Meet Todd Rider, Inventor of DRACO

Todd Rider, a biomedical engineer at MIT, Double-stranded RNA Activated Caspase Oligomerizer (DRACO).

Take me back to when you first discovered DRACOs. Did you immediately see their potential?

Because there were so few existing antiviral therapeutics, and those tended to be specific just for individual viruses or even just particular strains of individual viruses, I was motivated to develop new antiviral therapeutics that would be effective against a very broad spectrum of viruses. Rather than trying to invent something from scratch, I decided to borrow from what nature has already invented. Our cells have natural ways of detecting viral double-stranded RNA, and natural ways of triggering suicide in certain cells. I invented DRACO to combine those two natural systems and kill virus-infected cells. Just as the development of antibiotics completely revolutionized the treatment and prevention of bacterial infections in the mid-20th century, I believe that DRACO has the potential to completely revolutionize the treatment and prevention of viral infections in the 21st century.

You might think that a potential cure for all viruses would somehow generate sufficient interest and funding. Why hasn’t this happened?

Modest amounts of funding from the National Institutes of Health have enabled the previous proof-of-concept experiments in cells and mice, but that funding grant is now over. Major pharmaceutical companies have the resources and expertise to carry new drugs like DRACO through the manufacturing scale-up, large-scale animal trials, and human trials required for FDA approval. However, before committing any of their own money, those companies want to see that DRACOs have already been shown to be effective against major clinically relevant viruses (such as members of the herpesvirus family), not just the proof-of-concept viruses (such as rhinovirus) that were previously funded by NIH. Thus the Valley of Death is the financial and experimental gap between the previously funded NIH proof-of-concept experiments and the threshold for convincing major pharmaceutical companies to advance DRACOs toward human trials.

It seems as though DRACOs aren’t a silver bullet — separate therapies would have to be developed and tested individually, each at great cost.

In theory, one DRACO design should be effective against a very broad spectrum of viruses, and effective in a wide range of people. Starting from our initial proof-of-concept work, it may take some experimental optimization to find that best DRACO design.

What do you imagine a DRACO-based treatment would actually look like, if it were developed?

We have demonstrated that the initial version of DRACO can be successfully administered to mice as an injection or via inhalation. My ultimate goal is to develop DRACO in a pill form, but first I have to teach the mice how to swallow pills.

Do you believe the goal of curing all viral disease through DRACOs is attainable?

If we can successfully demonstrate and optimize DRACOs against clinically relevant viruses in cells, we believe those results should persuade pharmaceutical companies to carry DRACOs through large-scale animal trials and hopefully into human trials. The timeline depends on funding levels (including how much funding pharmaceutical companies are willing to commit later) and whether any unforeseen scientific difficulties arise in the experiments. However, if everything goes well, we hope that DRACO could enter human trials.

Broad-Spectrum Antiviral Strategies

Current antiviral drugs cover only a few of the hundreds of human viruses.

Over 200 viruses are known to cause disease in humans, yet currently approved antiviral drugs are available to treat only about 10 of these viral infections. - Preparing for the next viral threat with broad-spectrum antivirals

To “cover all viruses,” research focuses on broad-spectrum agents and combinations. One key example is DRACO (dsRNA-Activated Caspase Oligomerizer) – a fusion protein that binds any viral double-stranded RNA and triggers apoptosis in infected cells. Because most actively replicating viruses (RNA or DNA viruses during transcription) produce dsRNA intermediates, DRACO kills cells infected by viruses like influenza, dengue, arenaviruses, etc., without harming healthy cells. In fact, DRACO killed at least 15 different viruses in cell culture (flaviviruses, arenaviruses, bunyaviruses, H1N1 influenza) and protected mice from lethal influenza. In principle then, DRACO-like drugs could cover all viruses that generate any dsRNA. However, truly latent infections (e.g. herpesviruses, HIV provirus) produce no viral RNA (and hence no dsRNA) in their dormant state, so DRACO would not trigger apoptosis in those cases.

For example, Ebola virus is an enveloped filovirus with surface glycans. Novel synthetic carbohydrate receptor drugs bind viral surface sugars to block entry and have inhibited six unrelated viruses (Ebola, Nipah, Marburg, SARS-CoV-1/2) in cell culture and protected mice.

A new antiviral blocks 6 deadly viruses in mice but faces a long road ahead

Such approaches – along with DRACO and others – aim to treat multiple virus families with one agent.

Besides DRACO, several broad-spectrum antivirals are in development or use:

1. Nucleoside Analogues (RNA Polymerase Inhibitors): These target viral replication enzymes shared by many RNA viruses. Examples include remdesivir and molnupiravir (RdRp inhibitors approved for SARS-CoV-2) and favipiravir (approved in Japan for influenza). The classic broad-spectrum drug ribavirin inhibits both RNA and DNA synthesis. In practice, ribavirin is used against RSV and HCV, and favipiravir against influenza. These drugs will hit most RNA viruses (including those DRACO covers) as well as some DNA viruses (e.g. HBV).
2. Host-Directed Metabolic Inhibitors: Some approved drugs target host cell pathways essential for many viruses. For example, the antidiabetic biguanides metformin/phenformin activate innate immunity (AMPK-IFN pathways) and have shown antiviral effects in animals (metformin reduced influenza and dengue severity in mice; phenformin cut SARS-CoV-2 and dengue replication in cells and hamster). Other metabolic targets include atpenin A5 (a mitochondrial inhibitor) which also reduced diverse virus replication in vitro. These drugs work against multiple virus families because many viruses co‑opt similar host metabolism.
3. Entry/Fusion Inhibitors: Broad entry blockers include agents that bind viral envelopes or host receptors. The dye LJ001 (a photosensitizer) irreversibly damages viral lipid envelopes, blocking entry of enveloped viruses (poxviruses, filoviruses, arenaviruses, influenza, etc.) in vitro. Similarly, arbidol (umifenovir, used in Russia for flu) acts on viral membrane fusion and has broad anti-influenza and coronavirus activity. Newer approaches mimic this idea: e.g. synthetic carbohydrate receptor molecules bind conserved N-glycan sites on virus surfaces (as in Ebola and SARS-CoV) to prevent attachment. In mice, one such compound enabled 90% survival after SARS-CoV-2 infection. These entry inhibitors add coverage for enveloped viruses (and would complement DRACO).
4. Nuclear Export and Budding Inhibitors: Many RNA viruses export nucleocapsids or use the ESCRT pathway. The exportin-1 inhibitor verdinexor/KPT-335 blocked multiple influenza strains in cells and protected mice, and also inhibits some DNA viruses (e.g. HSV). Proteins like TSG101 (ESCRT-I) are essential for budding; compounds like FGI-104 and others targeting TSG101 block Ebola, influenza, HIV and HSV budding (in mice). These host-targeted agents act on a common step of enveloped virus life cycles, potentially covering any enveloped virus (especially if combined).
5. Broad-Acting Approved Drugs: Several known drugs show multi-virus activity. For example, nitazoxanide (an antiparasitic) inhibits replication of diverse RNA and DNA viruses (influenza, dengue, HIV, HBV, JEV, even HSV), likely by disrupting viral protein maturation. Nitazoxanide is FDA-approved and in trials for influenza/COVID-19. Likewise, broad-spectrum antibiotics (e.g. azithromycin) and immunomodulators (e.g. IFN-α) have activity against multiple viruses, though resistance and toxicity limit use.
6. Anti-Latency Strategies: No drug directly “kills” truly latent viruses, but strategies are being explored. The “shock-and-kill” approach uses epigenetic drugs to reactivate latent virus; for example, selective HDAC inhibitors (e.g. BRD3308 targeting HDAC3) can induce HIV expression from latency. Analogous approaches are studied for herpesviruses (e.g. arginine-butyrate or other HDAC inhibitors can wake latent HSV or EBV, followed by antiviral treatment). Gene-editing methods (CRISPR/Cas systems) are being developed to excise latent proviruses (HIV, HBV, HSV, etc.) though these are experimental. Immune therapies (e.g. broadly reactive antiviral T cells) can help control latent virus reactivation (as in transplant patients). In short, latent infections would require reactivation + clearance or gene therapies rather than conventional antivirals.

In sum, a minimal “pan-viral” arsenal would combine drugs from several classes. For example, DRACO (or similar dsRNA-triggered therapeutics) covers almost all replicating viruses; broad polymerase inhibitors (remdesivir, favipiravir, ribavirin) cover most RNA viruses; entry/fusion blockers (e.g. carbohydrate-receptor analogs) could stop any enveloped virus; host-targeted agents (e.g. verdinexor, phenformin) add redundancy across families; and epigenetic or gene therapies aim to purge latent reservoirs.

The table below summarizes key approaches and examples (approved drugs or candidates) covering different virus categories. Combining just a few complementary mechanisms could in principle provide effective treatment against all viruses.

Virus category / scenario                                 
Broad-spectrum agent(s) or approach                        
Notes and status (examples)                                            
 
 
 
**Viruses with dsRNA (most replicating RNA/DNA viruses)** 
DRACO (dsRNA-activated apoptosis)                          
Experimental; killed ≥15 virus types in cells, protected mice          
Polymerase inhibitors (remdesivir, favipiravir, ribavirin) 
Approved or in trials; active vs broad RNA viruses (also some DNA/HBV) 
**Enveloped viruses (entry inhibitors)**                  
LJ001/JL122 (envelope lipid oxidizer)                      
Research; blocks fusion of many enveloped viruses in vitro             
Synthetic glycan-binding drugs (e.g. “SCR” compounds)      
In development; blocked Ebola/Nipah/SARS etc. in cells and mice        
Arbidol (umifenovir)                                       
Approved (Russia); broad activity vs influenza, some coronaviruses     
**General host-targeting antivirals**                     
Verdinexor/KPT-335 (XPO1 inhibitor)                        
Preclinical; blocked influenza and other viruses in animals            
Phenformin (biguanide)                                     
Repurposed diabetes drug; inhibited SARS-CoV-2 and dengue in models    
Nitazoxanide                                               
Approved (antiprotozoal); broad antiviral activity in vitro and trials 
**DNA viruses**                                           
Cidofovir/Valacyclovir (nucleoside analogs)                
Approved; cover herpesviruses, CMV, adenovirus (some cross-coverage)   
Cidofovir prodrug NPP-669                                  
Preclinical; potent vs CMV, adenovirus in animals                      
**Latent/chronic infections**                             
HDAC inhibitors (e.g. BRD3308)                             
Research; reactivates latent HIV (shock-and-kill strategy)             
Adoptive antiviral T cells / immune therapy                
Clinical; used post-transplant to control EBV/CMV reactivation         
CRISPR/Cas gene-editing (experimental)                     
In development; could excise proviral genomes (HIV, HBV, herpes)       
**Others / adjuncts**                                     
Interferons (IFN-α/β) and immune modulators                
Approved; broad but limited by toxicity and viral evasion              
Combination immunomodulation (e.g. mRNA-induced ISG15)     
Experimental mRNA therapies boosting host defenses                     

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87.5% Broad Spectrum AntiViral Across 3 Methods

Interventions: DRACO + broad polymerase/replication inhibitor class + latency-targeting elimination strategy (3 interventions).

Coverage achieved (conservative mapping of 24 common human virus families): 21/24 → 87.5% covered.

Not covered (3 families, 12.5%): Papillomaviridae (HPV), Parvoviridae (B19), Anelloviridae (TTV). For these, practical responses are vaccines, local therapy/IVIG, or no therapy required respectively; future gene-editing could close gaps.

1. DRACO (broad dsRNA-triggered apoptosis). DRACO status: DRACO is experimental (proof-of-concept in cells & mice). I treat it as a valid candidate broad-spectrum agent against viruses that produce accessible long dsRNA during replication. Strengths: Directly kills infected cells only when viral dsRNA is present → broad across viruses that produce long dsRNA replication intermediates (many RNA viruses, some DNA viruses during transcription). Very broad, rapid antiviral action. Weaknesses: Experimental; some viruses hide dsRNA or express dsRNA-sequestering proteins (poxviruses, coronaviruses sequester in DMVs) that reduce DRACO accessibility.
2. Broad polymerase/replication inhibitor class. “Polymerase inhibitor” role: I use the phrase to mean a broadly-acting nucleoside/nucleotide analog strategy (examples: ribavirin-type broad inhibitors, remdesivir/molnupiravir classes for RdRp; separate approved drugs exist for DNA viruses — e.g., cidofovir/acyclovir class). This entry stands for the class of polymerase/replication inhibitors that can be applied (one or more clinical agents belonging to the class may be required in practice). Strengths: Targets viral replication machinery across many virus families (RdRp for RNA viruses; DNA polymerase inhibitors for DNA viruses). This class fills DRACO blind spots (viruses that hide dsRNA but still require polymerase activity). Several approved examples already exist (and more in trials). Weaknesses: Different families often require different specific drugs (a single small-molecule rarely works equally well across all families), toxicity and resistance are concerns; in the real world you’d select the best polymerase agent for the virus family.
3. Latency-targeting elimination strategy. “Latency-targeting” strategy: includes “shock-and-kill” epigenetic latency reversal (HDAC/other modulators) + immune clearance (adoptive T cells, therapeutic vaccines) and/or gene-editing strategies (CRISPR) aimed at eliminating provirus/cccDNA reservoirs. This is treated as one combined strategy for our minimal set. Strengths: Required to cure or eliminate latent/persistent infections (HIV provirus, herpesvirus latency, HBV cccDNA, polyomaviruses). Approaches include latency reversal (HDAC/other epigenetic drugs) + immune clearance, adoptive T cells, therapeutic vaccines, and experimental gene-editing (CRISPR/Cas) to excise provirus. Weaknesses: Mostly experimental; safety and off-target risks exist; combination with immune therapies likely necessary.

87.5% Oral Broad Spectrum AntiViral Polypill

• Proposed Oral Broad-Spectrum Antiviral Polypill

The current proposal suggests a 4 agent cocktail of Galidesivir, Brincidofovir, Nitazoxanide, Tamoxifen, and Lamivudine.

The same concept was proposed to Qwen which excelled at the task, mentioning NV-387. Here is that report.

Instead of trying to build the "perfect" antiviral pill all at once, the best approach is to do it in three smart steps:

Step 1: Start with a strong, safe core

Combine three modern, well-tolerated, oral drugs:

• VV116 (a powerful antiviral for many RNA viruses like coronaviruses),
• Nitazoxanide (boosts the body’s virus-fighting system and works against flu, RSV, etc.), and
• CDI-988 (a new drug that blocks a key virus enzyme in norovirus, flu, and more).

This gives broad protection with low side effects and is easy to take by mouth.

Step 2: Add coverage for missing viruses

Add two more drugs to cover viruses the first three don’t touch:

• Acyclovir → works against HPV (which causes warts and some cancers).
• Brincidofovir → works against Parvovirus B19 (which can be dangerous in pregnancy or for people with weak immune systems).

Now you have a 5-drug pill that covers nearly all major virus families, including the ones the original design missed.

Step 3: Test a game-changing alternative

There’s a brand-new type of antiviral called NV-387—it’s not a traditional drug but a nanoparticle that tricks viruses into binding to it instead of your cells. It might work against dozens of viruses at once—possibly even more than the 5-drug combo—and early tests show it’s very safe and works when taken by mouth.

So, the final step is to compare the 5-drug pill head-to-head with NV-387 alone in studies.

If NV-387 works just as well (or better) with only one ingredient, it could become the simplest, safest, and most powerful option—making complex pills obsolete.

In short:

• Build a smart, safe 3-drug base.
• Expand to 5 drugs to cover everything important.
• Test if one futuristic drug (NV-387) can do it all by itself.

This way, you get immediate progress now while staying open to a revolutionary breakthrough in the near future.

• A Strategic Framework for the Design of an Optimal Oral Broad-Spectrum Antiviral Polypill

We are all pushed into a program of thinking that is what is specific to the virus, a protein in its structure or anything else that is not present in humans, and then develop a chemical that is specific only to that difference to treat the virus, but NV-387 is out of the program.

NanoViricides Has Received Approval to Start Phase II Clinical Trial of NV-387 for the Treatment of MPox by the Regulatory Agency ACOREP of the Democratic Republic of Congo

December 9, 20259:33 PM GMT+7 - Updated December 9, 2025

NanoViricides / Source: NanoViricides (EZ Newswire)

SHELTON, CT, December 9, 2025 (EZ Newswire) -- NanoViricides, Inc. (NYSE American: NNVC (the “Company”) today reported that it has received approval to start a Phase II clinical trial of NV-387 for the treatment of MPox from the regulatory agency ACOREP of the Democratic Republic of the Congo (DRC).

The proposed Phase II clinical trial to evaluate safety and effectiveness of NV-387 for the treatment of patients with MPox disease caused by hMPXV infection is now cleared to proceed subject to filing of certain documents.

"This is an important milestone in regulatory development of NV-387," said Anil R. Diwan, PhD, president and executive chairman of the Company.

There is no drug available for the treatment of hMPXV infection that causes the MPox disease. A clinical trial of tecovirimat (TPOXX®, SIGA) failed to demonstrate any effectiveness over placebo, as per a NIH press release on August 15, 2024. Another drug, brincidofovir (TEMBEXA®, EBS) entered into a clinical trial called "MOSA" with fanfare in January, 2025, with early topline results expected by the end of the quarter. The status of this clinical trial is not publicly known as of now.

MPox Clade II has become endemic in the USA but it affects a limited population of Men-having-Sex-with-Men (MSM), because of transmission during sexual activity.

Most recently, three new cases of MPox Clade I have been found in California in unconnected persons, with no travel to Africa; yet the MPXV viral genomes were found to be in the same cluster, suggesting that community spread of the MPXV Clade I is likely already occurring, according to the CDC.

"NV-387, our broad-spectrum antiviral drug is poised to cause a revolution in treatment of viral diseases, just as antibiotics revolutionized the treatment of bacterial diseases," said Anil R. Diwan, Ph.D., adding "NV-387 is designed to mimic human cells to trap and destroy the virus. This single drug can target over 90% to 95% of human pathogenic viruses due to this biomimicry, which is reminiscent of the antibiotic penicillin that targets a large number of human pathogenic bacteria."

The Company previously announced in May, 2025 that it has received an approval from the Ethics Committee CNES of the national regulatory agency in DRC that NV-387 can be considered for a Phase II clinical trial for the treatment of MPox. This approval was based on a summary package of information regarding NV-387 regulatory development until then. This Ethics Committee approval cleared the path for us to engage with the regulatory agency ACOREP and prepare the documentation required for their evaluation and approval as instructed by them.

We have now completed submission of substantial required documentation in the draft forms as requested. We are now in the process of compiling all of this documentation together into the final form Clinical Trial Application, along with associated certifications and disclosures. These documents will be translated into French as required by the DRC. Both French and English sets of documents, certified to be accurately translated, will then be submitted to the ACOREP regulatory agency. The approval to start recruiting patients will then become effective.

MPox disease, caused by the human MPox virus (hMPXV) has been causing a regional pandemic encompassing several countries in the WHO African Region that includes the Democratic Republic of Congo (DRC), Uganda, and other countries. It led to the WHO declaring a Public Health Emergency of International Concern ("PHEIC") on August 14, 2024 that was closed in September, 2025. However, the MPox epidemic has continued to spread in the DRC, Uganda, and neighboring countries and the number of new weekly cases is still increasing in the WHO African Region. Therefore, the Africa CDC has maintained the status of the MPox pandemic as Public Health Emergency of Continental Security ("PHECS").

NV-387 was found to be highly effective in increasing survival in lethal animal models of influenza virus, surpassing existing drugs Tamiflu®, Rapivab® and Xofluza® by a large margin.

NV-387 led to a complete cure of lethal RSV lung infection in an animal model study. There is no approved drug for RSV treatment.

NV-387 was found to be highly effective in increasing survival in lethal animal models of Coronavirus infection (a stand-in model for SARS-CoV-2 infection), surpassing existing drug remdesivir by a large margin.

NV-387 was also found to be highly effective against lethal lung infection by Measles virus in a humanized (hCD150+knock-in/IfnR-/-) mouse model.

NV-387 was found to possess strong antiviral activity against an orthopoxvirus in an animal model that is considered an important model to establish potential effectiveness against MPox and Smallpox viruses, as all of these viruses belong to the same family of orthopoxviruses.

In fact, NV-387 effectiveness matched the effectiveness of the small chemical drug tecovirimat in two different models of infection, one was direct skin infection, and the other was a direct lung infection, by the virus.

Escape of virus from tecovirimat can occur by a single point mutation in a viral protein called VP-37.

Vaccines, antibodies, and small chemical drugs such as tecovirimat for MPox/Smallpox, or oseltamivir (Tamiflu®), baloxavir (Xofluza®) for Influenza are readily escaped by viruses simply by introduction of small changes that viruses undergo when they are faced with these challenges in the field.

In contrast, escape of virus from NV-387 is highly unlikely because no matter how much the virus changes in the field, it continues to use sulfated proteoglycans such as HSPG as "attachment receptor" in order to cause cell infection. NV-387 mimics the sulfated proteoglycan signature feature that the viruses require.

NV-387 is a host-mimetic drug that "looks like a cell" to the virus, displaying numerous ligands that mimic the sulfated proteoglycan, enticing the virus to bind to and become engulfed by the NV-387 dynamic shape-shifting polymeric micelle.

Therefore development of NV-387, a broad-spectrum host-mimetic, direct-acting antiviral drug that the viruses cannot escape even as they change constantly, will be revolutionary once the drug undergoes regulatory development for approval for use in humans.

New viruses and existing viruses acquiring greater pathology and infectivity are bound to keep appearing in time. To combat such threats, we need to develop broad-spectrum drug arsenal that the viruses cannot escape. Vaccines and antibodies simply will not do, and their limitations have become clearly evident during the COVID-19 pandemic.

About NanoViricides

NanoViricides, Inc. (the "Company") is a clinical stage company that is creating special purpose nanomaterials for antiviral therapy. The Company's novel nanoviricide™ class of drug candidates and the nanoviricide™ technology are based on intellectual property, technology and proprietary know-how of TheraCour Pharma, Inc. The Company has a Memorandum of Understanding with TheraCour for the development of drugs based on these technologies for all antiviral infections. The MoU does not include cancer and similar diseases that may have viral origin but require different kinds of treatments. For more information, visit www.nanoviricides.com.

The Company has obtained broad, exclusive, sub-licensable, field licenses to drugs developed in several licensed fields from TheraCour Pharma, Inc. The Company's business model is based on licensing technology from TheraCour Pharma Inc. for specific application verticals of specific viruses, as established at its foundation in 2005.

Our lead drug candidate is NV-387, a broad-spectrum antiviral drug that we plan to develop as a treatment of RSV, COVID, Long COVID, Influenza, and other respiratory viral infections, as well as MPOX/Smallpox infections. Our other advanced drug candidate is NV-HHV-1 for the treatment of Shingles. The Company cannot project an exact date for filing an IND for any of its drugs because of dependence on a number of external collaborators and consultants. The Company is currently focused on advancing NV-387 into Phase II human clinical trials.

NV-CoV-2 (API NV-387) is our nanoviricide drug candidate for COVID-19 that does not encapsulate remdesivir. NV-CoV-2-R is our other drug candidate for COVID-19 that is made up of NV-387 with remdesivir encapsulated within its polymeric micelles. The Company believes that since remdesivir is already US FDA approved, our drug candidate encapsulating remdesivir is likely to be an approvable drug, if safety is comparable. Remdesivir is developed by Gilead. The Company has developed both of its own drug candidates NV-CoV-2 and NV-CoV-2-R independently.

The Company is also developing drugs against a number of viral diseases including oral and genital Herpes, viral diseases of the eye including EKC and herpes keratitis, H1N1 swine flu, H5N1 bird flu, seasonal Influenza, HIV, Hepatitis C, Rabies, Dengue fever, and Ebola virus, among others. NanoViricides' platform technology and programs are based on the TheraCour® nanomedicine technology of TheraCour, which TheraCour licenses from AllExcel. NanoViricides holds a worldwide exclusive perpetual license to this technology for several drugs with specific targeting mechanisms in perpetuity for the treatment of the following human viral diseases: Human Immunodeficiency Virus (HIV/AIDS), Hepatitis B Virus (HBV), Hepatitis C Virus (HCV), Rabies, Herpes Simplex Virus (HSV-1 and HSV-2), Varicella-Zoster Virus (VZV), Influenza and Asian Bird Flu Virus, Dengue viruses, Japanese Encephalitis virus, West Nile Virus, Ebola/Marburg viruses, and certain Coronaviruses. The Company intends to obtain a license for RSV, Poxviruses, and/or Enteroviruses if the initial research is successful. As is customary, the Company must state the risk factor that the path to typical drug development of any pharmaceutical product is extremely lengthy and requires substantial capital. As with any drug development efforts by any company, there can be no assurance at this time that any of the Company's pharmaceutical candidates would show sufficient effectiveness and safety for human clinical development. Further, there can be no assurance at this time that successful results against coronavirus in our lab will lead to successful clinical trials or a successful pharmaceutical product.

Forward-Looking Statements

This press release contains forward-looking statements that reflect the Company's current expectation regarding future events. Actual events could differ materially and substantially from those projected herein and depend on a number of factors. Certain statements in this release, and other written or oral statements made by NanoViricides, Inc. are "forward-looking statements" within the meaning of Section 27A of the Securities Act of 1933 and Section 21E of the Securities Exchange Act of 1934. You should not place undue reliance on forward-looking statements since they involve known and unknown risks, uncertainties and other factors which are, in some cases, beyond the Company's control and which could, and likely will, materially affect actual results, levels of activity, performance or achievements. The Company assumes no obligation to publicly update or revise these forward-looking statements for any reason, or to update the reasons actual results could differ materially from those anticipated in these forward-looking statements, even if new information becomes available in the future. Important factors that could cause actual results to differ materially from the company's expectations include, but are not limited to, those factors that are disclosed under the heading "Risk Factors" and elsewhere in documents filed by the company from time to time with the United States Securities and Exchange Commission and other regulatory authorities. Although it is not possible to predict or identify all such factors, they may include the following: demonstration and proof of principle in preclinical trials that a nanoviricide is safe and effective; successful development of our product candidates; our ability to seek and obtain regulatory approvals, including with respect to the indications we are seeking; the successful commercialization of our product candidates; and market acceptance of our products.

The phrases "safety", "effectiveness" and equivalent phrases as used in this press release refer to research findings including clinical trials as the customary research usage and do not indicate evaluation of safety or effectiveness by the US FDA.

Where stated with an ®, the name is a registered trademark, which belongs to the owner of the trademark name.

FDA refers to US Food and Drug Administration. IND application refers to "Investigational New Drug" application. cGMP refers to current Good Manufacturing Practices. CMC refers to "Chemistry, Manufacture, and Controls". CHMP refers to the Committee for Medicinal Products for Human Use, which is the European Medicines Agency's (EMA) committee responsible for human medicines. API stands for "Active Pharmaceutical Ingredient". WHO is the World Health Organization. R&D refers to Research and Development.

Media Contact

NanoViricides, Inc.

info@nanoviricides.com

Public Relations Contact

ir@nanoviricides.com

SOURCE: NanoViricides

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