Does Molnupiravir represent a second front in the battle to abolish natural immunity, or something even more sinister?
Millions of doses already produced and pre-purchased by the US government, FDA “emergency” authorization seemingly around the corner1 based on “promising” trial results that are still only publicly available in the form of a press release, and a possible risk of cancer generation and birth defects which might be so high that “risk” is a bit of a misnomer: That’s Molnupiravir. At least, so it would seem as of last week.
In one experiment which has made the rounds since the press release, out of UNC Chapel Hill and involving virtual tests with animal cells (rather than real-world animal trials), for example:
[The metabolite of Molnupiravir] also displays host mutational activity in an animal cell culture assay, consistent with RNA and DNA precursors sharing a common intermediate of a ribonucleoside diphosphate. These results indicate highly active mutagenic ribonucleosides may hold risk for the host.2
This is what millions of patients with SARS-CoV-2 will receive this winter - even, potentially, for early treatment? In advance of a single study of long-term effects?!
Improving upon this general impression, however, would require my sudden acquisition of a rough understanding of that most tedious and arcane3 of subjects, molecular biology. Thus, I was not in any position to author a post on the topic.4 To my eyes, after all, it’s just obvious that there can not be such a thing as interfering with a “viral replication” process; any named “viral” process must necessarily be endogenous and essential to cellular operation, as well. There is nothing a virus “does” that does not originate from cellular division, communication, or metabolism; and in fact the genes of our own bodies are, at default, more tightly gate-kept in terms of unbridled replication than the genes of our viruses.5 If disabling the core means of viral replication were a good idea, the immune system would do it.
But, for me to rant on that effect probably does not offer much value to the reader.
So in the last seven days I have acquired a rough understanding of molecular biology. After which, I have come to realize Molnupiravir is an even worse idea than I thought.
Here are the highlights for what Molnupiravir can do inside the body “according to a rough understanding of molecular biology,” if the currently described mechanism against SARS-CoV-2 is actually correct (I have my doubts). As is my wont, I will avoid abbreviations as much as possible, because they make things look more complicated than they are. Elements which are part of the official, narrow explanation of the mechanism are in bold. The rest is my wild ranting.
Molnupiravir will or might:
1 - Insinuate into viral mRNA, causing errors in replication and translation.
Replication is performed by proteins called polymerases; translation (turning mRNA into proteins) by RNA-protein complexes called ribosomes.
In the model used by coronaviruses, the mRNA that is initially released into the cell is read by an available ribosome which skips over most of the code, settling on the portion coding the creation of a “viral” polymerase protein. The polymerase, upon creation, takes over reading of the original viral mRNA.
The polymerase, first, reads the original strand of mRNA and makes a “negative” copy of it from available 3phosphate+2OHthing+A/U/G/C bits. It then goes back and reads the negative, creating not only new copies for the future virus, but smaller segments that direct and orchestrate further protein synthesis back in the cell’s ribosomes; we can call these small worker bits.
Molnupiravir starts out as blablabla+2OHthing+M, and is transformed after ingestion, mostly, into 3phosphate+2OHthing+M. In this form, it can be confused for 3phosphate+2OHthing+C by polymerases inside cells. (Note that at least one source seems to suggest that competition with “U” is more important to what happens next; for now, I will work with the above construction.7)
That’s rather bad for the virus, which at the moment we left it was reading its own mRNA with the viral polymerase. The polymerase will create a “negative” of the mRNA that sometimes has M where it should have C. When it goes back to read the resulting mRNA(M) “negative,” it will sometimes think M means C, so “write U” (correct) and sometimes think it means U, so “write C” (wrong). The insertion of C where the original code called for a U (as well as additional insertions of M where “write U” is called) results in the creation of nonsense / mutant mRNA(M) “positive” copies and, more importantly, nonsense / mutant small RNA(M) worker bits.
When the cell’s ribosomes read the RNA(M) worker bits they potentially create mis-folded proteins, or read the code in novel, suboptimal ways, or get stuck due to early “stop” codes written by the polymerase, prompting cleanup, though cleanup factors (exosome complexes8) may quickly become exhausted by all the work. They may also take up and read the “positive” mRNA(M) copies in novel ways, producing more chaos. Because of this layered sabotage, the original viral mRNA has no chance of making virus happen. Presumably, the infected cell is so stressed-out at this point that it either self-triggers cell death, or nearby cells, detecting the chaos, put it out of its misery.
All the A/U/T/G/C and M bits in the destroyed cell, with whatever else is attached to them, don’t just disappear. They may be salvaged by metabolic pathways and reused by other cells, or processed by the liver and kidneys for excretion (see below). Any mis-folded proteins go on to do who knows what.
Almost certainly, the destruction of cells with mutant viral elements alters antigen-presenting-cell behavior compared to normal infection (and cellular destruction prompted by successful viral replication), implying possibilities for adaptive immunity “silencing” (and thus, prompt reinfection) and auto-immunity (based on mis-folded proteins with similar peptide motifs as self-proteins).
2 - Insinuate into nuclear RNA.
I mean, duh. This is just so astoundingly obvious I have to wonder why anyone considers “nucleoside analogs” a promising “antiviral” platform at all, rather than an obvious bioweapon.
Ingested M will end up in all sorts of cells throughout the body, not just cells with virus in them. The 3phosphate+2OHthing+M form of M will be confused for 3phosphate+2OHthing+C during transcription of DNA in the nucleus.9
DNA is transcribed into RNA inside the nucleus by, guess what, polymerase. Nuclear polymerase selects from free-floating 3phosphate+2OHthing+A/U/G/C in accordance with the A/T/G/C code in the portion of DNA being transcribed. M will be substituted for C by nuclear polymerase just as frequently as by “viral” polymerase.
Resulting pre-mRNA(M) will presumably be spliced in novel ways, with M appearing within introns prompting alterations to the invisible Cryptic Unstable Transcript-regulated algorithms that mediate gene expression. Or, errors during splicing may prompt error-checking action and cleanup by exosomes; resulting in gene silencing or reattempted gene expression.
If splicing is nonetheless non-destructive, the resulting mature mRNA(M) will exit the nucleus and get taken up by, guess what, available ribosomes. Ribosomes will occasionally mis-read M as U instead of C, prompting novel read behaviors (leaky scanning, etc.), early stops, and mis-folded proteins.
But nuclear DNA is also transcribed into, guess what, functional “worker” RNA molecules and RNA-protein complexes, including, guess what, ribosomes themselves. M will be placed where C ought to go in:
Splicer “snRNA,” potentially distorting or halting genetic expression (which would imply that pre-RNA(M), since it can’t be processed by splicer RNA complexes, can’t even leave the nucleus, and must wait for exosome degradation; generally speaking, genetic expression is useful - including in the function of the immune system - and should not be halted willy-nilly).
Ribosomal “rRNA,” potentially resulting in mutant ribosome(M) complexes that become mutant protein factories, or in nonfunctional ribosomes, leading to silenced gene expression and inefficient cell division.
Workspace-modifying “tRNA” which move appropriate elements into place and function as proofreading markers during translation of mRNA in the ribosome. Incorporation of “M” into tRNA may lead to defects during subsequent modification (when tRNA is made “functional” by modifications to specific A/U/G/C bits), resulting in nonfunctional tRNA. Creation of tRNA(M), “functional” or otherwise, could result in inefficient gene expression or mis-folded proteins.
3 - Insinuate into mitochondrial RNA.10
Mitochondria have their own set of DNA which is translated by, guess what, polymerase, implying that analogs to all the above will also occur in mitochondria, implying disruption of cellular metabolism - the cell will starve to death.
To sum up the many elements of cellular function which depend on functioning transcription of DNA via RNA polymerase, perhaps we should consult the Wikipedia description:11
“RNA polymerase is essential to life, and is found in all living organisms and many viruses.”
Oh, OK then!
4 - Compete with free-floating 3phosphate+2OHthing+C (CTP) during the production of cell membranes (glycerophospholipids), and the preparation of certain protein structures (glycosylation) which are critical for general metabolism - as well as for the post-translation preparation of coronavirus spike proteins.
That’s right - “C” has lots of other essential uses besides going into (DNA and) RNA!
Note that this could be relevant to the actual mechanism of action against reproduction of SARS-CoV-2 in vivo; implying that efficient substitution of M for C in RNA might not actually be taking place.
5 - Be converted into forms that compete with methylcytosines, leading to who knows what.
6 - Be translated from 2phosphate+2OHthing+M into 2phosphate+1OHthing+M (via ribonucleotide reductase).
Subsequent 3phosphate+1OHthing+M would thereafter actively compete with 3phosphate+1OHthing+C for, guess what, placement into replicated DNA during DNA repair and cellular division, leading to DNA(M) - nonsense / mutant DNA in cell nuclei and mitochondria. There, M will presumably be misread by polymerase as T instead of C, resulting in cellular metabolic failure leading to apoptosis, or carcinogenesis - conversion into cancer cells.
7 - This would include in germ cells, implying direct infertility in males (unable to produce sperm without mutations12) and indirect fertility in women (fertilized eggs unable to replicate without mutations).
8 - Escape into the environment.
As with virally-infected cells in the first example, apoptosis of cells containing M would merely release A/U/T/G/C and M bits into the body, where they might be salvaged or excreted. M, unlike most drugs, is possibly not going to ever be truly “metabolized” out of potential active forms. It will only alternate between 2/3phosphate+1/2OHthing+ forms, bounce from cell to cell, and repeat the same interactions until degraded. The “half-life” for M - when it ceases to be available in actively employable forms - in the real world is probably unknowable.
Excreted M, for example, could enter the microbiotic genome (bacteria in the gut and elsewhere), potentially producing mutant bacteria. Even upon the death of bacterial cells due to lethal mutations during DNA repair and cellular division, M could still be recycled to other bacteria. These bacteria could, of course, carry M to other organisms, conceivably resulting in “wild-caught M-induced carcinogenesis and infertility” throughout every kingdom of life.
Non-excreted, free-floating cellular M, once reduced to lower levels, could end up incorporated into viable RNA and DNA viruses, and transmitted from the original recipient.
Humans will merely be the vector for some amount of M to “infect” the entire nucleoside-metabolic cycle of the Earth, until finally degraded.13
Within “anti-Covid-vaxx” world, Molnupiravir has been lambasted as a glorified, high-dollar ivermectin imitator. After all, Molnupiravir “stops replication,” and ivermectin “stops replication,” so they must be the same drug - hence the derisive moniker “ivermercktin” for the newcomer.
But this is not really the case. Ivermectin is not a nucleoside analog, and thus is not similar to Molnupiravir in potential mechanism or harms. Ivermectin has dozens of theoretical antiviral, anti-SARS-CoV-2, and anti-“Covid” (as in, inflammation, etc.) properties, only one of which comes close to the mechanism believed to be responsible for Molnupiravir’s “efficacy”: Binding to the coronavirus polymerase.14 The polymerase, again, is the first protein created after coronavirus mRNA is read by an available ribosome of the host cell; it then turns around and creates the “negative” copy of the mRNA. It is not that ivermectin sabotages the copying process; it merely (possibly) physically blocks it.
Outside of the body, however - in the world of human semantics - the extent of Molnupiravir’s imitation of ivermectin is indeed galling. The mainstream narrative heralding the drug’s arrival exceeds all possible bounds of tolerable cognitive dissonance; it is difficult to read a word of it without access to a nearby pillow to scream into. From yesterday’s AP report of the FDA emergency authorization request, for example:
If cleared by the Food and Drug Administration — a decision that could come in a matter of weeks — it would be the first pill shown to treat the illness. […]
An antiviral pill that people could take at home to reduce their symptoms and speed recovery could prove groundbreaking [you don’t say!], easing the crushing caseload on U.S. hospitals and helping to curb outbreaks in poorer countries with weak health care systems.15
And the price-tag accompanying this successful imitation act is mind-boggling. Ivermectin, whose patent (once held by Merck themselves) has elapsed, is incredibly affordable everywhere in the world it is not actively suppressed by health boards - as are most of the other prominent repurposed drugs recommended for treatment of SARS-CoV-2 by the FLCCC, save for the mid-range Fluvoxamine. Molnupiravir will be priced at $700 a course. The US government’s pre-purchase, as announced by Merck in their press release celebrating their own trial results, amounts to $910 million.
For an incisive and satisfying criticism of this obvious, broad-daylight-clad fraud, see the recent article by Justus R. Hope, “Ivermectin - Truth and Totalitarianism.”16 Hope characterizes the suppression of ivermectin by its former patent-holder, Merck, and the timing of the coming approval as one giant exercise in corporate welfare Kabuki theatre:
Just as Moderna was choreographed to go first in the vaccine rollout, Merck was first with the antiviral, and Pfizer first with the booster. They would take turns as there was more than enough profit to go around. Soon it would be Pfizer’s turn at the antiviral trough, but they had to be patient for now. There was an order and method to this.
But the craftiest strategy of all was Merck's: Accuse the other side [i.e., ivermectin] of that which you are guilty.
This quote has been variously attributed to Karl Marx, Vladimir Lenin, and Joseph Goebbels, the Nazi propaganda minister. Regardless of its source, it has proven remarkably effective as a propaganda tactic throughout modern history, and Merck was betting on this to sell the public on Molnupirivar. However, the move backfired. In the case of Ivermectin, they falsely argued that it was ineffective and unsafe while their own drug suffered from both.
For example, one could argue, "There is a concerning lack of safety data" regarding Molnupirivar. Indeed, it does not have decades of safety data like Ivermectin; it does not even have years. The little safety data pertains to a dearth of Phase II and Phase III clinical trials, which total less than a few thousand patients.
While Ivermectin's safety data with over 40 years of treatment in over 3.7 billion doses is truly robust, Molnupiravir's safety numbers are barely rudimentary. In short, Molnupiravir's safety data is concerning because of its lack.
But upon reading about the mechanism of Molnupiravir last week, my first thought was that the truth is potentially even more sinister.
What if Molnupiravir is not intended as a stand-in for ivermectin, but for the harms caused by the Covid vaccines?
Consider the timing: Molnupiravir is set to be aggressively prescribed for outpatient treatment for infection with SARS-CoV-2 starting basically yesterday - potentially reaching millions of patients in the coming months alone. This is the same time-window for carcinogenic, fertility, and neurological harms from the Covid vaccines to potentially become visible on a wide scale. If Molnupiravir’s roll-out is an intentional “mistake” - another disaster drug to add to the Hall of Infamy, leading to cancers, birth defects, infertility, and prion-based neurological disorders, not just in recipients but in secondary carriers of “M” - the potential for obscuring and deflecting from the same exact harms caused by the Covid vaccines is obvious.
And just as with the “lab leak” fiasco, the delayed acknowledgement of the openly visible “fraud” - preceded by months of excruciating media Fact Checks™ declaring the acknowledgement impossible - will itself be handy cover for a possible intentional release.
In fact, such a sweeping campaign of sleight-of-hand wouldn’t even require Molnupiravir to actually be toxic at all. These $700 molecular boondoggles could, for all we know, turn out not to effectively compete with cellular CTP in vivo. The behind-closed-doors “success” announced in Merck’s own trial could easily be a sham; in India, for example, a simultaneous trial for the drug has just been cancelled for a lack of efficacy in “moderate” infections with SARS-CoV-2.17 The point - that Molnupiravir can be blamed for the harms it is mechanistically “likely” to cause - does not require that it actually causes them.
What else to make, after all, of a certain figure appearing in the author roll of the paper seeding the narrative that Molnupiravir is mutagenic in the first place:
Molnupiravir would not be the first “antiviral” nucleoside analog on the market, but it appears, potentially, more “potent” in competing for polymerase selection and inducing viral mutagenesis (rather than inhibition of translation) than predecessors. To return to taking the mechanism at face value, we can quote from the “intriguing” UNC paper again (emphasis added):
β-d-N4-hydroxycytidine (NHC, initial metabolite of molnupiravir) is >100-fold more active than ribavirin or favipiravir against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), with antiviral activity correlated to the level of mutagenesis in virion RNA.18
This names the two nucleoside analogs which were considered as possible repurposed drugs to combat SARS-CoV-2.
Ribavirin, significantly, has been used for decades, predominately in the “treatment” of chronic infection with Hepatitis C virus. What is notable about this practice is that the use of ribavirin as an antiviral precedes understanding of its mechanism as a nucleoside analog, which did not emerge until about two decades ago.19 It only seems by accident, therefor, that the last two decades have featured intense efforts at developing novel “antiviral” nucleoside analogs despite the fact that mechanism is so intrinsically destructive that it is simultaneously employed in the pursuit of novel cancer therapies.
Hence, the great overlap between Ribavirin and anti-cancer drug Fluorouracil, which is not a nucleoside analog, but operates by making the nucleotide version of “T” unavailable inside cells. Both of them sound like something out of the first step in a Pinky and the Brain plot; and both should only even be considered for use for severely ill patients. So, do the results of these two separate modes of attack on gene expression and replication resemble each other in real life?
See for yourself, whether you can tell which monograph excerpts represent the “antiviral,” and which the cancer therapy:
Principal toxicity of oral [..] is hemolytic anemia which may result in worsening of cardiac disease and has resulted in fatal and nonfatal MI. Do not use […] in patients with a history of clinically important or unstable cardiac disease.
Myocardial ischemia/infarction, heart failure, arrhythmias, and angina (including Prinzmetal variant angina) reported.
Teratogenic and/or embryocidal effects demonstrated in all animal species exposed to […]. […] has a long half-life (12 days after multiple doses) and may persist in nonplasma compartments for as long as 6 months. Contraindicated in pregnant women and male partners of pregnant women. Extreme care must be used to avoid pregnancy during and for 6 months following […] therapy in female patients and female partners of male patients receiving […]. Must use at least 2 reliable forms of contraception during and for 6 months following completion of treatment.
Advise women of childbearing potential and men with such female partners to use effective contraceptive methods during […] therapy and for up to 3 months after the last dose of the drug. […] Results of animal studies suggest that […] may impair male and female fertility.
Not known whether […] or its metabolites are distributed into human milk. Discontinue nursing or the drug.
Not known whether […] is distributed into human milk. Discontinue nursing or delay or discontinue the drug.
Initiation of aerosolized […] in infants has resulted in sudden deterioration of respiratory function.
Safety and efficacy in children not established.
Disorientation, confusion, ataxia, visual disturbances, and acute cerebellar syndrome reported. Insufficient data on risks of resuming […] after resolution of neurologic adverse effects. […] Myelosuppression (e.g., neutropenia, thrombocytopenia, anemia), sometimes severe or fatal, reported.
Other adverse psychiatric effects (depression, emotional lability, somnolence), anemia, and neutropenia reported as in adults.20
Molpunivir implies a great leap in the scale of an experiment that hasn’t even finished the first stages. Ribavirin’s long-term effects have essentially gone unstudied, presumably as a result of the delayed recognition of its activity on the genome. The primary novel “antiviral” nucleoside analogs in use in the wake of Ribavirin are Favipiravir21 - approved for limited use against influenza in Japan for the last eight years or so - and Remdesivir. Long-term data on adverse effects like cancer is not yet possible for either of these (particularly in the latter case, as Remdesivir appears efficient at making “long term” anything impossible).
Perhaps even more significantly, Molpunivir represents the amplification of a potential release of nucleoside analogs into the “global nucleoside-metabolic cycle” that has been ongoing for decades via, once again, Ribavirin. For all we know, this drug, passed on via incorporation into microbial DNA in place of adenine and guanine, has been impacting us all for years. It could be responsible for increased rates of cancer, or auto-immune diseases, or reality TV viewership, or, who knows - plummeting sperm counts for men.
Is “wild-caught” Ribavirin ending up in genomes or RNA of other species and of ourselves? The absurdity of the fact that this hasn’t even been looked into is only exceeded by the stupidity of waiting until it’s looked into to take action. Nucleoside analogs are obvious toxins. Anyone who manufactures, promotes, or prescribes them is committing harm - including, potentially, to themselves.
(Related: An update on Molnupiravir development and risks.)
What emergency, again?
Zhou, S. et al. “β-d-N4-hydroxycytidine Inhibits SARS-CoV-2 Through Lethal Mutagenesis But Is Also Mutagenic To Mammalian Cells.” The Journal of Infectious Diseases. 2021 Aug 1; 224(3): 415–419.
This paper was criticized by authors associated with Merck, who claim that Zhou et al. used levels and durations of exposure which exceed typical practice. See Troth, S. et al. “Letter to the Editor in Response to Zhou et al.” The Journal of Infectious Diseases:
These in vivo mutation assays evaluated MOV at doses and durations significantly greater than those being used in the clinic […]
Thus, based on the totality of genotoxicity data (including two distinct in vivo rodent mutagenicity models in which MOV did not demonstrate evidence of mutagenicity or genotoxicity in vivo), MOV is considered of low risk for genotoxicity in clinical use.
It is important to note that the assay conditions used for the in vitro HPRT assay by Zhou et al were significantly different from standard protocols conducted under regulatory test guidelines.
Readers familiar with Bret Weinstein’s podcast will already be aware that most lab rodent breeds have outlandishly long telomeres due to generations of rapid-breeding (which removes any fitness benefit conferred from longevity in the wild), which render them both impervious to drug harms and universal cancer-forming-factories by default. This renders any attempt to screen a drug for mutagenicity using rodent models a pointless farce.
My write-up of the syncytin-1 study from Singapore, which required figuring out ELISA and dispelling a certain mystified naïvety over log scales, represents the normal limits of my appetite for knowledge.
A statement of the cellular world’s ambivalence to viral replication which ought to communicate something to us about where our priorities should lie!
See Menéndez-Arias, L. “Decoding molnupiravir-induced mutagenesis in SARS-CoV-2.” Journal of Biological Chemistry. 2021 Jul;297(1):100867.
At a certain point, most of the possible “mutagenic” and gene silencing effects become redundant anyway. And I was clearly all but out of space in my notes on molecular biology:
The term “exosome” is used for both extracellular vesicles and the intracellular molecules which degrade RNA.
See Feng, J. et al. (2015.) “Role of Mitochondrial RNA Polymerase in the Toxicity of Nucleotide Inhibitors of Hepatitis C Virus.” Antimicrobial Agents and Chemotherapy. 2016 Feb; 60(2): 806–817 (emphasis added):
“The mechanisms for toxicity of ribonucleotide analogs have not been well characterized but could theoretically arise from incorporation into cellular RNA by human [nuclear] RNA polymerases I, II, III (PolI, PolII, and PolIII) and the mitochondrial RNA polymerase (PolRMT).”
(Feng, J. et al.) This paper represents the current research - it is still the end point for the citation in a more recent review attached to a rephrasing of the same claim. See Sticher, Z. et al. (2020.) “Analysis of the Potential for N4-Hydroxycytidine To Inhibit Mitochondrial Replication and Function.” Antimicrobial Agents and Chemotherapy. 2020 Feb; 64(2): e01719-19:
“Since phosphorylated ribonucleoside analogs mimic natural ribonucleotides, they may also be incorporated into human RNA by the mitochondrial DNA-dependent RNA polymerase (POLRMT) or by nuclear RNA polymerase (Pol) I, II, or III, resulting in undesired side effects.”
Observations of possible higher incorporation of M into mitochondrial RNA may, as the papers by Feng et al. and Lu et al. suggest, be a result of a lack of proofreading in mitochondrial polymerase. Or, it may be that nuclear gene expression is suppressed in the artificial conditions in which tissue samples are studied, whereas mitochondrial expression (cellular metabolism) does not require (natural) external stimulus.
Deformation or inhibition of specialized gene-silencing proteins (“piwi” proteins) in sperm cells via polymerase interference with “M” could also contribute to high rates of apoptosis.
I don’t know about you, but I have a pretty high estimation of the ability of bacteria to keep a molecule in circulation. And do you know where the molecules that bacterias keep in circulation end up? Our food.
This is based on computer modeling. See Swargiary, A. “Ivermectin as a promising RNA-dependent RNA polymerase inhibitor and a therapeutic drug against SARS-CoV2: Evidence from in silico studies.” researchsquare.com.
Perron, Matthew. “Merck asks US FDA to authorize promising anti-COVID pill.” (2021, October 12.) AP.
Singh, Shivani. “Two Indian drugmakers to end trials of generic Merck pill for moderate COVID-19.” (2021, October 8.) Reuters.
(Zhou, S. et al.)
See Cameron, C. Castro, C. (2001.) “The mechanism of action of ribavirin: lethal mutagenesis of RNA virus genomes mediated by the viral RNA-dependent RNA polymerase.” Curr Opin Infect Dis. 2001 Dec;14(6):757-64.
See Pilkington, Victoria. “A review of the safety of favipiravir – a potential treatment in the COVID-19 pandemic?” Journal of Virus Eradication. 2020 Apr; 6(2): 45–51:
[H]yperuricaemia, [yawn] teratogenicity [development of birth defects!] and QTc prolongation [a precursor to cardiac arrhythmias!] have not yet been adequately studied. Favipiravir may be safe and tolerable in short-term use, but more evidence is needed to assess the longer-term effects of treatment. Given the limitations of the evidence and unresolved safety concerns, caution is warranted in the widespread use of favipiravir against pandemic COVID-19.