Over 12,000
compounds predicted to reduce risk—SARS-CoV-2 easily
disabled
SARS-CoV-2 infection involves a complex interplay of over 500
host and viral proteins and other factors1-172, providing many therapeutic targets.
Scientists have identified 12,528+
compounds173 potentially beneficial
for COVID-19. Hundreds of compounds inhibit SARS-CoV-2 in vitro,
including many with known pharmacokinetics and proven safety.
c19early.org
Efficacy confidence - low-cost systemic
p < 0.00000001
p < 0.00000001
p < 0.00000001
p < 0.00000001
p = 0.00000001
p < 0.00000001
p = 0.00000006
p = 0.0000004
p = 0.000002
p = 0.000005
p = 0.00003
p = 0.00005
p = 0.0001
p = 0.0006
p = 0.0007
p = 0.002
P-values indicate the confidence that studies show a significant effect. p = 0.05 is the typical threshold for significance, with lower values indicating higher confidence. See the individual analyses for details of efficacy for specific outcomes and conditions.
if you say anything in favor of ivermectin you will be cast out of civilization and thrown into the circle of social hell…
Scott Alexander
Astral Codex Ten1201
Hydroxychloroquine
Extensive preclinical research supports efficacy41,1202-1238 .
Viruses like SARS-CoV-2 that depend on low pH for endosomal
entry1239,1240 can be inhibited with endosomal
acidification inhibitors like
HCQ(b),1215,1229,1240 .
Direct clinical measurement shows that HCQ reaches therapeutic concentrations
in COVID-19 patients1241, and analysis of lung cells from COVID-19
patients shows inhibition in early target cell types1242,1243.
Analysis of 426 controlled
clinical studies174,175,285-711 shows
strong evidence for efficacy with early treatment
(p<0.00000001) and prophylaxis (p<0.00000001), confirmed in multiple additional meta-analyses174,587,1244-1252 .
The largest HCQ/CQ RCT—the 4,652 patient Oxford/MORU COPCOV
RCT—shows 57% lower symptomatic PCR+ COVID-19 (p=0.0002, results withheld for over two years)(c),174.
In 2021 Naggie et al.654 showed that HCQ prophylaxis
significantly reduced COVID-19 cases based on 2 US RCTs(d). This is now known with
p=0.000005 for RCTs and
p=0.00000001 for observational studies.
The Oxford PRINCIPLE RCT, withheld for 5 years, shows significantly faster recovery
with HCQ(e),175.
HCQ shows poor results with late treatment and excessive dosage, and the
combination shows harm.
HCQ may exacerbate cytokine storm in late-stage COVID-19 patients1255, and
late-stage treatment may enhance viral egress via lysosomal
deacidification(f),1253,1254 . Research also suggests potential
cardioprotective effects at lower doses, but cardiotoxicity with excessive
dosage1219.
Combined use of HCQ and remdesivir is contraindicated1256, but was commonly done.
The RECOVERY trial, key to the worldwide campaign against HCQ, used very late treatment
with an excessive toxic dose349.
HCQ studies focused on late treatment (89%). Early/
preventive trials—more likely to be positive—did not report results at a 3x higher rate.
Studies for HCQ are inconsistent with the logical use of
antivirals. 89% of treatment studies analyzed late treatment,
5+ days after the onset of symptoms712.
This makes it easy to generate meta-analyses showing poor efficacy by
including large late treatment studies1257, although the results
are not relevant to recommended usage.
Results have not been reported for 37 RCTs1258-1294, and an
additional 65 RCTs were terminated with <30
patients1295-1353.
it is often possible to make clinical trials come out pretty much any way you want
Marcia Angell
former NEJM editor1354
HCQ was the first treatment confirmed
effective1355, however alternatives
may offer advantages. Lung pharmacokinetics show high inter-individual
variability1241; dosage is relatively challenging, with dependence
on cholesterol1222, lung pH1212, and renal
impairment1212, delayed attainment of therapeutic
concentrations, and a relatively narrow range of regimens showing efficacy
while limiting side effects; and ~2.5%1356 of patients may have
contraindications.
Longer-term use of endosomal acidification modifiers raises
concern for potential off-target effects, including disruption of cellular
processes, impaired lysosomal function, reduced immune
response1357, and altered cellular signaling.
Fake tablets are common in some locations1358-1361.
The largest ivermectin RCT shows faster recovery with probability >0.999 and 36% lower long COVID, p<0.0001, despite extreme bias and very suboptimal design(g),263.
The largest RCT, with a design highly favoring
finding no efficacy, found superiority with probability >0.999 for
recovery(g),263. Improved recovery is strongly associated
with lower mortality, p<0.00000000001(g),263. The trial also
found 36% lower long COVID (p<0.0001) despite very suboptimal
use(g),263.
A post-exposure prophylaxis RCT shows 96% lower cases with high viral load with ivermectin282. A long COVID RCT shows 4x faster resolution of anosmia256.
Extensive preclinical research supports efficacy(h),52,124,1223,1373,1375,1376,1381,1383-1412,1414-1465 .
This includes mechanisms relevant to all stages: blocking initial infection, minimizing viral replication, and mitigating secondary complications. Specifically, for blocking initial infection: spike-ACE2 disruption1384,
lipid raft attachment inhibition1401,
glycan binding1385,1466, and CD147
inhibition1397-1400; for minimizing viral replication:
importin-α/β nuclear transport blockade1373,1375,1376,1383 , 3CLpro
inhibition1391, and RdRp interference1392; and for mitigating
secondary complications: inhibiting fibrin clots1390, reducing lung
fibrosis1388,1404,1405 , protecting against myocarditis1394,1407, and
dampening cytokine storm1402,1403.
Ivermectin also has the most carefully analyzed evidence base
in history, resulting in the retraction of a few studies which has improved
the quality of the evidence base, and improved the dose-response and treatment
delay-response relationships. However the analysis team showed strong bias, focusing
only on issues with positive
results1467-1469,
and disregarding flaws and fraud in the major trials
claiming no effect284.
For example, the main author claims the Together Trial was "incredibly well-done"
and a "masterpiece of science" despite the trial reporting multiple impossible
numbers, blinding being broken with external sharing during the trial, randomization
failure, refusal to share data despite pledging to, no response from the authors, and many
protocol violations201. The metformin arm was retracted due to incorrect
data and compromised integrity >3 years later1470, however for ivermectin both
the authors and the journal do not respond.
There is a clear signal that IVM works in COVID patients…
Ed Mills
Together Trial co-principal investigator1471
Optimal use of ivermectin may involve synergy with combined treatments,
administration taking into account the lipophilic nature, and sublingual,
spray, or inhaled formulations for direct respiratory tract treatment.
Pharmacokinetics show significant inter-individual variability1472.
Injectable formulations may reduce variability and provide faster onset
of action1454.
Liposomal formulations show increased antiviral activity and lower
cytotoxicity1449.
Synergistic results are seen with polytherapy1223,1447,1453 .
Efficacy varies depending on the manufacturer1473, underdosed
and contaminated ivermectin is common1474-1477,
and fake tablets with no active ingredient have been
reported1361,1478.
c19early.org
Results vary as expected across studies—only possible with a real treatment effect
Meta-analysis shows very strong confidence in efficacy, however experts that claimed no efficacy early in the pandemic fall back on their last refuge—claiming that all studies are garbage or critically flawed. This is a plausible claim for people unfamiliar with the studies because it is true in certain domains. However, for ivermectin this is easily disproved. Analysis shows that the results across studies varies as expected based on the biological mechanisms. This is not possible without a real treatment effect.
| Treatment delay | Meta-regression of efficacy as a function of treatment delay matches expectations (p = 0.0038). |
| Gradient across stages |
Preclinical studies show mechanisms relevant to all stages: blocking initial infection, minimizing viral replication, and mitigating secondary complications; therefore we expect benefits to combine and increase for earlier treatment, and again for prophylaxis—as intervention is delayed the benefit of specific mechanisms is reduced or lost. Meta-regression confirms this relationship with p < 0.0000001. (Specifically, for blocking initial infection: spike-ACE2 disruption1384,
lipid raft attachment inhibition1401,
glycan binding1385,1466, and CD147
inhibition1397-1400; for minimizing viral replication:
importin-α/β nuclear transport blockade1373, |
| Fed vs. fasting | Administration with a high-fat meal is expected to significantly increase bioavailability, but also support distribution to the lung, bypassing hepatic first-pass metabolism. Studies specifying fed vs. fasting administration show 3.1 times greater efficacy, interaction p = 0.03). |
Systemic vs. topical
application
Dosing and minimizing side effects may be easier with inhaled or
nasal/oral spray formulations, which have been widely proposed for
HCQ1217,1479-1484 and
ivermectin256,1438,1460,1461,1465,1485-1487 .
These formulations may prevent progression to other tissues and improve
utility for less severe cases without significant progression beyond the
respiratory tract.
All studies to date reporting clinical results for HCQ/ivermectin treatment with
inhaled/spray formulations report significant positive
results198,256,944,1484 .
Erasing efficacy
For HCQ, meta-analysis including late stage / excessive
dose trials—where results are poor and trials were large—hides positive results for early treatment and prophylaxis1257.
For ivermectin overdosing is more difficult and late treatment shows
efficacy. How did Cochrane generate a null result? Their meta-analysis1488,1489
required unprecedented measures for a politically acceptable outcome, and has extreme
COI—many authors also did the paxlovid analysis.
•Authors created a
retrospective analysis excluding most studies, splitting results across
multiple analyses, and disregarding efficacy if independent
evidence is combined1488.
•Authors pledged to update the analysis
but only did so once in >5 years. The second version required voiding the protocol
and using novel mechanisms to exclude even more studies, for example specific registration requirements (applied selectively)1489.
•Are authors restricting to
high quality trials? No, their quality evaluation is highly inaccurate, e.g.,
including (violating their own protocol1490) and claiming
low risk of bias for the Together trial, however
the trial has very high actual known bias—reporting multiple
impossible numbers, refusing to release data despite pledging to,
breaking blinding (even externally), and having randomization
failure, extreme COI, many protocol violations, and other issues201.
•Three pre-exposure prophylaxis RCTs,
all showing significant efficacy, were
ignored by specifying post-exposure only.
In contrast, many of the same authors include pre-exposure studies for
paxlovid. In 2023, an ivermectin post-exposure RCT showed efficacy with
p<0.00000000001—no update has been made since 2022.
•Authors claimed updates would be
made as new results were available, however they have only released
two versions, both retrospective with separate protocols specified after all
included results were known.
[Cochrane] has degenerated into a politically expedient organisation that doesn't care much about the trustworthiness of the science or the public…
Peter C. Gøtzsche
Cochrane co-founder1491
Metformin
114 metformin clinical
studies (4 RCTs)584,590,713-824 show
efficacy, confirmed in multiple additional meta-analyses1492-1514.
Studies also show efficacy for acute respiratory failure1515 and influenza A1516.
Extensive preclinical research supports efficacy(i),102,112,116,719,800,1418,1517-1531 .
Antiandrogens
49 antiandrogen clinical
studies (17 RCTs)826-874 show
efficacy, confirmed in multiple additional meta-analyses1532,1533.
Preclinical research supports efficacy1534-1538.
Potential mechanisms include inhibition of TMPRSS2 expression, reduction of
androgen-mediated viral entry, modulation of the immune response, and
attenuation of inflammation.
Antihistamine H1RAs
17 antihistamine H1RA clinical
studies (4 RCTs)876-892 show
efficacy.
Extensive preclinical research supports efficacy878,886,1539-1546 .
Curcumin
28 curcumin clinical
studies (21 RCTs)924-951 show
efficacy, confirmed in multiple additional meta-analyses1547-1552.
Extensive preclinical research supports efficacy(u),166,1203,1216,1416,1418,1443,1553-1600 .
Curcumin has low bioavailability and stability1601—COVID-19 efficacy may depend
heavily on advanced formulations1602 for improved bioavailability.
Melatonin
18 melatonin clinical
studies (8 RCTs)953-970 show
efficacy, confirmed in multiple additional meta-analyses1603-1609.
Extensive preclinical research supports efficacy(v),1610-1617 .
Potential mechanisms include antioxidant, anti-inflammatory, and
antithrombotic effects, immune modulation, regulation of autophagy, modulation
of the renin-angiotensin system, promotion of sleep and circadian rhythm, and
mitigation of cytokine storm.
Colchicine
54 colchicine clinical
studies (30 RCTs)584,972-1024 show
efficacy, confirmed in multiple additional meta-analyses1618-1627.
Preclinical research supports efficacy122,1584.
Potential mechanisms include direct antiviral activity,
immunomodulatory and anti-inflammatory effects, cardioprotective effects, and
prevention of microvascular thrombosis.
Results are poor with very late treatment988—risks due
to side effects may exceed benefits.
Probiotics
29 probiotics clinical
studies (17 RCTs)1026-1054 show
efficacy, confirmed in multiple additional meta-analyses1628,1629.
Studies also show efficacy for upper respiratory infections1630, respiratory tract infections1631, and the common cold1632.
Preclinical research supports efficacy1633,1634.
NAC
26 N-acetylcysteine clinical
studies (11 RCTs)1099-1124 show
efficacy, confirmed in multiple additional meta-analyses1635,1636.
Efficacy has also been shown for influenza1637.
Extensive preclinical research supports efficacy(w),1418,1584,1613,1638-1649 .
Fluvoxamine
21 fluvoxamine clinical
studies (10 RCTs)1126-1146 show
efficacy, confirmed in multiple additional meta-analyses1650-1658.
See Kirsch et al. for additional evidence and analysis1659.
Preclinical research supports efficacy(x),148,1660-1662 .
Potential mechanisms include ASM inhibition, σ-1 receptor activation,
antiplatelet effects, endolysosomal interference, HO-1 increase, reduced cytokine
storm, and elevated melatonin.
Azvudine
42 azvudine clinical
studies (2 RCTs)1056-1097 show
efficacy, confirmed in multiple additional meta-analyses1663-1667.
Preclinical research supports efficacy1096,1668.
Nigella Sativa
15 nigella sativa clinical
studies (11 RCTs)1148-1162 show
efficacy, confirmed in multiple additional meta-analyses1669-1671.
Extensive preclinical research supports efficacy1203,1672-1689 .
Potential mechanisms include direct antiviral activity, and immunomodulatory,
antioxidant, and anti-inflammatory action.
Famotidine
29 famotidine clinical
studies (4 RCTs)579,584,1164-1189 show
efficacy, confirmed in another meta-analysis1690.
Preclinical research supports efficacy71,1691.
Potential mechanisms include direct antiviral activity,
anti-inflammatory effects and reduced cytokine release, reduced acidity
altering conditions for viral replication, immune modulation, and
anticoagulant effects.
TMPRSS2 inhibitors
29 TMPRSS2 inhibitor clinical
studies (25 RCTs)894-922 show
efficacy.
Extensive preclinical research supports efficacy1202,1416,1421,1692-1699 .
Quercetin
9 quercetin clinical
studies (9 RCTs)1191-1199 show
efficacy, confirmed in multiple additional meta-analyses1700,1701.
Extensive preclinical research supports efficacy(as),18,25,32,166,1203,1205,1416,1554,1558,1563,1569,1572,1573,1581,1586,1702,1704-1765 .
Potential mechanisms include direct antiviral activity, antioxidant and
anti-inflammatory activity, and immune support.
COVID-19 efficacy may depend heavily on advanced formulations for improved bioavailability.
Systemic antivirals may be less
applicable to low-risk infections As SARS-CoV-2 has evolved, the frequency of
serious cases has reduced. Systemic antivirals may have a more limited
effect if infection does not spread beyond the upper respiratory tract.
Protocols combine multiple
treatments No single treatment is guaranteed to be effective and safe for a specific individual.
Leading evidence-based protocols combine multiple treatments.
Combined treatment increases efficacy
Monotherapy (single)
27%
[24–30%]
Polytherapy (combined)
71%
[60–79%]
Complementary/synergistic actions,
viral evolution, escape risk suggest polytherapy
There are many complementary mechanisms of action for COVID-19 treatments, with
over 500 therapeutic targets1766.
Studies show complementary and
synergistic effects with polytherapy248,1223,1233,1428,1444,1445,1447,1453,1456,1696,1697,1767-1780 .
For example, Jitobaom et al.1223 shows >10x reduction in
IC50 with ivermectin and niclosamide, an RCT by Said et
al.1770 showed the combination of nigella sativa and vitamin D was
more effective than either alone, and an RCT by Wannigama et
al.1137 showed improved results with fluvoxamine combined with
additional treatments, compared to fluvoxamine alone.
SARS-CoV-2 can rapidly acquire mutations altering infectivity,
disease severity, and drug resistance even without selective
pressure1781-1788.
Antigenic drift can undermine more
variant-specific treatments like monoclonal antibodies and more specific
antivirals. Treatment with targeted antivirals may select for escape
mutations1789.
The efficacy of treatments varies depending on cell
type1790 due to differences in viral receptor expression, drug
distribution and metabolism, and cell-specific mechanisms.
Efficacy may also vary based on genetic
variants1791-1801.
Variable efficacy across variants, cell types, tissues, and
host genetics, along with the complementary and synergistic actions of different
treatments, all point to greater efficacy with polytherapy.
In many studies, the standard of care given to all patients includes other
treatments—efficacy seen in these trials may rely in part on
synergistic effects.
Less variant specific treatments and polytherapy targeting multiple viral and
host proteins may be more effective.
Meta-analysis of all early treatment trials shows 71% [60‑79%] lower risk
for studies using combined treatments, compared to 27% [24‑30%] for single
treatments.
c19early.org
Combined treatment is more effective
SARS-CoV-2 involves the complex interplay of 500+ host and viral proteins and factors, providing many therapeutic targets. Many compounds have antiviral activity for SARS-CoV-2, with many different mechanisms including blocking attachment, entry, and replication. Combinations of treatments, with careful attention to potential side effects, allows improved efficacy via complementary and synergistic mechanisms.
| Tissue and cell coverage | Different compounds have different tissue penetration profiles and efficacy across cell types |
| Variant coverage | Compounds with different viral resistance profiles |
| Intra/extracellular | Disabling and removing intracellular and extracellular viral particles |
| Resistance | Minimizing persistence and emergence of resistant variants |
| Genetics | Robustness against individual variations in efficacy based on genetics |
| Lower doses | Potentially lower doses of individual agents, reducing toxicity |
| Viral and host-directed | Antivirals targeting viral and host proteins |
| Immune system function | Supporting or enhancing natural immune system function |
| Disease phases | Addressing multiple disease phases (viral replication, inflammation, secondary complications) |
Contact.
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Conflicts of interest.
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We have no affiliation with any pharmaceutical companies, supplement companies, governments, political parties, or advocacy organizations.AI.
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ChatGPT) tasked with functioning as additional peer-reviewers to check for errors, suggest
improvements, and review spelling and grammar. Any corrections are manually verified. Our preference for em dashes is independent of AI.Updates.
Our COVID-19 meta-analyses involve the extraction of over 229,000
datapoints from thousands of papers for 227 treatments. We thank the
thousands of scientists, physicians, and other contributors that have provided updates,
suggestions, feedback, and corrections. These are all welcome and can be submitted
below.
Dedication.
This work is dedicated to top
evidence-based physicians that worked tirelessly to analyze evidence and greatly reduce
mortality and morbidity during the pandemic. In alphabetical order:
Dr. Thomas J. Borody, Dr. Mary Talley Bowden, Dr. Flavio Cadegiani, Dr. Shankara Chetty,
Dr. Ryan Cole, Dr. George Fareed, Dr. Sabine Hazan, Dr. Pierre Kory, Dr. Tess Lawrie, Dr.
Robert Malone, Dr. Paul Marik, Dr. Peter McCullough, Dr. Didier Raoult, Dr. Harvey Risch,
Dr. Jackie Stone, Dr. Brian Tyson, Dr. Joseph Varon, and Dr. Vladimir Zelenko.
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Defined as ≥3 studies showing ≥10% improvement or >0% harm with statistical significance in meta-analysis.
The efficacy of endosomal entry inhibitors varies
across SARS-CoV-2 variants, depending on their reliance on the endosomal
pathway for entry. SARS-CoV-2 uses two major pathways for host cell entry:
endosomal entry via cathepsin proteases and TMPRSS2-mediated plasma membrane
fusion. Studies show increased reliance on TMPRSS2-mediated entry for the
Delta variant compared to the original strain. Conversely, Omicron variants
have shown significantly greater reliance on endosomal entry, suggesting
increased efficacy of endosomal acidification inhibitors. Specific
sub-variants may vary. A dual-inhibition strategy targeting both pathways
may be preferred.
COPCOV has the largest number of treated patients of all HCQ/CQ RCTs.
Authors include their own meta-analysis of RCTs confirming significant efficacy.
Due to the politicization,
the most relevant data is hidden within the body of the paper and the supplementary data.
Note that the post-hoc serology based analysis is unreliable as discussed in the paper—due to the high false negative rate of serum/DBS serology, false negative baseline serology may account for many/most of the seroconversion cases174.
The analysis showing significantly lower COVID-19 cases with HCQ across 2 US RCTs is in the preprint only—it was deleted from the journal version.
The other arms of this trial confirm that the efficacy is not due to the open label design175. Significant improvement is seen consistently across all symptoms, and across all variants of the recovery outcome.
When administered late in infection, HCQ may enhance viral egress by further increasing
lysosomal pH beyond the effect of ORF3a's water channel activity, thereby promoting
lysosomal exocytosis, inactivating degradative enzymes, and facilitating the release of
SARS-CoV-2 particles into the extracellular environment1253,1254.
Page 358 in the appendix shows 36% lower ongoing persistent COVID-19 specific symptoms (p<0.0001) when combining the individual symptom results. Authors report a 28% reduction (p=0.015), not mentioned in the abstract or conclusion. This appears to be a one of any symptom analysis,
effectively increasing the weight of the more common “fatigue”, reducing the perceived effect
(the difference does not appear to be due to adjustments - the adjustments in Table S6 to
Table S39 make minimal difference). This is for very late and poorly administered treatment taken
by only 89% of patients in a relatively low-risk population - benefits may
be much greater with recommended usage and in high-risk patients.
Prof. Sander Greenland demonstrates176 that the Bayesian model applied an extremely tight, null-centered prior that was never reported in the paper. This prior pulls the frequentist hazard ratio for time-to-recovery down and slashes the posterior probability that the benefit reaches the trial's own “clinically meaningful” threshold of HR≥1.2. Even with the shrinkage, the posterior probability of any benefit exceeds 0.9999, well above the protocol's 0.99 superiority bar, however authors label ivermectin “unlikely to provide clinically meaningful improvement.” Greenland argues that the unexplained prior acts like a hidden penalty, lacks empirical justification, and biases the analysis toward the null, thereby allowing the authors to downplay results their own decision rules would otherwise classify as superior. Author notes the strong priors are not justified by previous trials and suggests that they reflect social pressure to discredit ivermectin.
Ivermectin, better known for antiparasitic activity, is a broad spectrum antiviral with activity against many viruses including H7N71373, Dengue124,1374,1375 , HIV-11375, Simian virus 401376, Zika124,1377,1378 , West Nile1378, Yellow Fever1379,1380, Japanese encephalitis1379, Chikungunya1380, Semliki Forest virus1380, Human papillomavirus1381, Epstein-Barr1381, BK Polyomavirus1382, and Sindbis virus1380.
Ivermectin inhibits importin-α/β-dependent nuclear import of viral proteins1373,1375,1376,1383 , shows spike-ACE2 disruption at 1nM with microfluidic diffusional sizing1384, binds to glycan sites on the SARS-CoV-2 spike protein preventing interaction with blood and epithelial cells and inhibiting hemagglutination1385,1386, shows dose-dependent inhibition of wildtype and omicron variants1387, exhibits dose-dependent inhibition of lung injury1388,1389, may inhibit SARS-CoV-2 via IMPase inhibition124, may inhibit SARS-CoV-2 induced formation of fibrin clots resistant to degradation1390, inhibits SARS-CoV-2 3CLpro1391, may inhibit SARS-CoV-2 RdRp activity1392,1393, may minimize viral myocarditis by inhibiting NF-κB/p65-mediated inflammation in macrophages1394, may be beneficial for COVID-19 ARDS by blocking GSDMD and NET formation1395, may interfere with SARS-CoV-2's immune evasion via ORF8 binding1396, may inhibit SARS-CoV-2 by disrupting CD147 interaction1397-1400, may inhibit SARS-CoV-2 attachment to lipid rafts via spike NTD binding1401, shows protection against inflammation, cytokine storm, and mortality in an LPS mouse model sharing key pathological features of severe COVID-191402,1403, may be beneficial in severe COVID-19 by binding IGF1 to inhibit the promotion of inflammation, fibrosis, and cell proliferation that leads to lung damage1404, significantly mitigates bleomycin-induced pulmonary fibrosis by reducing collagen accumulation and inflammatory cell infiltration1405, improves oxidative stress markers while suppressing myofibroblast proliferation1405, mitigates lung pathology and anosmia in vivo while regulating the CXCL10/CXCL5 inflammatory axis via P2X4 and α7nAChR receptor modulation1406, may minimize SARS-CoV-2 induced cardiac damage1407,1408, may counter immune evasion by inhibiting NSP15-TBK1/KPNA1 interaction and restoring IRF3 activation52, may disrupt SARS-CoV-2 N and ORF6 protein nuclear transport and their suppression of host interferon responses1409, reduces TAZ/YAP nuclear import, relieving SARS-CoV-2-driven suppression of IRF3 and NF-κB antiviral pathways1410, increases Bifidobacteria which play a key role in the immune system1411, has immunomodulatory1412 and anti-inflammatory1413,1414 properties, and has an extensive and very positive safety profile1415.
A systematic review and meta-analysis of 15 non-COVID-19 preclinical studies showed that metformin inhibits pulmonary inflammation and oxidative stress, minimizes lung injury, and improves survival in animal models of acute respiratory distress syndrome (ARDS) or acute lung injury (ALI)1517.
Metformin inhibits SARS-CoV-2 in vitro719,1518, minimizes LPS-induced cytokine storm in a mouse model1519, minimizes lung damage and fibrosis in a mouse model of LPS-induced ARDS800, may protect against SARS-CoV-2-induced neurological disorders1520, may be beneficial via inhibitory effects on ORF3a-mediated inflammasome activation1521, reduces UUO and FAN-induced kidney fibrosis800, increases mitochondrial function and decreases TGF-β-induced fibrosis, apoptosis, and inflammation markers in lung epithelial cells800, may reduce inflammation, oxidative stress, and thrombosis via regulating glucose metabolism1522, attenuates spike protein S1-induced inflammatory response and α-synuclein aggregation1523, may protect against COVID-19 cognitive impairment by suppressing HIF-1α stabilization and reducing neurodegenerative protein aggregation112, may reduce COVID-19 severity and long COVID by inhibiting NETosis via suppression of protein kinase C activation1524, enhances interferon responses and reduces SARS-CoV-2 infection and inflammation in diabetic models by suppressing HIF-1α signaling1525, may improve COVID-19 outcomes by preventing VDAC1 mistargeting to the plasma membrane, reducing ATP loss, and preserving immune cell function during cytokine storm116, reduces hyperglycemia-induced hepatic ACE2/TMPRSS2 up-regulation and SARS-CoV-2 entry1526, may reduce COVID-19 severity by suppressing monocyte inflammatory responses and glycolytic activation via AMPK pathway modulation1527, may reduce glycolytic capacity and restrict SARS-CoV-2 replication via boosting mitochondrial OXPHOS with AMPK/PGC-1α activation102, and may improve outcomes via modulation of immune responses with increased anti-inflammatory T lymphocyte gene expression and via enhanced gut microbiota diversity1528.
The trimeric spike (S) protein is a glycoprotein that mediates viral entry by binding to the host ACE2 receptor, is critical for SARS-CoV-2's ability to infect host cells, and is a target of neutralizing antibodies. Inhibition of the spike protein prevents viral attachment, halting infection at the earliest stage.
The receptor binding domain is a specific region of the spike protein that binds ACE2 and is a major target of neutralizing antibodies. Focusing on the precise binding site allows highly specific disruption of viral attachment with reduced potential for off-target effects.
The main protease or Mpro, also known as 3CLpro or nsp5, is a cysteine protease that cleaves viral polyproteins into functional units needed for replication. Inhibiting Mpro disrupts the SARS-CoV-2 lifecycle within the host cell, preventing the creation of new copies.
RNA-dependent RNA polymerase (RdRp), also called nsp12, is the core enzyme of the viral replicase-transcriptase complex that copies the positive-sense viral RNA genome into negative-sense templates for progeny RNA synthesis. Inhibiting RdRp blocks viral genome replication and transcription.
The papain-like protease (PLpro) has multiple functions including cleaving viral polyproteins and suppressing the host immune response by deubiquitination and deISGylation of host proteins. Inhibiting PLpro may block viral replication and help restore normal immune responses.
The angiotensin converting enzyme 2 (ACE2) protein is a host cell transmembrane protein that serves as the cellular receptor for the SARS-CoV-2 spike protein. ACE2 is expressed on many cell types, including epithelial cells in the lungs, and allows the virus to enter and infect host cells. Inhibition may affect ACE2's physiological function in blood pressure control.
The nucleocapsid (N) protein binds and encapsulates the viral genome by coating the viral RNA. N enables formation and release of infectious virions and plays additional roles in viral replication and pathogenesis. N is also an immunodominant antigen used in diagnostic assays.
Non-structural protein 10 (nsp10) serves as an RNA chaperone and stabilizes conformations of nsp12 and nsp14 in the replicase-transcriptase complex, which synthesizes new viral RNAs. Nsp10 disruption may destabilize replicase-transcriptase complex activity.
The helicase, or nsp13, protein unwinds the double-stranded viral RNA, a crucial step in replication and transcription. Inhibition may prevent viral genome replication and the creation of new virus components.
The interaction between the SARS-CoV-2 spike protein and the human ACE2 receptor is a primary method of viral entry, inhibiting this interaction can prevent the virus from attaching to and entering host cells, halting infection at an early stage.
Transmembrane protease serine 2 (TMPRSS2) is a host cell protease that primes the spike protein, facilitating cellular entry. TMPRSS2 activity helps enable cleavage of the spike protein required for membrane fusion and virus entry. Inhibition may especially protect respiratory epithelial cells, buy may have physiological effects.
In silico studies predict inhibition of SARS-CoV-2 with curcumin or metabolites via binding to the spike(j),1416,1553-1559 (and specifically the receptor binding domain(k),1560-1565 ), Mpro(l),1416,1554,1555,1557,1558,1561-1563,1566-1573 , RNA-dependent RNA polymerase(m),1416,1558,1562,1563,1574 , PLpro(n),1416, ACE2(o),1203,1556,1564,1572 , nucleocapsid(p),1443,1575 , nsp10(q),1443, and helicase(r),1576 proteins, and inhibition of spike-ACE2 interaction(s),1565,1577 .
In vitro studies demonstrate inhibition of the spike(j),1216 (and specifically the receptor binding domain(k),1578), Mpro(l),1216,1573,1579,1580 , ACE2(o),1578, and TMPRSS2(t),1578 proteins, and inhibition of spike-ACE2 interaction(s),1577,1581 .
Curcumin decreases pro-inflammatory cytokines induced by SARS-CoV-2 in peripheral blood mononuclear cells1582, alleviates SARS-CoV-2 spike protein-induced mitochondrial membrane damage and oxidative stress1583, may limit COVID-19 induced cardiac damage by inhibiting the NF-κB signaling pathway which mediates the profibrotic effects of the SARS-CoV-2 spike protein on cardiac fibroblasts1584, is predicted to inhibit the interaction between the SARS-CoV-2 spike protein receptor binding domain and the human ACE2 receptor for the delta and omicron variants1560, lowers ACE2 and STAT3, curbing lung inflammation and ARDS in preclinical COVID-19 models1585, inhibits SARS-CoV-2 ORF3a ion channel activity, which contributes to viral pathogenicity and cytotoxicity1586, has direct virucidal action by disrupting viral envelope integrity1587, may inhibit viral replication and modulate inflammatory pathways like NF-κB via SIRT1 activation166, and can function as a photosensitizer in photodynamic therapy to generate reactive oxygen species that damage the virus1587.
Melatonin may restore altered redox homeostasis in COVID-191610, modulates type III interferon responses and reduces inflammatory cytokine production in TLR3 receptor agonist stimulated viral inflammation while preserving tissue integrity1611, and negatively regulates genes critical for viral entry in lung tissue, including reduced expression of FURIN and components of the CD147 complex, while potentially disrupting TMPRSS2/ACE2-mediated entry mechanisms1612.
Melatonin reduces oxidative stress, inhibits NET formation, and protects tissues through anti-inflammatory and antioxidant actions1613.
Severe COVID-19 is marked by endotheliopathy with elevated von Willebrand factor (VWF) levels and platelet/VWF-rich microthrombi; N-acetylcysteine can reduce VWF multimers and lyse VWF-dependent clots in vivo, potentially helping to alleviate thrombosis associated with COVID-191638-1640.
N-acetylcysteine shows dose-dependent inhibition of SARS-CoV-21641-1643, shows anti-inflammatory and immunomodulatory effects against SARS-CoV-2-induced immune responses in combination with bromelain1644, suppressed virus-induced reactive oxygen species and blocked viral replication in a humanized mouse model and in human lung cells1645, may limit COVID-19 induced cardiac damage by boosting cellular antioxidant defenses and potentially mitigating the oxidative stress caused by spike protein-induced ROS production in cardiac fibroblasts1584, and reduces disulfide bonds in proteins and exhibits antioxidant properties that may inhibit viral replication and modulate inflammatory responses1646.
NAC may be beneficial for COVID-19 by replenishing glutathione stores and reinforcing the glutathione peroxidase-4 pathway to inhibit ferroptosis, an oxidative stress-induced cell death pathway implicated in COVID-191647.
NAC reinforces glutathione levels, reduces ROS, and minimizes ferroptosis and cytokine storm1613.
Fluvoxamine may inhibit SARS-CoV-2 cell entry by preventing the formation of ceramide platforms that facilitates viral uptake1660, may help restore autophagic processes disrupted by NSP6, thereby reducing SARS-CoV-2 replication and improving host cellular defenses1661, and may reduce COVID-19 thrombotic complications by inhibiting serotonin reuptake and decreasing platelet activation148.
The endoribonuclease, also known as NendoU or nsp15, cleaves specific sequences in viral RNA which may help the virus evade detection by the host immune system. Inhibition may hinder the virus's ability to mask itself from the immune system, facilitating a stronger immune response.
The NSP16/10 complex consists of non-structural proteins 16 and 10, forming a 2'-O-methyltransferase that modifies the viral RNA cap structure. This modification helps the virus evade host immune detection by mimicking host mRNA, making NSP16/10 a promising antiviral target.
Cathepsin L is a host lysosomal cysteine protease that can prime the spike protein through an alternative pathway when TMPRSS2 is unavailable. Dual targeting of cathepsin L and TMPRSS2 may maximize disruption of alternative pathways for virus entry.
Wingless-related integration site (Wnt) ligand 3 is a host signaling molecule that activates the Wnt signaling pathway, which is important in development, cell growth, and tissue repair. Some studies suggest that SARS-CoV-2 infection may interfere with the Wnt signaling pathway, and that Wnt3a is involved in SARS-CoV-2 entry.
The frizzled (FZD) receptor is a host transmembrane receptor that binds Wnt ligands, initiating the Wnt signaling cascade. FZD serves as a co-receptor, along with ACE2, in some proposed mechanisms of SARS-CoV-2 infection. The virus may take advantage of this pathway as an alternative entry route.
Low-density lipoprotein receptor-related protein 6 is a cell surface co-receptor essential for Wnt signaling. LRP6 acts in tandem with FZD for signal transduction and has been discussed as a potential co-receptor for SARS-CoV-2 entry.
The ezrin protein links the cell membrane to the cytoskeleton (the cell's internal support structure) and plays a role in cell shape, movement, adhesion, and signaling. Drugs that occupy the same spot on ezrin where the viral spike protein would bind may hindering viral attachment, and drug binding could further stabilize ezrin, strengthening its potential natural capacity to impede viral fusion and entry.
The Adipocyte Differentiation-Related Protein (ADRP, also known as Perilipin 2 or PLIN2) is a lipid droplet protein regulating the storage and breakdown of fats in cells. SARS-CoV-2 may hijack the lipid handling machinery of host cells and ADRP may play a role in this process. Disrupting ADRP's interaction with the virus may hinder the virus's ability to use lipids for replication and assembly.
Neuropilin-1 (NRP1) is a cell surface receptor with roles in blood vessel development, nerve cell guidance, and immune responses. NRP1 may function as a co-receptor for SARS-CoV-2, facilitating viral entry into cells. Blocking NRP1 may disrupt an alternative route of viral entry.
EP300 (E1A Binding Protein P300) is a transcriptional coactivator involved in several cellular processes, including growth, differentiation, and apoptosis, through its acetyltransferase activity that modifies histones and non-histone proteins. EP300 facilitates viral entry into cells and upregulates inflammatory cytokine production.
Prostaglandin G/H synthase 2 (PTGS2, also known as COX-2) is an enzyme crucial for the production of inflammatory molecules called prostaglandins. PTGS2 plays a role in the inflammatory response that can become severe in COVID-19 and inhibitors (like some NSAIDs) may have benefits in dampening harmful inflammation, but note that prostaglandins have diverse physiological functions.
Heat Shock Protein 90 Alpha Family Class A Member 1 (HSP90AA1) is a chaperone protein that helps other proteins fold correctly and maintains their stability. HSP90AA1 plays roles in cell signaling, survival, and immune responses. HSP90AA1 may interact with numerous viral proteins, but note that it has diverse physiological functions.
Matrix metalloproteinase 9 (MMP9), also called gelatinase B, is a zinc-dependent enzyme that breaks down collagen and other components of the extracellular matrix. MMP9 levels increase in severe COVID-19. Overactive MMP9 can damage lung tissue and worsen inflammation. Inhibition of MMP9 may prevent excessive tissue damage and help regulate the inflammatory response.
The interleukin-6 (IL-6) pro-inflammatory cytokine (signaling molecule) has a complex role in the immune response and may trigger and perpetuate inflammation. Elevated IL-6 levels are associated with severe COVID-19 cases and cytokine storm. Anti-IL-6 therapies may be beneficial in reducing excessive inflammation in severe COVID-19 cases.
The interleukin-10 (IL-10) anti-inflammatory cytokine helps regulate and dampen immune responses, preventing excessive inflammation. IL-10 levels can also be elevated in severe COVID-19. IL-10 could either help control harmful inflammation or potentially contribute to immune suppression.
Vascular Endothelial Growth Factor A (VEGFA) promotes the growth of new blood vessels (angiogenesis) and has roles in inflammation and immune responses. VEGFA may contribute to blood vessel leakiness and excessive inflammation associated with severe COVID-19.
RELA is a transcription factor subunit of NF-kB and is a key regulator of inflammation, driving pro-inflammatory gene expression. SARS-CoV-2 may hijack and modulate NF-kB pathways.
A mouse model expressing the human ACE2 receptor under the control of the K18 promoter.
A mouse model of obesity and severe insulin resistance leading to type 2 diabetes due to a mutation in the leptin receptor gene that impairs satiety signaling.
A mouse model commonly used in infectious disease and cancer research due to higher immune response and susceptibility to infection.
In silico studies predict inhibition of SARS-CoV-2, or minimization of side effects, with quercetin or metabolites via binding to the spike(j),1205,1416,1554,1558,1572,1702-1710 (and specifically the receptor binding domain(k),1563), Mpro(l),1205,1416,1554,1558,1563,1569,1572,1705,1706,1708,1711-1725 , RNA-dependent RNA polymerase(m),1416,1558,1563,1708,1726,1727 , PLpro(n),1416,1713,1718 , ACE2(o),1203,1572,1704,1709,1713,1714,1728 , TMPRSS2(t),1704, nucleocapsid(p),1416, helicase(r),1416,1712,1729 , endoribonuclease(y),1702, NSP16/10(z),1730, cathepsin L(aa),1731, Wnt-3(ab),1704, FZD(ac),1704, LRP6(ad),1704, ezrin(ae),1732, ADRP(af),1205, NRP1(ag),1709, EP300(ah),1733, PTGS2(ai),1714, HSP90AA1(aj),1714,1733 , matrix metalloproteinase 9(ak),1734, IL-6(al),1735,1736 , IL-10(am),1735, VEGFA(an),1736, and RELA(ao),1736 proteins, and inhibition of spike-ACE2 interaction(s),1737.
In vitro studies demonstrate inhibition of the Mpro(l),1573,1720,1738,1739 protein, and inhibition of spike-ACE2 interaction(s),1581.
Animal studies demonstrate efficacy in K18-hACE2 mice(ap),1740, db/db mice(aq),1741,1742 , BALB/c mice(ar),1743, and rats1744.
Quercetin reduced proinflammatory cytokines and protected lung and kidney tissue against LPS-induced damage in mice1743, inhibits LPS-induced cytokine storm by modulating key inflammatory and antioxidant pathways in macrophages1745, may block ACE2-spike interaction and NLRP3 inflammasome, limiting viral entry and inflammation18, upregulates the SIRT1/AMPK axis to inhibit oxidative injury and accelerate viral clearance166, inhibits SARS-CoV-2 ORF3a ion channel activity, which contributes to viral pathogenicity and cytotoxicity1586, may alleviate COVID-19 ARDS via inhibition of EGFR and JAK2 inflammatory targets32, may destabilize the Spike protein, IL-6R, and integrins via conserved residues, blocking viral entry, hyperinflammation, and platelet aggregation25, and may reduce COVID-19 neuroinflammation and cognitive dysfunction through anti-inflammatory mechanisms and neuroprotective effects1746.
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