 0.50μM, which is far superior to Pfizer’s nirmatrelvir, which has an EC50 (in vitro efficacy) of 6.76μM to 14.81μM:

In the past, all HIV-1 protease inhibitors had their best efficacy against retroviruses and failed against RNA viruses. Kaletra (lopinavir plus ritonavir) is a combination of two HIV-1 protease inhibitors that had some efficacy against retroviruses but failed against RNA viruses:

Pfizer’s 3CL protease inhibitor, PF-07321332 (nirmatrelvir), needs to be swallowed together with the HIV-1 protease inhibitor, ritonavir:

Pfizer’s Paxlovid (nirmatrelvir plus ritonavir) comprises of 3 pills that need to be swallowed twice daily for never more than 5 days.
Shionogi’s Xocova (ensitrelvir) comprises of just 1 pill that needs to be swallowed once each day for 5 days.

In Emi Takashita’s in vitro study, Merck’s molnupiravir was 17.84 times more effective than Pfizer’s nirmatrelvir against the Delta variant and 29.56 times more effective than Pfizer’s nirmatrelvir against the Omicron variant. All 10 monoclonal antibody drugs in Emi Takashita’s Japanese in vitro study failed even more severely against the Omicron variant than Pfizer’s nirmatrelvir:

In the past, all HIV-1 protease inhibitors, including RITONAVIR, were cell-damaging pro-oxidants and had a long list of BAD SIDE EFFECTS (artery wall damage, arthralgia, bleeding among hemophiliacs, blood clots among normal people, bone damage, brain damage, dysgeusia, endocrine system damage, endoplasmic reticulum damage, fatty liver, gingivitis, Golgi damage, hair loss, hearing loss, heart damage, hyperlipidemia, hypertension, hypertriglyceridemia, insulin resistance, kidney damage, kidney stones, liver damage, metallic mouth, mitochondria damage, muscle damage, nervous system damage, oxidative stress, pancreatitis, sexual dysfunction, skin damage, vision loss):

RITONAVIR causes platelet aggregation (blood clots):

RITONAVIR causes bleeding in hemophiliacs, who can catch HIV or hepatitis from their frequent blood transfusions:

RITONAVIR causes endothelial dysfunction (artery wall damage):

RITONAVIR causes vision loss (retina damage):

RITONAVIR causes hearing loss (inner ear damage):

RITONAVIR causes sexual dysfunction (erectile dysfunction, loss of sex drive, sperm quality damage, testicle damage):

RITONAVIR causes oxidative stress and nitrosative stress (reactive oxygen species and reactive nitrogen species):

RITONAVIR causes insulin resistance (new-onset diabetes):

RITONAVIR causes pancreatitis (inflammation of the pancreas):

RITONAVIR causes endocrine system dysfunction (damage to adrenal glands and other glands):

RITONAVIR causes lipolysis, lipoatrophy, lipohypertrophy, lipodystrophy (unwanted relocation of body fat), and atherosclerotic lesions:

RITONAVIR causes hair loss (hair follicle damage):

RITONAVIR causes hypermenorrhea (excessive menstrual bleeding, new-onset gastrointestinal bleeding)

RITONAVIR causes CNS (cental nervous system) dysfunction (nerve damage):

RITONAVIR causes intracellular dysfunction (endoplasmic reticulum damage, mitochondria damage):

RITONAVIR and other HIV drugs worsen the gut microbiota (more gas, more diarrhea, and less beneficial, health-protecting, probiotic chemicals):

RITONAVIR boosts the amount of toxic metals (arsenic, barium, beryllium, cadmium, lead, and mercury) inside of the human body by potently inhibiting CYP3A4, the most important of the hepatic, drug-metabolizing enzymes:

RITONAVIR causes eryptosis (red blood cell apoptosis):

RITONAVIR causes muscle loss (muscle damage):

RITONAVIR causes bone loss (bone damage):

RITONAVIR causes hypertension (high blood pressure):

RITONAVIR causes cognitive dysfunction (brain damage):

RITONAVIR penetrates the blood-brain barrier and remains trapped in the brain’s capillaries:

RITONAVIR causes hyperlipidemia and hypertriglyceridemia (blood cholesterol ratio damage):

RITONAVIR causes gingivitis (worsens gum health):

RITONAVIR causes cardiovascular dysfunction (heart damage):

RITONAVIR can reactivate hepatitis B or hepatitis C in people who have already been exposed to these 2 hepatitis viruses in the past:

RITONAVIR causes hepatic steatosis (fatty liver disease):

RITONAVIR causes renal calculi or nephrolithiasis (kidney stones that are composed of pure ritonavir):

RITONAVIR causes renal dysfunction (kidney damage):

NIRMATRELVIR causes even more renal dysfunction (kidney damage) than ritonavir:

PAXLOVID or RITONAVIR (swallowed alone) can sometimes cause hives (skin rash):

PAXLOVID or RITONAVIR (swallowed alone) always causes a bitter, metallic taste:

PAXLOVID can sometimes cause dysgeusia (loss or alteration of taste):

PAXLOVID is a nightmare for organ transplant recipients, for whom Paxlovid is frequently prescribed because they qualified for it by being “high-risk” for bad outcomes from COVID-19:

We’ll see if Pfizer, Shionogi, Enanta, Todos, Zhongsheng, and Simcere can live up to their exaggerated claims after the bad side effects and inadequate efficacies of their protease inhibitors are first discovered in unauthorized foreign research studies:

Dozens of 3CL protease inhibitors have been discovered, ranging from very safe (vitamin B12) to poorly tolerated (cancer chemotherapy drugs):

HIV-1 protease inhibitors for treating human immunodeficiency virus (HIV) are highly vulnerable to drug resistance:

NS3/4A protease inhibitors for treating hepatitis C virus (HCV) are highly vulnerable to drug resistance:

3CL proteae inhibitors, including nirmatrelvir, are highly vulnerable to drug resistance:

However, RNA-dependent RNA polymerase (RdRp) inhibitors (favipiravir, ribavirin) are less likely to encounter viral drug resistance. Ribavirin, which was invented in 1972, continues to be used today to treat hepatitis C virus (HCV) patients:

Although most governments have been eager to purchase and try both Paxlovid and molnupiravir, the demand among the people for these 2 poorly tested antivirals has been unexpectedly low. This has forced the US FDA to extend the shelf life of Paxlovid to prevent huge quantities of this expensive (inflationary) drug from being discarded into the trash can by pharmacists:

Merck recently reminded us that ritonavir-boosted protease inhibitors, including Pfizer’s Paxlovid, have the longest list of bad drug interactions of any drugs in history. Although both nirmatrelvir and ritonavir are pro-oxidants that will damage every cell in the human body if used longer than 5 days, ritonavir causes 621 out of the 627 bad drug interactions caused by Paxlovid, while ritonavir causes 221 out of the 227 “major” bad drug interactions caused by Paxlovid:

In their zeal to dispense Paxlovid, proper vetting for Paxlovid’s 627 bad drug interactions isn’t being done:

Many people say that their COVID-19 viral load and symptoms got better, then worse, after swallowing Paxlovid:

Reports are emerging of the restarting of full-fledged COVID-19 among people who swallowed Paxlovid:

In his 5-31-2022 study, Dr. Michael Charness of the VA Medical Center in Boston warns that Paxlovid swallowers can still be superspreaders, even if if they were among the 10% to 20% of Paxlovid swallowers who tested false negative on Day 2:

Pfizer wants to block all scientific studies that they don’t control with their billions of dollars in bribe money. Pfizer especially fears scientific studies that force Paxlovid to be compared in efficacy against molnupiravir, favipiravir, or Shionogi’s Xocova (ensitrelvir):

Here’s the truth about Paxlovid in Hong Kong, which first received Paxlovid on 3-14-2022, which is AFTER their Omicron wave had nearly ended:

By 4-23-2022, Hong Kong’s Omicron wave had ended:

Hong Kong reported on 4-23-2022 that almost nobody had been prescribed Paxlovid between 3-14-2022 and 4-23-2022, when Paxlovid was, and still is, in abundant oversupply:

In the Pfizer-funded, Hong Kong clinical trial by Cheuk Fung Yip, molnupiravir had 17% more hospitalizations than the control group, while Paxlovid had only 21% less hospitalizations than the control group, not 89% less hospitalizations than the control group as Pfizer had been claiming:

“Conclusion: Both antivirals did not reduce the risk of COVID-19-associated ventilator use, ICU occupancy, or death:”

In the Pfizer-funded, Israeli clinical trial by Ronen Arbel, in the 40-to-64 age bracket, Paxlovid had only 22% less hospitalizations than the control group, not 89% less hospitalizations than the control group as Pfizer had been claiming. In the 40-to-64 age bracket, Paxlovid INCREASED mortality by 64%:

Of the 42,819 Israelis over age 65 who were eligible, only 2,504 of them, or 5.85% of them, agreed to swallow the Paxlovid pills, while 94.15% of these 42,819 Israelis refused.
Of the 66,394 Israelis aged 40-to-64 who were eligible, only 1,435 of them, or 2.16% of them, agreed to swallow the Paxlovid pills, while 97.84% of these 66,394 Israelis refused.
“and even those in the older [65-plus age] group who were vaccinated or recovered saw [only] a relatively small benefit from Paxlovid:”

On 5-24-2022, Shanghai Junshi Biosciences reported that their nucleoside analog (RdRp inhibitor), VV116 (JT001), defeated the 3C-like protease (3CLpro) inhibitor, Paxlovid, in a Phase 3 clinical trial. The VV116 molecule is more similar to the molecule of Gilead Sciences’ GS-441524 than to the molecules of the nucleoside analogs, ribavirin, favipiravir, or molnupiravir:

In India, on 1-12-2022, the Indian Council of Medical Research (ICMR) dropped molnupiravir from India’s national treatment protocol for COVID-19:

In India, on 5-7-2022, the Indian Council of Medical Research (ICMR) dropped Paxlovid from India’s national treatment protocol for COVID-19: