COVID-19 treatment: systemic agents
• Many systemic agents reduce risk
@CovidAnalysis, August 21, 2025
We do not provide medical advice. No treatment is
100% effective, and all may have side effects. Protocols combine multiple
treatments. Consult a qualified physician for personalized
risk/benefit analysis.
Over 10,000
compounds predicted to reduce risk—SARS-CoV-2 is easily
disabled
SARS-CoV-2 infection and replication involves a complex
interplay of over 200 host and viral proteins and other
factors1-8, providing many therapeutic
targets.
Scientists have identified 10,157+
compounds9 potentially beneficial
for COVID-19. Hundreds of compounds inhibit SARS-CoV-2 in vitro,
including many with known pharmacokinetics and proven safety.
Figure 1. Efficacy vs. cost for COVID-19 treatments.
Figure 2. Efficacy as a function of treatment delay.
Early treatment is easier and more
effective
As infection progresses, SARS-CoV-2 may spread to the lower respiratory tract
and throughout the body.
Toro et al.10 detected SARS-CoV-2 in the serum of 23% of patients.
Nebulization can target the lower respiratory tract, while spread throughout
the rest of the body may require systemic treatments.
Systemic treatments may delay the onset of action, increase side effect risk,
and present challenges for accurately attaining target therapeutic concentrations
across tissues.
SARS-CoV-2 cell entry, and the antiviral activity of treatments, can be very
different across cell types, for example lung vs. cardiac
cells11. Therefore, treatment is more complex as
infection spreads.
Figure 2 shows efficacy in studies from the 178 treatments
covered as a function of the delay from onset to treatment
initiation(b). Early treatment is more effective.
c19early.org
| Efficacy confidence - low-cost systemic agents | ||
| Hydroxychloroquine | p<0.0000000001 | |
| Ivermectin | p<0.0000000001 | |
| Metformin | p<0.0000000001 | |
| Curcumin | p=0.000000006 | |
| Melatonin | p=0.00000001 | |
| Antiandrogens | p=0.00000006 | |
| Azvudine | p=0.0000001 | |
| Colchicine | p=0.0000002 | |
| Probiotics | p=0.000001 | |
| N-acetylcysteine | p=0.00003 | |
| Antihistamine H1RAs | p=0.00007 | |
| Fluvoxamine | p=0.0001 | |
| Nigella Sativa | p=0.0002 | |
| Famotidine | p=0.0003 | |
| TMPRSS2 inhibitors | p=0.0007 | |
| Quercetin | p=0.002 | |
| Efficacy confirmed March 2020 (HCQ)(c),15 | ||
❝
if you say anything in favor of ivermectin you will be cast out
of civilization and thrown into the circle of social hell..
Scott Alexander1028
Politicization Hydroxychloroquine and ivermectin have become the most politicized treatments of
all time. As Scott Alexander
said1028:
"if you say anything in favor of ivermectin you will be cast out of
civilization and thrown into the circle of social hell reserved for Klan
members and 1/6 insurrectionists. All the health officials in the world will
shout 'horse dewormer!' at you and compare you to Josef Mengele."
❝
it is often possible to make
clinical trials come out pretty much any way you want
Marcia Angell, former NEJM editor1029
Analysis of 424 controlled
clinical studies12,13,122-546 shows
strong evidence for efficacy with early treatment
(p<0.0000000001) and prophylaxis (p<0.0000000001), confirmed in multiple additional meta analyses423,1070-1077 .
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)(e),12.
In 2021 Naggie et al.490 showed that HCQ pre-exposure prophylaxis
significantly reduced COVID-19 cases based on 2 US RCTs. This is now known with
p=0.00004 for RCTs and
p=0.00000001 for observational studies.
The Oxford PRINCIPLE RCT, withheld for 5 years, shows significantly faster recovery
with HCQ(f),13.
HCQ shows poor results with late treatment and excessive dosage, and the
combination shows harm.
Late-stage treatment may enhance viral egress via lysosomal
deacidification(g),1078,1079 . Research also suggests potential
cardioprotective effects at lower doses, but cardiotoxicity with excessive
dosage1046. Bobrowski et al. show that HCQ and remdesivir should
not be used together.
The RECOVERY trial, key to the worldwide campaign against HCQ, used very late treatment
with an excessive toxic dose186. Strong evidence for harm with the dose used
was known from a dose comparison RCT on April 241081.
It is unclear how the trial, with reported IDMC interim reviews every two weeks, could
justify starting and continuing this dose until June 5.
Studies for HCQ are inconsistent with the logical use of
antivirals. 90% of treatment studies analyzed late treatment,
5+ days after the onset of symptoms547.
This makes it easy to generate meta analyses showing poor efficacy by
including large late treatment studies1082, although the results
are not relevant to recommended usage.
Results have not been reported for 37 RCTs1083-1119, and an
additional 65 HCQ RCTs were terminated with <30
patients1120-1178.
HCQ was the first treatment confirmed
effective1179, however alternatives
may offer advantages. Lung pharmacokinetics show high inter-individual
variability1067; dosage is relatively challenging, with dependence
on cholesterol1049, lung pH1040, and renal
impairment1040, delayed attainment of therapeutic
concentrations, and a relatively narrow range of regimens showing efficacy
while limiting side effects; and ~2.5%1180 of patients may have
contraindications.
Longer-term use of endosomal acidification modifiers for prophylaxis raises
concern for potential off-target effects, including disruption of cellular
processes, impaired lysosomal function, reduced immune
response1181, and altered cellular signaling.
Fake tablets are common in some locations1182-1184.
❝
There is a clear signal that IVM works in COVID patients..
Ed Mills, Together Trial co-principal
investigator1185
The largest RCT, with a design highly favoring
finding no efficacy, found superiority with probability > 0.999 for
recovery(h),101. Improved recovery is strongly associated
with lower mortality, p<0.00000000001(h),101. The trial also
found 36% lower long COVID (p<0.0001) despite very suboptimal
use(h),101.
Extensive preclinical research supports efficacy(i),1194,1196-1198,1203,1205-1231,1233-1284 .
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
results1285-1287,
and disregarding flaws and fraud in the major trials
claiming no effect121.
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 violations41.
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 treatment to the respiratory tract.
Pharmacokinetics show significant inter-individual variability1288.
Injectable formulations may reduce variability and provide faster onset
of action1273.
Liposomal formulations show increased antiviral activity and lower
cytotoxicity1268.
Synergistic results are seen with polytherapy1265,1267,1272 .
Efficacy varies depending on the manufacturer1289, underdosed
and contaminated ivermectin is common1290-1293,
and fake tablets with no active ingredient have been
reported1294.
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
HCQ1044,1295-1300 and
ivermectin94,1258,1279,1280,1284,1301-1303 .
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
results38,94,771,1300 .
Metformin
106 metformin clinical
studies420,426,548-651 show
efficacy, confirmed in multiple additional meta analyses1304-1325.
Efficacy has also been shown for influenza A1326.
Extensive preclinical research supports efficacy(j),555,632,1238,1327-1340 .
Antiandrogens
49 antiandrogen clinical
studies653-701 show
efficacy, confirmed in multiple additional meta analyses1341,1342.
Preclinical research supports efficacy1343-1346.
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
studies703-719 show
efficacy.
Extensive preclinical research supports efficacy705,713,1347-1354 .
Curcumin
28 curcumin clinical
studies751-778 show
efficacy, confirmed in multiple additional meta analyses1355-1358.
Extensive preclinical research supports efficacy(v),1031,1043,1236,1238,1263,1359-1402 .
Curcumin has low bioavailability and stability1403—COVID-19 efficacy may depend
heavily on advanced formulations1404 for improved bioavailability.
Melatonin
20 melatonin clinical
studies780-799 show
efficacy, confirmed in multiple additional meta analyses1405-1411.
Extensive preclinical research supports efficacy(w),1412-1419 .
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
57 colchicine clinical
studies420,801-856 show
efficacy, confirmed in multiple additional meta analyses1420-1429.
Preclinical research supports efficacy1388.
Potential mechanisms include direct antiviral activity,
immunomodulatory and anti-inflammatory effects, cardioprotective effects, and
prevention of microvascular thrombosis.
Results are poor with very late treatment819—risks due
to side effects may exceed benefits.
Probiotics
28 probiotics clinical
studies858-885 show
efficacy, confirmed in multiple additional meta analyses1430,1431.
Studies also show efficacy for respiratory tract infections1432 and the common cold1433.
Preclinical research supports efficacy1434,1435.
NAC
24 N-acetylcysteine clinical
studies925-948 show
efficacy, confirmed in multiple additional meta analyses1436,1437.
Efficacy has also been shown for influenza1438.
Extensive preclinical research supports efficacy(x),1238,1388,1415,1439-1446 .
Fluvoxamine
21 fluvoxamine clinical
studies950-970 show
efficacy, confirmed in multiple additional meta analyses1447-1455.
Preclinical research supports efficacy(y),1456-1459 .
Potential mechanisms include ASM inhibition, σ-1 receptor activation,
antiplatelet effects, endolysosomal interference, HO-1 increase, reduced cytokine
storm, and elevated melatonin.
Azvudine
37 azvudine clinical
studies887-923 show
efficacy, confirmed in multiple additional meta analyses1460-1463.
Preclinical research supports efficacy1464.
Nigella Sativa
14 nigella sativa clinical
studies972-985 show
efficacy, confirmed in multiple additional meta analyses1465,1466.
Extensive preclinical research supports efficacy1031,1467-1484 .
Potential mechanisms include direct antiviral activity, and immunomodulatory,
antioxidant, and anti-inflammatory action.
Famotidine
30 famotidine clinical
studies415,420,987-1013 show
efficacy.
Preclinical research supports efficacy1485.
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
studies721-749 show
efficacy.
Extensive preclinical research supports efficacy1030,1236,1241,1486-1493 .
Quercetin
12 quercetin clinical
studies1015-1026 show
efficacy, confirmed in multiple additional meta analyses1494,1495.
Extensive preclinical research supports efficacy(at),1031,1033,1236,1360,1364,1368,1373,1376,1377,1385,1390,1496,1498-1554 .
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.
Protocols typically combine multiple
treatments No single treatment is guaranteed to be effective and safe for a specific individual.
Leading evidence-based protocols combine multiple treatments.
c19early.org
| Combined treatments increase efficacy | |
|---|---|
| Monotherapy | 33% [30‑36%] |
| Polytherapy | 68% [57‑77%] |
Complementary and
synergistic actions There are many complementary mechanisms of action
across treatments, and studies show complementary and synergistic effects
with polytherapy86,1059,1265,1267,1272,1275,1490,1491,1555-1563 .
For example, Jitobaom et al.1267 shows >10x reduction in
IC50 with ivermectin and niclosamide, an RCT by Said et
al.1558 showed the combination of nigella sativa and vitamin D was
more effective than either alone, and an RCT by Wannigama et
al.961 showed improved results with fluvoxamine combined with
additional treatments, compared to fluvoxamine alone.
Treatment efficacy may vary significantly across SARS-CoV-2 variants. For
example new variants may gain resistance to targeted
treatments1564-1570, and
the role of TMPRSS2 for cell entry differs across variants1571.
The efficacy of specific treatments varies depending on cell
type11 due to differences in viral receptor expression, drug
distribution and metabolism, cell-specific mechanisms, and the relevance of
drug targets to specific cells.
Efficacy may also vary based on genetic
variants1572-1580.
Variable efficacy across SARS-CoV-2 variants, cell types, different 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.
Meta analysis of all early treatment trials shows 68% [57‑77%] lower risk
for studies using combined treatments, compared to 33% [30‑36%] for single
treatments.
SARS-CoV-2 evolution and the risk of
escape mutants suggests treatments with broader mechanisms of action and
polytherapy SARS-CoV-2 can rapidly acquire mutations altering infectivity,
disease severity, and drug resistance even without selective
pressure1581. Antigenic drift can undermine more
variant-specific treatments like monoclonal antibodies and more specific
antivirals. Treatment with targeted antivirals may select for escape
mutations1582.
Less variant specific treatments and polytherapy targeting multiple viral and
host proteins may be more effective.
Systemic antivirals may be less
applicable to low-risk infections As SARS-CoV-2 has evolved, the frequency of
serious infections has reduced. Systemic antivirals may have a more limited
effect if infection does not spread beyond the upper respiratory tract.
Treatments with few studies are not shown.
Analysis includes all studies that specify the time between the
onset of symptoms and treatment. This analysis focuses on individual
treatments—typical protocols combine treatments and may maintain higher efficacy at
later times.
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 cases12.
The other arms of this trial confirm that the efficacy is not due to the open label design13. 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 environment1078,1079.
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 demonstrates14 that the Bayesian model applied an extremely tight, null-centred 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 H7N71194, Dengue1195-1197, HIV-11196, Simian virus 401198, Zika1197,1199,1200 , West Nile1200, Yellow Fever1201,1202, Japanese encephalitis1201, Chikungunya1202, Semliki Forest virus1202, Human papillomavirus1203, Epstein-Barr1203, BK Polyomavirus1204, and Sindbis virus1202.
Ivermectin inhibits importin-α/β-dependent nuclear import of viral proteins1194,1196,1198,1205 , shows spike-ACE2 disruption at 1nM with microfluidic diffusional sizing1206, binds to glycan sites on the SARS-CoV-2 spike protein preventing interaction with blood and epithelial cells and inhibiting hemagglutination1207,1208, shows dose-dependent inhibition of wildtype and omicron variants1209, exhibits dose-dependent inhibition of lung injury1210,1211, may inhibit SARS-CoV-2 via IMPase inhibition1197, may inhibit SARS-CoV-2 induced formation of fibrin clots resistant to degradation1212, inhibits SARS-CoV-2 3CLpro1213, may inhibit SARS-CoV-2 RdRp activity1214, may minimize viral myocarditis by inhibiting NF-κB/p65-mediated inflammation in macrophages1215, may be beneficial for COVID-19 ARDS by blocking GSDMD and NET formation1216, may interfere with SARS-CoV-2's immune evasion via ORF8 binding1217, may inhibit SARS-CoV-2 by disrupting CD147 interaction1218-1221, shows protection against inflammation, cytokine storm, and mortality in an LPS mouse model sharing key pathological features of severe COVID-191222,1223, may be beneficial in severe COVID-19 by binding IGF1 to inhibit the promotion of inflammation, fibrosis, and cell proliferation that leads to lung damage1224, may minimize SARS-CoV-2 induced cardiac damage1225,1226, may counter immune evasion by inhibiting NSP15-TBK1/KPNA1 interaction and restoring IRF3 activation1227, may disrupt SARS-CoV-2 N and ORF6 protein nuclear transport and their suppression of host interferon responses1228, reduces TAZ/YAP nuclear import, relieving SARS-CoV-2-driven suppression of IRF3 and NF-κB antiviral pathways1229, increases Bifidobacteria which play a key role in the immune system1230, has immunomodulatory1231 and anti-inflammatory1232,1233 properties, and has an extensive and very positive safety profile1234.
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)1327.
Metformin inhibits SARS-CoV-2 in vitro555,1328, minimizes LPS-induced cytokine storm in a mouse model1329, minimizes lung damage and fibrosis in a mouse model of LPS-induced ARDS632, may protect against SARS-CoV-2-induced neurological disorders1330, may be beneficial via inhibitory effects on ORF3a-mediated inflammasome activation1331, reduces UUO and FAN-induced kidney fibrosis632, increases mitochondrial function and decreases TGF-β-induced fibrosis, apoptosis, and inflammation markers in lung epithelial cells632, may reduce inflammation, oxidative stress, and thrombosis via regulating glucose metabolism1332, attenuates spike protein S1-induced inflammatory response and α-synuclein aggregation1333, may reduce COVID-19 severity and long COVID by inhibiting NETosis via suppression of protein kinase C activation1334, enhances interferon responses and reduces SARS-CoV-2 infection and inflammation in diabetic models by suppressing HIF-1α signaling1335, may improve COVID-19 outcomes by preventing VDAC1 mistargeting to the plasma membrane, reducing ATP loss, and preserving immune cell function during cytokine storm1336, reduces hyperglycemia-induced hepatic ACE2/TMPRSS2 up-regulation and SARS-CoV-2 entry1337, and may improve outcomes via modulation of immune responses with increased anti-inflammatory T lymphocyte gene expression and via enhanced gut microbiota diversity1338.
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(k),1236,1359-1364 (and specifically the receptor binding domain(l),1365-1369 ), Mpro(m),1236,1360,1361,1363,1364,1366-1368,1370-1377 , RNA-dependent RNA polymerase(n),1236,1364,1367,1368,1378 , PLpro(o),1236, ACE2(p),1031,1362,1369,1376 , nucleocapsid(q),1263,1379 , nsp10(r),1263, and helicase(s),1380 proteins, and inhibition of spike-ACE2 interaction(t),1381.
In Vitro studies demonstrate inhibition of the spike(k),1043 (and specifically the receptor binding domain(l),1382), Mpro(m),1043,1377,1383,1384 , ACE2(p),1382, and TMPRSS2(u),1382 proteins, and inhibition of spike-ACE2 interaction(t),1381,1385 .
Curcumin decreases pro-inflammatory cytokines induced by SARS-CoV-2 in peripheral blood mononuclear cells1386, alleviates SARS-CoV-2 spike protein-induced mitochondrial membrane damage and oxidative stress1387, 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 fibroblasts1388, 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 variants1365, lowers ACE2 and STAT3, curbing lung inflammation and ARDS in preclinical COVID-19 models1389, inhibits SARS-CoV-2 ORF3a ion channel activity, which contributes to viral pathogenicity and cytotoxicity1390, has direct virucidal action by disrupting viral envelope integrity1391, and can function as a photosensitizer in photodynamic therapy to generate reactive oxygen species that damage the virus1391.
Melatonin may restore altered redox homeostasis in COVID-191412, modulates type III interferon responses and reduces inflammatory cytokine production in TLR3 receptor agonist stimulated viral inflammation while preserving tissue integrity1413, 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 mechanisms1414.
Melatonin reduces oxidative stress, inhibits NET formation, and protects tissues through anti-inflammatory and antioxidant actions1415.
N-acetylcysteine shows dose-dependent inhibition of SARS-CoV-21439-1441, shows anti-inflammatory and immunomodulatory effects against SARS-CoV-2-induced immune responses in combination with bromelain1442, suppressed virus-induced reactive oxygen species and blocked viral replication in a humanized mouse model and in human lung cells1443, 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 fibroblasts1388, and reduces disulfide bonds in proteins and exhibits antioxidant properties that may inhibit viral replication and modulate inflammatory responses1444.
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-191445.
NAC reinforces glutathione levels, reduces ROS, and minimizes ferroptosis and cytokine storm1415.
Fluvoxamine may inhibit SARS-CoV-2 cell entry by preventing the formation of ceramide platforms that facilitates viral uptake1456, may help restore autophagic processes disrupted by NSP6, thereby reducing SARS-CoV-2 replication and improving host cellular defenses1457, and may reduce COVID-19 thrombotic complications by inhibiting serotonin reuptake and decreasing platelet activation1458.
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(k),1033,1236,1360,1364,1376,1496-1504 (and specifically the receptor binding domain(l),1368), Mpro(m),1033,1236,1360,1364,1368,1373,1376,1499,1500,1502,1505-1519 , RNA-dependent RNA polymerase(n),1236,1364,1368,1502,1520,1521 , PLpro(o),1236,1507,1512 , ACE2(p),1031,1376,1498,1503,1507,1508,1522 , TMPRSS2(u),1498, nucleocapsid(q),1236, helicase(s),1236,1506,1523 , endoribonuclease(z),1496, NSP16/10(aa),1524, cathepsin L(ab),1525, Wnt-3(ac),1498, FZD(ad),1498, LRP6(ae),1498, ezrin(af),1526, ADRP(ag),1033, NRP1(ah),1503, EP300(ai),1527, PTGS2(aj),1508, HSP90AA1(ak),1508,1527 , matrix metalloproteinase 9(al),1528, IL-6(am),1529,1530 , IL-10(an),1529, VEGFA(ao),1530, and RELA(ap),1530 proteins, and inhibition of spike-ACE2 interaction(t),1531.
In Vitro studies demonstrate inhibition of the Mpro(m),1377,1514,1532,1533 protein, and inhibition of spike-ACE2 interaction(t),1385.
Animal studies demonstrate efficacy in K18-hACE2 mice(aq),1534, db/db mice(ar),1535,1536 , BALB/c mice(as),1537, and rats1538.
Quercetin reduced proinflammatory cytokines and protected lung and kidney tissue against LPS-induced damage in mice1537, inhibits LPS-induced cytokine storm by modulating key inflammatory and antioxidant pathways in macrophages1539, may block ACE2-spike interaction and NLRP3 inflammasome, limiting viral entry and inflammation1540, and inhibits SARS-CoV-2 ORF3a ion channel activity, which contributes to viral pathogenicity and cytotoxicity1390.
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