Main Research Findings

1) Mitoquinone mesylate decreased brain inflammation in an animal model of chronic HIV infection.

2) Treatment with mitoquinone mesylate protected against transmission of the SARS-Cov2 infection highlighting the antiviral properties of the compound.

 

 

Selected Data
1) The study by Satta et al was designed to investigate whether MitoQ, a mitochondria-targeted antioxidant, could reduce brain inflammation in a humanized mouse model of chronic HIV infection receiving suppressive antiretroviral therapy (ART). Although modern ART effectively suppresses viral replication and prolongs survival in people living with HIV, many patients continue to develop HIV-associated neurocognitive disorders (HAND), which remain among the most common neurological complications of chronic HIV infection. Persistent viral reservoirs and chronic immune activation are believed to contribute to ongoing oxidative stress, mitochondrial dysfunction, neuroinflammation, and neuronal injury despite successful viral suppression. Because mitochondria are a major source of reactive oxygen species (ROS) within the brain, the investigators hypothesized that selectively reducing mitochondrial oxidative stress with MitoQ would decrease inflammatory signaling and attenuate neuroinflammation in a preclinical model of chronic treated HIV infection. The primary objective of the study was therefore to determine whether long-term MitoQ administration could reduce proinflammatory cytokine and chemokine production within the brains of HIV-infected humanized mice maintained on effective ART [1].
To investigate this hypothesis, the researchers utilized NOD scid gamma (NSG) Bone Marrow-Liver-Thymic (BLT) humanized mice, a well-established experimental model that supports human immune cell development and HIV infection while closely reproducing important aspects of human HIV immunopathogenesis. Equal numbers of male and female mice were included to minimize potential sex-related differences in inflammatory responses. In total, twenty-seven humanized mice were generated according to previously validated protocols and maintained under institutional and federally approved animal care guidelines. Humanized BLT mice possess functional human immune cells capable of supporting HIV replication and therefore provide an appropriate platform for evaluating persistent immune activation during chronic infection despite antiretroviral therapy.
After successful engraftment, the mice were experimentally infected with the dual-tropic HIV-1 89.6 viral strain to establish chronic HIV infection. Once infection was established, all infected animals received combination antiretroviral therapy consisting of tenofovir disoproxil fumarate (8.75 mg/kg), emtricitabine (13 mg/kg), and raltegravir (17.5 mg/kg). These medications were administered daily throughout the experimental period to achieve sustained suppression of viral replication. The antiretroviral regimen had previously been validated by the investigators and closely resembles combination therapy used clinically to control HIV infection. The purpose of maintaining effective ART throughout the study was to reproduce the clinical situation in which patients exhibit well-controlled plasma viral loads but continue to experience chronic neuroinflammation and are therefore at risk for HIV-associated neurocognitive disorders [1].
To evaluate the therapeutic effects of mitochondrial antioxidant treatment, MitoQ was administered orally through the drinking water at a concentration of 500 μmol/L. Mice received continuous MitoQ supplementation for approximately ninety days while remaining on suppressive antiretroviral therapy. Control animals received flavored drinking water without MitoQ. Three experimental groups were established for comparison. Group A consisted of five uninfected humanized mice that served as healthy controls. Group B included twelve HIV-infected mice receiving antiretroviral therapy alone, representing chronic treated HIV infection without antioxidant intervention. Group C consisted of ten HIV-infected mice receiving both ART and MitoQ supplementation, allowing investigators to directly evaluate whether mitochondrial antioxidant therapy reduced neuroinflammation beyond the effects achieved with antiretroviral treatment alone. This three-group design enabled comparisons between healthy animals, chronically infected treated animals, and infected animals receiving adjunctive antioxidant therapy. [1]
At the conclusion of the treatment period, brain tissue was collected from every animal for detailed immunological analysis. The primary outcome measure consisted of quantifying inflammatory cytokines and chemokines within brain tissue as biomarkers of neuroinflammation. Both human-derived cytokines produced by engrafted human immune cells and murine cytokines produced by resident mouse cells were evaluated to characterize inflammatory responses originating from multiple cellular sources. Cytokine concentrations were measured using highly sensitive multiplex Luminex immunoassays according to the manufacturer’s standardized protocols. This technology enabled simultaneous quantification of numerous inflammatory mediators from relatively small tissue samples while providing highly sensitive and reproducible measurements. Protein concentrations were normalized to total tissue protein determined by bicinchoninic acid (BCA) protein assay to account for differences in tissue sample size and protein content between animals.
The investigators measured several proinflammatory cytokines and chemokines previously implicated in the pathogenesis of HIV-associated neurocognitive disorders. Human inflammatory markers included interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-alpha (TNF-α), CCL2, CCL3, CCL5, CXCL10, and the anti-inflammatory cytokine IL-10. Equivalent murine cytokines, including IL-1β, IL-6, TNF-α, IL-10, CCL2, CCL3, CCL5, and CXCL10, were also quantified to evaluate inflammatory signaling originating from resident mouse brain cells such as microglia and other innate immune cells. By simultaneously measuring both human and murine inflammatory mediators, the investigators were able to distinguish immune responses contributed by the engrafted human immune system from those generated by the murine central nervous system environment [1].
Throughout the study, suppression of HIV replication was monitored to ensure that observed changes in neuroinflammation were attributable to MitoQ treatment rather than differences in viral control. As reported previously by the investigators, plasma viremia was effectively suppressed in all HIV-infected animals after four weeks of combination ART, thereby creating a stable model of chronic treated HIV infection that closely resembles virologically suppressed patients receiving long-term antiretroviral therapy. Because viral replication remained controlled across infected groups, subsequent comparisons focused specifically on differences in inflammatory biomarker expression within brain tissue.
Cytokine concentrations were expressed as protein levels normalized to tissue protein content, and data were presented as box-and-whisker plots displaying minimum, median, and maximum values, with each individual data point representing one mouse. This statistical approach allowed investigators to determine whether adjunctive MitoQ therapy significantly reduced brain inflammation in HIV-infected humanized mice receiving effective antiretroviral treatment. Overall, the study combined a clinically relevant humanized mouse model, long-term combination antiretroviral therapy, targeted mitochondrial antioxidant supplementation, and comprehensive multiplex cytokine analysis to evaluate the potential of MitoQ as a novel therapeutic strategy for reducing chronic neuroinflammation associated with HIV infection [1].
2) The study by Chen et al was designed as an exploratory, single-center, pragmatic, open-label, non-randomized pilot clinical trial to evaluate whether mitoquinone mesylate (Mito-MES) could serve as an effective post-exposure prophylactic treatment against SARS-CoV-2 infection in humans. The investigators developed the study in response to the continued need for novel antiviral therapies that remain effective despite the emergence of new SARS-CoV-2 variants and the potential development of antiviral resistance. Although vaccines have substantially reduced severe COVID-19, there remains no FDA-approved medication specifically indicated for post-exposure prophylaxis following high-risk exposure to SARS-CoV-2. Previous laboratory studies from the research group demonstrated that Mito-MES possesses potent antiviral, anti-inflammatory, and anti-apoptotic activity against SARS-CoV-2 in cultured cells and in infected mouse models [2].
Eligible participants were adults between 18 and 65 years of age who had experienced a documented high-risk exposure to an individual with confirmed SARS-CoV-2 infection within the previous five days. High-risk exposure was defined as prolonged contact lasting more than 24 hours at a distance of less than six feet from the infected individual without face masks or other personal protective equipment in poorly ventilated indoor environments. Both vaccinated and unvaccinated individuals were eligible regardless of previous SARS-CoV-2 infection history because circulating Omicron variants were known to evade immunity acquired through prior infection or vaccination. Individuals with severe uncontrolled medical conditions, recent corticosteroid use, pregnancy, significant cardiac or pulmonary disease, or other conditions that could interfere with study participation were excluded. Equal attention was given to recruiting both male and female participants to ensure sex balance between treatment groups.
The investigation employed a pragmatic open-label, non-randomized design consisting of two matched groups of forty participants each. Participants who agreed to receive Mito-MES were assigned to the intervention group, while individuals who declined treatment but agreed to participate in follow-up assessments served as matched controls. Matching was based primarily on demographic characteristics, including age and sex. Because the study reflected real-world clinical practice, investigators did not administer placebo capsules, and neither participants nor investigators were blinded to treatment allocation.
To reduce potential clustering bias, only one participant per unique SARS-CoV-2 exposure event was enrolled whenever possible, although some independent household members exposed to the same infected individual were included. Statistical analyses later accounted for household clustering. Baseline demographic information, smoking history, vaccination status, household size, comorbidities, and risk factors for severe COVID-19 were recorded before intervention. Approximately one-fifth of participants in each group were considered high risk because of immunosuppression or multiple chronic medical conditions [2].
Participants assigned to the treatment group received oral Mito-MES at a daily dose of 20 mg for fourteen consecutive days following SARS-CoV-2 exposure. The medication consisted of four 5-mg capsules taken once daily after an overnight fast to maximize absorption based on previously established pharmacokinetic studies. Investigators selected the 20-mg dosage because earlier clinical trials demonstrated excellent tolerability while achieving favorable tissue concentrations. The fourteen-day treatment duration was chosen to cover the entire period of highest infection risk and to address concerns regarding viral rebound observed with shorter antiviral regimens. Mito-MES was provided immediately after informed consent so that participants could begin treatment as soon as possible following exposure. Among treated participants, twenty-two initiated therapy within 24 hours of exposure, four began treatment within 48 hours, and the remaining participants started treatment between three and five days after exposure because the precise timing of exposure could not be reliably established. Adherence was assessed through participant diaries, pill counts, and structured questionnaires completed during follow-up [2].
The primary outcome measure was the development of laboratory-confirmed SARS-CoV-2 infection during the fourteen-day follow-up period. Infection was defined by at least one positive FDA-authorized polymerase chain reaction (PCR) or rapid antigen test (RAT). A second primary endpoint evaluated whether Mito-MES prevented progression to severe COVID-19. Secondary outcomes included symptom severity, duration of illness, time to symptom onset, need for hospitalization, oxygen supplementation, and overall disease progression. Symptom severity was quantified using a standardized scoring system incorporating fourteen common COVID-19 symptoms, including fever, cough, sore throat, fatigue, myalgia, headache, gastrointestinal symptoms, anosmia, and shortness of breath. Each symptom was assigned a severity score ranging from one (mild) to three (severe), producing a maximum possible cumulative score of forty-two. Additional points were added for new-onset hypoxia. Investigators categorized infections as mild, moderate, or severe according to predefined symptom thresholds and oxygen saturation criteria.
Participants underwent regular follow-up throughout the study period. Telephone assessments were conducted on study days 1, 7, and 14, with an additional safety follow-up on day 21. Participants completed daily symptom diaries documenting medication adherence, body temperature, and symptom severity using standardized FDA guidance for outpatient COVID-19 clinical trials. Unlike highly controlled randomized trials, diagnostic testing occurred within real-world healthcare settings rather than according to a fixed research protocol. Participants obtained PCR or rapid antigen tests through community testing centers or routine clinical care based on perceived exposure risk [2].
Nevertheless, to ensure reliable exclusion of infection, all participants with initially negative tests were required to complete at least four FDA-approved COVID-19 diagnostic tests during the follow-up period, with some high-risk individuals undergoing as many as ten separate tests. Positive test results and symptom reports were verified by the study investigators throughout follow-up. Overall, the investigators employed a clinical trial design that reflected real-world post-exposure management while incorporating rigorous outcome assessment and statistical methodology to evaluate the potential effectiveness of Mito-MES as a novel post-exposure prophylactic therapy against SARS-CoV-2 infection [2].

 

Discussion
1) The study by the research team of Satta et al demonstrated that MitoQ significantly reduced neuroinflammation in a humanized mouse model of chronic HIV infection despite effective suppression of viral replication with combination ART. Although ART successfully controlled systemic HIV infection, persistent inflammatory activity remained evident within the brains of HIV-infected mice, reflecting the chronic immune activation that contributes to HAND. Administration of MitoQ markedly attenuated several key proinflammatory cytokines and chemokines implicated in neurodegeneration, providing the first preclinical evidence that a mitochondria-targeted antioxidant may reduce chronic brain inflammation associated with treated HIV infection. These findings support the hypothesis that mitochondrial oxidative stress continues to promote inflammatory signaling even after viral replication has been effectively suppressed and suggest that antioxidant therapy may represent a promising adjunctive treatment strategy for preventing or slowing the development of HAND [1].
Before evaluating the effects of MitoQ, the investigators first confirmed that the antiretroviral regimen effectively suppressed HIV replication throughout the study. Consistent with their previous investigations using the same humanized mouse model, all HIV-infected animals receiving combination ART achieved suppression of plasma viremia within four weeks of treatment. This finding was critical because it established that subsequent differences in inflammatory markers could not be attributed to uncontrolled viral replication but instead reflected persistent immune activation despite successful ART. The model therefore closely resembled the clinical situation observed in many individuals living with HIV, in whom viral replication remains well controlled while chronic inflammation and neurocognitive impairment continue to develop over time. By maintaining equivalent viral suppression across infected groups, the investigators created an experimental framework that isolated the specific effects of MitoQ on neuroinflammation independent of antiviral activity.
Analysis of brain tissue demonstrated that HIV infection continued to promote significant inflammatory responses despite long-term ART. Compared with uninfected control animals, HIV-infected mice receiving ART alone exhibited significantly elevated concentrations of several important human-derived inflammatory cytokines within the brain. Levels of human IL-1β, IL-8, and TNF-α were all significantly increased in the HIV-infected ART-treated group. Additionally, investigators observed a strong trend toward elevated concentrations of the chemokine human CCL2, although this increase narrowly missed conventional statistical significance. These findings demonstrated that substantial neuroinflammation persisted despite effective antiviral treatment, supporting previous evidence that suppression of circulating HIV does not completely eliminate inflammatory processes occurring within the central nervous system. Persistent activation of inflammatory cytokines such as IL-1β and TNF-α has been implicated in neuronal injury, synaptic dysfunction, and the cognitive impairment observed in patients with HIV-associated neurocognitive disorders [1].
The addition of MitoQ to suppressive antiretroviral therapy produced substantial reductions in multiple inflammatory mediators within the brain. Compared with HIV-infected mice receiving ART alone, animals treated with both ART and MitoQ demonstrated significantly lower concentrations of human IL-1β, IL-6, TNF-α, and CCL2. Each of these inflammatory markers declined significantly following MitoQ supplementation, indicating that mitochondrial antioxidant therapy effectively attenuated inflammatory signaling within the central nervous system. Among these biomarkers, IL-1β and TNF-α are recognized as major mediators of neurotoxicity and inflammasome activation, while IL-6 contributes to chronic neuroinflammation and CCL2 promotes recruitment of inflammatory immune cells into the brain. Simultaneous reductions in these cytokines therefore suggested that MitoQ broadly suppressed multiple inflammatory pathways rather than targeting only a single signaling mechanism. These findings strongly support the proposed role of mitochondrial reactive oxygen species in sustaining chronic neuroinflammation during treated HIV infection [1].
The investigators also evaluated inflammatory responses generated by resident murine cells within the brain to determine whether MitoQ influenced neuroinflammation originating from the host central nervous system. Similar to the changes observed for human cytokines, MitoQ significantly reduced murine IL-1β, IL-6, and TNF-α concentrations compared with HIV-infected animals receiving ART alone. These parallel reductions demonstrated that MitoQ attenuated inflammatory signaling arising from both engrafted human immune cells and endogenous murine brain cells, including microglia and other innate immune populations. The ability to simultaneously suppress inflammatory mediators from both cellular compartments suggests that mitochondrial oxidative stress contributes broadly to chronic neuroinflammatory processes regardless of cellular origin. Because activation of microglia represents a major pathological feature of HIV-associated neurocognitive disorders, these findings provide additional evidence that MitoQ may interrupt important mechanisms underlying neuronal injury during chronic treated HIV infection.
Not all inflammatory mediators were altered by treatment, however. The investigators found no significant differences among experimental groups in concentrations of either human or murine IL-10, CCL3, CCL5, or CXCL10. These results indicate that MitoQ selectively modulated specific proinflammatory signaling pathways without globally suppressing all cytokine production. Preservation of IL-10, an important anti-inflammatory cytokine, suggests that MitoQ did not broadly impair normal immune regulation. Likewise, the absence of significant changes in several chemokines indicates that the anti-inflammatory effects of MitoQ were relatively targeted toward cytokines closely associated with mitochondrial oxidative stress and inflammasome activation. This selective pattern of cytokine modulation may represent an important therapeutic advantage by reducing pathological inflammation while minimizing disruption of protective immune responses [1].
Based on these findings, the investigators concluded that MitoQ exerts both antioxidant and anti-inflammatory effects that may be particularly relevant for chronic HIV infection. They proposed that mitochondrial reactive oxygen species promote activation of the inflammasome, leading to increased production of IL-1β and other inflammatory mediators that contribute to neurotoxicity and cognitive decline. By selectively targeting mitochondria, MitoQ likely interrupts this cycle of oxidative stress and inflammatory activation, thereby reducing downstream cytokine production. The observed reductions in IL-1β, IL-6, TNF-α, and CCL2 are consistent with previous studies demonstrating anti-inflammatory effects of MitoQ in experimental models of multiple sclerosis, colitis, and other neurodegenerative disorders, further supporting a common mechanism involving suppression of mitochondrial oxidative stress and inflammasome activation.
Overall, this proof-of-concept study provided the first preclinical evidence that MitoQ can significantly reduce brain inflammation in a humanized mouse model of chronic HIV infection receiving suppressive antiretroviral therapy. Although the study focused exclusively on inflammatory biomarkers and did not directly assess cognitive function, neuronal survival, or behavioral outcomes, the substantial reductions in multiple cytokines and chemokines strongly support further investigation of MitoQ as an adjunctive therapy for HIV-associated neurocognitive disorders. The authors emphasized that MitoQ has been used safely as an oral dietary supplement and has demonstrated a favorable safety profile in previous human clinical trials, making it an attractive candidate for translation into clinical studies. They concluded that additional research should evaluate the effects of MitoQ on other mechanisms contributing to neuroinflammation and determine whether the reductions in inflammatory signaling observed in this study ultimately translate into improved neurological function and cognitive outcomes in people living with HIV [1].
2) The study performed by researchers Chen et al demonstrated that Mito-MES substantially reduced the risk of developing SARS-CoV-2 infection following high-risk exposure and was well tolerated when administered as post-exposure prophylaxis. Eighty participants completed the trial, with forty receiving Mito-MES and forty serving as untreated matched controls. Baseline characteristics were generally well balanced between the two groups with respect to age, sex, vaccination status, smoking history, and risk factors for severe COVID-19.
Approximately 20% of participants in each group were classified as high risk because of immunosuppression or multiple chronic medical conditions. Many exposures occurred within households, particularly among parents caring for infected children, resulting in prolonged and repeated close contact that represented a particularly challenging exposure setting. Every participant who initially tested negative underwent at least four FDA-approved SARS-CoV-2 diagnostic tests during follow-up, with some high-risk participants completing as many as ten PCR or rapid antigen tests over a twenty-one-day period to minimize the possibility of false-negative results. This rigorous testing protocol strengthened confidence that differences between groups reflected true treatment effects rather than incomplete case detection [2].
The primary endpoint showed a marked reduction in laboratory-confirmed SARS-CoV-2 infection among participants treated with Mito-MES. Only 12 of the 40 participants (30%) receiving Mito-MES developed confirmed SARS-CoV-2 infection during the fourteen-day follow-up period, compared with 30 of the 40 control participants (75%). This represented an absolute risk reduction of 45 percentage points and demonstrated a statistically significant protective effect of post-exposure prophylaxis. Statistical modeling further showed that participants receiving Mito-MES were more than 80% less likely to test positive for SARS-CoV-2 than untreated controls, with the protective effect remaining significant after separate adjustment for vaccination status, age, sex, smoking history, and high-risk medical conditions. These findings indicate that the observed reduction in infection risk was not explained by demographic differences or baseline clinical characteristics but instead reflected a robust treatment effect associated with Mito-MES administration.
Timing of treatment initiation proved to be an important determinant of efficacy. Participants who began Mito-MES within the first 72 hours following exposure experienced the greatest protection against SARS-CoV-2 infection. Of the forty treated participants, twenty-two initiated therapy within twenty-four hours of exposure and four more began treatment within forty-eight hours, meaning that most participants received the intervention during the earliest stages of viral incubation. Figures presented in the study demonstrated that early initiation within this seventy-two-hour window produced the lowest infection rates and the greatest reduction in symptomatic disease. In contrast, participants who began treatment three to five days after exposure still appeared to benefit, but the protective effect against infection was less pronounced. The authors therefore concluded that the antiviral efficacy of Mito-MES was greatest when treatment was initiated as soon as possible after high-risk exposure, consistent with the biological expectation that early inhibition of viral replication provides the greatest opportunity to prevent establishment of infection [2].
Among participants who nevertheless became infected despite treatment, Mito-MES appeared to lessen disease severity. Of the fourteen individuals who initiated treatment three to five days after exposure, ten developed asymptomatic infection while only four developed mild symptomatic disease. None progressed to moderate or severe illness. By comparison, 23 of the 40 untreated controls (57.5%) became symptomatic, including five individuals who developed moderate COVID-19 and eighteen who experienced mild symptomatic illness. Among the thirty control participants with confirmed infection, nineteen developed symptoms, representing a substantially higher proportion of symptomatic disease than observed in the Mito-MES group. Statistical analyses demonstrated significantly lower rates of symptomatic infection and mild symptomatic disease among treated participants compared with controls. These findings suggest that even when Mito-MES did not completely prevent infection, it frequently reduced progression from asymptomatic viral detection to clinically apparent illness [2].
The intervention also improved several measures of symptom burden. Among participants with symptomatic SARS-CoV-2 infection, the median duration of illness was reduced from five days in the control group to only three days in the Mito-MES group, representing a median reduction of two days. Furthermore, symptom onset occurred later in treated participants than in untreated controls, suggesting that Mito-MES delayed disease progression after viral exposure. Quantitative symptom severity scores based on fourteen standardized COVID-19 symptoms were also significantly lower among treated participants. Statistical analyses estimated that Mito-MES reduced symptom severity scores by nearly two points relative to controls, even after adjustment for important demographic and clinical variables. Together, these findings indicate that Mito-MES not only reduced infection rates but also attenuated the clinical manifestations of COVID-19 in participants who developed breakthrough infections.
Additional subgroup analyses demonstrated that the protective effects of Mito-MES remained consistent across multiple patient characteristics. The reduction in positive SARS-CoV-2 diagnostic tests persisted after adjustment for age, sex, smoking status, vaccination history, and high-risk medical conditions. Investigators also compared participants who received Mito-MES for seven days with those completing the full fourteen-day regimen and found no statistically reliable difference in infection risk between treatment durations. Likewise, treatment effectiveness appeared similar regardless of vaccination status or other baseline risk factors. Although the relatively small sample size limited statistical power for subgroup comparisons, these analyses suggested that Mito-MES exerted broadly consistent antiviral effects across diverse participant populations rather than benefiting only selected demographic groups [2].
Overall, the investigators concluded that this proof-of-concept pilot trial provided the first clinical evidence that Mito-MES possesses antiviral activity against SARS-CoV-2 in humans when used as post-exposure prophylaxis. Participants receiving Mito-MES experienced markedly lower rates of laboratory-confirmed infection, fewer symptomatic cases, reduced symptom severity, and shorter illness duration compared with untreated controls, while maintaining an excellent safety profile. The authors emphasized that the study was exploratory and acknowledged important limitations, including its open-label, non-randomized design, relatively small sample size, reliance on self-reported symptoms, and restriction to circulating Omicron variants during the study period. Nevertheless, because Mito-MES demonstrated substantial efficacy despite these limitations and has an established record of safety in humans, the investigators concluded that their findings provide strong justification for larger randomized, placebo-controlled clinical trials to determine whether Mito-MES can become an effective post-exposure prophylactic therapy for preventing SARS-CoV-2 infection and reducing COVID-19 disease severity [2].

 

Disclaimer

**LAB USE ONLY**
*This information is for educational purposes only and does not constitute medical advice. THE PRODUCTS DESCRIBED HEREIN ARE FOR RESEARCH USE ONLY. All clinical research must be conducted with oversight from the appropriate Institutional Review Board (IRB). All preclinical research must be conducted with oversight from the appropriate Institutional Animal Care and Use Committee (IACUC) following the guidelines of the Animal Welfare Act (AWA).

 

 

Citation

[1] Satta S, Hugo C, Sharma M, et al. Mitoquinone mesylate attenuates brain inflammation in humanized mouse model of chronic HIV infection. AIDS. 2022;36(11):1609-1611. doi:10.1097/QAD.0000000000003291

[2] Chen K, Jackson NJ, Kelesidis T. Mitoquinone mesylate as post-exposure prophylaxis against SARS-CoV-2 infection in humans: an exploratory single center pragmatic open label non-randomized pilot clinical trial with matched controls. EBioMedicine. 2024;102:105042. doi:10.1016/j.ebiom.2024.105042

 

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