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Fluvoxamine: A Review of Its Mechanism of Action and Its Role in COVID-19

Vikas P. Sukhatme, Angela M. Reiersen, Sharat J. Vayttaden and 1 more

Frontiers in Pharmacology · 2021 · CC BY

doi:10.3389/fphar.2021.652688

Abstract

Fluvoxamine is a well-tolerated, widely available, inexpensive selective serotonin reuptake inhibitor that has been shown in a small, double-blind, placebo-controlled, randomized study to prevent clinical deterioration of patients with mild coronavirus disease 2019 (COVID-19). Fluvoxamine is also an agonist for the sigma-1 receptor, through which it controls inflammation. We review here a body of literature that shows important mechanisms of action of fluvoxamine and other SSRIs that could play a role in COVID-19 treatment. These effects include: reduction in platelet aggregation, decreased mast cell degranulation, interference with endolysosomal viral trafficking, regulation of inositol-requiring enzyme 1α-driven inflammation and increased melatonin levels, which collectively have a direct antiviral effect, regulate coagulopathy or mitigate cytokine storm, which are known hallmarks of severe COVID-19.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 23, 2026. Paragraph numbers are ours, so an answer can point at one.

Introduction

Initially used to treat obsessive-compulsive disorder (OCD), fluvoxamine (FLV) has been shown to have the strongest activity of all SSRIs at the sigma-1 receptor (S1R) with low-nanomolar affinity. FLV agonism on S1R potentiates nerve-growth factor (NGF)-induced neurite outgrowth in PC 12 cells. S1R is a chaperone protein at the endoplasmic reticulum with anti-inflammatory properties. FLV’s anti-inflammatory effects likely stem from its regulation of S1R, which modulates innate and adaptive immune responses. S1R is also an important regulator of inositol-requiring enzyme 1α (IRE1)-driven inflammation (Figure 1).

FLV and other SSRIs regulate inflammatory cytokine activity and gene expression in both cell and animal models of inflammation. The potential of FLV to dampen cytokine storm has implications in COVID-19. COVID-19 severity is associated with an increased level of inflammatory mediators including cytokines and chemokines. Other S1R agonists like fluoxetine have been reported to have antiviral activity. These studies have raised interest in the potential therapeutic role of FLV and S1R agonists in COVID-19.

This review illustrates mechanisms of action underlying anti-inflammatory and antiviral properties of FLV. It covers preclinical studies on effects of FLV and S1R agonists on inflammation, and summarizes currently available clinical data for FLV treatment in COVID-19.

Indications for Fluvoxamine

Fluvoxamine maleate is available as immediate release tablets and controlled-release capsules. FLV is indicated to treat obsessions and compulsions in patients with OCD. The half-life of FLV is 9–28 h depending on its formulation, and the recommended dosage is 100–300 mg/day.

Serotonin Transporter Inhibition

FLV blocks reuptake of serotonin at the sodium-dependent serotonin transporter (SERT) of the neuronal membrane, enhancing actions of serotonin on 5HT1A autoreceptors. FLV has negligible affinity for α1-, α2-, β-adrenergic, muscarinic, dopamine D2, histamine H1, GABA-benzodiazepine, opiate, 5-HT1, or 5-HT2 receptors.

Platelet Aggregation

Platelets lack the enzyme to synthesize serotonin. A SERT enables rapid uptake of serotonin from plasma. During thrombosis platelets release serotonin, facilitating hemostasis through platelet aggregation (Figure 1), and promotes recruitment of neutrophils. SSRIs can therefore increase bleeding time or reduce serum serotonin by >80% and reduce neutrophil recruitment. Platelets from individuals treated with SSRIs, and platelets from SERT knockout mice, show decreased aggregation. Measures of coagulation and hemostasis were lower in patients with serotonergic antidepressant than in patients without serotonergic antidepressant. A hyperserotonergic state distinguishes COVID-19 and non-COVID-19 acute respiratory distress syndrome, biochemically and clinically. This is likely pathologic across a multitude of organs (akin to serotonin syndrome, F. Jalali—personal observation and communication) and may originate from an immune-mediated state of platelet hyperreactivity, resulting in florid platelet degranulation of serotonin into plasma.

A concomitant impairment of serotonin reuptake may exacerbate this hyperserotonergic state. Serotonin clearance relies on a healthy pulmonary endothelium, that is injured in COVID-19. Platelet serotonin liberation can be reduced with chronic or early de novo SSRI use, since SSRIs deplete serotonin content of platelets. Initiation of de novo SSRIs at later stages of moderate to severe COVID-19, however, may be unpredictably harmful given the existing hyperserotonergic state unless counterbalanced by other beneficial effects of SSRIs. Indeed, direct serotonin antagonism specifically targeting the serotonin 2 A, B and C receptors with drugs such as cyproheptadine or mirtazapine in this stage may be beneficial and is being explored (F. Jalali—personal communication).

Three trials assessing benefit of anticoagulants to treat COVID-19 have paused enrollment of critically ill COVID-19 patients who require intensive care unit (ICU) support. Therapeutic blood thinners did not reduce need for ICU admission in this patient-group. Since full doses of therapeutic anticoagulants increase risk of internal bleeding, FLV could perhaps inhibit blood clotting more safely.

Mast Cell Degranulation

Human mast cells (MCs) are a viral reservoir for RNA viruses like HIV. Retinoic acid-inducible gene-I-like receptors of mast cells can detect RNA viruses. Viruses can cause degranulation of MCs in a Sphingosine-1-Phosphate (S1P) -dependent pathway. MCs express angiotensin converting enzyme 2 (ACE2), the principal receptor for SARS-CoV-2 entry into cells, thus defining a route by which MCs could become hosts for this virus. Post-mortem lung biopsies of COVID-19 patients have linked pulmonary edema and thromboses to activated MCs. Antidepressants also decrease histamine release from MCs. SSRIs like fluoxetine decreased mRNA levels of protease-1 in MCs. Therefore, SSRIs like FLV could reduce cytokine storms in COVID-19 patients (Figure 1) because of atypical response of MCs to SARS-CoV-2.

Lysosomotropism

S1R agonists like FLV and fluoxetine are lysosomotropic. Fluvoxamine has a predicted pKa of 8.86 and is susceptible to protonation in the physiological pH range. Less polar, unionized form of basic drugs can easily cross membranes. Basic drugs like FLV can get protonated in the lysosome, which hinders the now-charged moieties from crossing membranes. β-coronaviruses, like SARS-CoV-2 and mouse hepatitis virus (MHV), use lysosomal trafficking to escape from infected cells (Figure 1). GRP78/BIP, a chaperone that facilitates coronavirus infectivity, is co-released with β-coronaviruses through this pathway. The SARS-CoV open reading frame protein 3A (ORF3a) is a viroporin that localizes to lysosomes, disrupts their acidification, and contributes to viral egress. Given the lysosomal egress of β-coronaviruses from infected cells, lysosomotropic drugs like FLV could have antiviral effects in the virus laden lysosomes (Figure 1).

Acid Sphingomyelinase

Lysosomotropic drugs displace acid sphingomyelinase (ASM) from lysosomal membranes leading to its degradation (Figure 1). Treatment of mice with S1R agonists like fluoxetine reduces both acid sphingomyelinase activity and protein levels in neurons. This is consistent with partial proteolysis of acid sphingomyelinase by fluoxetine. Fluoxetine can efficiently inhibit entry and propagation of SARS-CoV-2 in Vero-E6 cell lines. It also exerts antiviral activity against influenza A virus subtypes. S1R agonists like escitalopram and fluoxetine can prevent infection of Vero cells with vesicular stomatitis virus pseudoviral particles presenting SARS-CoV-2 spike protein (pp-VSV-SARS-CoV-2 spike). Antidepressants like amitriptyline also prevented infection of human Caco-2 cells with SARS-CoV-2 and treating volunteers with a low dose of amitriptyline prevented infection of freshly isolated nasal epithelial cells with pp-VSV-SARS-CoV-2 spike. Inhibition of acid sphingomyelase by these drugs can prevent the conversion of sphingomyelin to phosphorylcholine and ceramide. Because high ceramide in the cell membrane facilitates viral entry, this reduction in ceramide may prevent infection. Therefore, functional inhibition of acid sphingomyelinase by lysosomotropic drugs is another avenue of viral control by antidepressants.

Sigma-1 Receptor Activity

S1R was discovered in 1976 and cloned in 1996. It regulates ER-mitochondrial Ca2+ signaling and cell survival. Targeting S1R with FLV regulates cytokine production in human monocyte-derived dendritic cells. S1R knockout (KO) bone marrow-derived macrophages (BMDMs) were proinflammatory in endotoxic shock models. They had higher levels of IL-6 and IL-1β mRNA and increased IL-6 protein secretion compared to wild-type (WT) BMDMs. In contrast, anti-inflammatory cytokine IL-10 expression was unaffected in S1R KO BMDMs. S1R overexpression in HEKs expressing mTLR4/MD2/CD14 was anti-inflammatory in an endotoxic shock model. Compared to HEKs with normal levels of S1R, cells with higher levels of S1R had lower IL-8 levels on LPS stimulation (p < 0.05). In other systems, FLV upregulates IL-10. FLV via the S1R may therefore modulate SARS-CoV-2-induced hyperinflammatory state (Figure 1).

On the flip side, genetic perturbation screens have shown depletion of S1R, decreases SARS-CoV-2 viral replication in adenocarcinoma human alveolar basal epithelial cell lines expressing Angiotensin I Converting Enzyme 2 (A549-ACE2). Consistent with this genetic data, S1R agonists such as dextromethorphan can increase viral replication. However, in contrast, researchers reviewing medical billing data for nearly 740,000 COVID-19 patients in the US showed patients on antipsychotic drugs targeting S1R were half as likely as those on other types of antipsychotic drugs to require mechanical ventilation.

Neurotropism is one common feature for human coronaviruses. Various receptors could be involved in neurotropism and neuronal cell entry of SARS-CoV-2. Sigma receptors are widely expressed in the CNS. Downregulation of S1R protein expression impairs initiation of hepatitis C virus (HCV) RNA replication in human hepatoma cells. BD1047 a selective S1R antagonist blocked cocaine-mediated stimulation of human immune deficiency virus (HIV-1) expression in neuronal mononuclear phagocytes like microglia. S1R could therefore be involved in neuronal transmission of other RNA viruses like SARS-CoV-2.

Inositol-Requiring Enzyme 1α and Autophagy

Endotoxin-stimulated TLR4 activates IRE1 and regulates proinflammatory cytokine production. SARS-CoV E protein down-regulates IRE1 pathway and the SARS-CoV lacking the envelope (E) gene (rSARS-CoV-ΔE) is attenuated in vivo. IRE1 inhibitors like STF-083010 rescued S1R KO mice in a model of endotoxemia. IRE1 is essential for autophagy during infection with a gamma coronavirus-Infectious Bronchitis Virus (IBV). SARS-CoV replicase proteins nsp2, 3 and 8 occur in cytoplasmic complexes and colocalize with LC3, a protein marker for autophagic vacuoles. The viral replicase protein nsp6 of IBV activates autophagy in a screen. Other studies reviewed here suggest autophagy is not directly involved in SARS-CoV. These discrepancies are probably because of different viruses and cells tested in various studies.

Melatonin

SARS-CoV-2 virus can activate NLRP3 inflammasome, which along with NF-κB activation can induce cytokine storm. Melatonin can mitigate inflammation through these pathways and melatonin exposure post-intubation is associated with a positive outcome in COVID-19 (and non-COVID-19) patients. FLV can elevate melatonin levels via inhibition of CYP1A2, a member of the cytochrome P450 superfamily of enzymes (Figure 1).

Precedent for Using Selective Serotonin Reuptake Inhibitors to Treat Other Viral Infections

Enteroviruses are non-enveloped RNA viruses. Their nonstructural protein 2C is one of their most conserved proteins and contains ATPase activity and putative RNA helicase activity. Fluoxetine has in vitro antiviral activity against Enterovirus B and D species. Fluoxetine binds nonstructural protein 2C directly. Some fluoxetine resistant variants of enteroviruses like coxsackievirus B3 and B4 have mutations in protein 2C. This reinforces the idea that interaction between fluoxetine and protein 2C is essential for its antiviral effects.

Endoplasmic Reticulum Stress Response

Viral infection may trigger the unfolded protein response (UPR). This is an ER stress response because of ER overloading with virus-encoded proteins, and can also induce autophagy. ER signaling proteins like IRE1, PRKR-like ER kinase (PERK), and activating transcription factor 6 (ATF6) regulate UPR. The UPR is involved in viral replication and modulates host innate responses. Virus-induced ER stress is required for autophagy activation, viral replication, and pathogenesis in dengue. Murine cytomegalovirus activates the IRE1 pathway to relieve repression by X-box binding protein 1 unspliced mRNA. Coronavirus infection induces ER stress and triggers UPR. The S protein in β-coronaviruses modulates UPR to facilitate viral replication. The α-coronavirus, transmissible gastroenteritis virus (TGEV) triggers UPR-induced ER stress primarily through activation of PERK-eukaryotic initiation factor 2α axis. Thus ER stress response is critical in host-virus interactions in a variety of infections. We have discussed above how S1R is a regulator of IRE1 and autophagy. S1R agonists like FLV could therefore have a role in regulating viral infections beyond SARS-CoV-2 through its putative regulation of ER stress and UPR.

Preclinical Effects of Fluvoxamine on Inflammation

S1R KO mice display increased mortality compared to WT in sublethal models of sepsis. Peak serum TNF and IL-6 were increased in LPS-challenged S1R KO mice. S1R ligand FLV enhanced survival in mouse models of IRE1-mediated inflammation and fecal-induced peritonitis. FLV treatment protected WT mice from endotoxic shock-induced death, while no significant effect was observed in S1R KO animals suggesting the anti-inflammatory effects of FLV are likely mediated through S1R.

Multiple sclerosis (MS) is a chronic, inflammatory, demyelinating neurodegenerative disease. SSRIs like sertraline have been shown to have immunomodulatory effects in experimental autoimmune encephalomyelitis (EAE), a mouse model of MS, and in a rat model of rheumatoid arthritis. FLV reduces the severity in EAE in rats, even when treatment began 12 days post-induction of EAE. FLV-treated EAE rats showed a decrease in IFN-γ serum levels and an increase in IL-4, pro- and anti-inflammatory cytokines respectively, compared to untreated EAE rats. The dose of FLV used in these experiments extrapolates (by surface area) to FLV doses approved for human use.

Thus, FLV seems to ameliorate inflammation in different in vivo inflammation models. Data in non-human primates or a hamster model of SARS-CoV-2 infection would shed further light on whether FLV might be a useful drug for COVID-19 patients and on the mechanism(s) at play.

Clinical Effects of Fluvoxamine in COVID-19

In a double-blind, randomized, preliminary study of adult outpatients with symptomatic COVID-19, 80 patients treated with FLV, compared to 72 treated with placebo, had a lower likelihood of clinical deterioration over 15 days. Eligible patients were enrolled within 7 days of symptom development. These data are provocative with none of the FLV-treated patients deteriorating vs. 8.3% patients in the control arm who showed clinical deterioration. Participants received 50 mg FLV QD on day 1, then for 2 days 100 mg FLV BID, and then 100 mg FLV TID as tolerated through day 15 and then stopped. In a prospective study on use of FLV for early treatment of COVID-19 the incidence of hospitalization was 0% (0/65) with FLV and 12.5% (6/48) with observation alone. At 14 days, 0% (0/65) of FLV treated people had persistent residual symptoms compared to 60% (29/48) among people who opted for no therapy. Agonists of S1R like escitalopram and fluoxetine were associated with lower risk of intubation or death (p < 0.05) because of COVID-19 in a multicenter observational retrospective cohort study.

Given the multiple roles of S1R reviewed here in inflammation, platelet aggregation, antiviral activity etc. and the recent striking human data, it is likely that S1R agonists like FLV could have a major impact on disease progression of COVID-19 patients in the early stage of the disease.

Discussion

An 880 patient randomized study is underway and should provide some definitive answers. Patients nationally can join this study from home and at no cost. However, given the current crisis, which is expected to worsen before a vaccine takes effect, one wonders if the FLV evidence in COVID-19 is strong enough to consider a change in practice guidelines, to even more quickly accumulate data on outcomes in COVID-19 patients. A small group of healthcare systems could consider this approach and simultaneously set up tools, e.g., a local or regional repository to track outcomes in real-time. If the efficacy is similar to the small randomized trial, it should be evident in such data. Out of caution, the practice guidelines could urge caregivers to consider administering FLV only to those COVID-19 + patients at highest risk for disease progression, and who do not have access to one of the monoclonal antibodies that have been given emergency use authorizations by the FDA. Also, these guidelines could be revised at any time.

Small biomarker intensive trials should be planned to assess antiviral, immunomodulatory, anti-thrombotic effects or other effects in patients treated with FLV. One could incorporate tools such as single cell RNA and protein analysis in such studies. While human data is being gathered, additional preclinical data in cell culture systems like co-cultures of human epithelial and immune cells would be useful. Data from non-human primate and hamsters would provide valuable information on optimal timing of drug, amount needed for efficacy, and which among the myriad mechanisms of action might be most relevant.

There may be a role for serotonin modulation in the inpatient setting. Indeed, if this drug is not working primarily as an antiviral but rather through other mechanisms (e.g., immunomodulatory, anti-platelet), it may be efficacious in this setting where hyperinflammatory responses and thrombotic events drive disease pathology. However, there will need to be vigilance for emergence of a hyperserotonergic state with similarities to serotonin syndrome, as noted earlier. Thus it may make sense to initiate fluvoxamine in the less severe hospitalized patients but administer a serotonin 2 A, B and C receptor antagonist such as cyproheptadine or mirtazapine in the more severe patients (along with fluvoxamine). It is also tempting to speculate on a role for FLV in COVID-19 long-haulers. There are likely to be subsets in this heterogeneous group that may have an aberrant immune response that has lingered on, in which FLV may be efficacious. Finally, there may be a role for FLV in the treatment of other viral illnesses in which there is some version of a cytokine storm present.

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