Claromers® Fight Epstein-Barr Virus
A Breakthrough in the Fight Against the Silent Pandemic

The Epstein-Barr virus (EBV), also known as human herpesvirus 4, is one of the most common and elusive viral infections in the world. It is responsible for infectious mononucleosis ("mono") and is associated with a range of chronic and autoimmune conditions—including Multiple Sclerosis, certain cancers, lupus, rheumatoid arthritis, and Irritable Bowel Disease. Estimates show that nearly 95% of the global population carry EBV for life.

For decades, EBV has remained dormant and unpredictable, persisting in the body and evading both treatments and immunity. Modern antiviral therapies, like acyclovir, have proven ineffective at stopping EBV’s long-term incubation—leaving billions at risk.

A 3D rendering of a virus with a spherical shape, textured surface in light green and orange, and spike-like protrusions in green, purple, and black against a blurred green background.

“Epstein-Barr is the quietest and most widespread pandemic in human history—it lives inside 95 percent of us for life, and modern medicine has never had a real tool against it… These results are the first sign that Maxwell’s Claromer technology may finally be that tool.” — Scotch McClure, Founder & CEO

Immune-Inspired Solutions: Claromers®
At Maxwell Biosciences, we believe tackling the world’s most persistent infections requires a new way of thinking. Our novel Claromer® platform—immune-inspired, broad-spectrum small molecules—mimics and enhances the body’s natural defenses, destroying pathogens without harming healthy cells or the microbiome.

In a recent third-party laboratory study, Claromers® demonstrated groundbreaking results against the Epstein-Barr virus. 

Two Claromer® compounds achieved over 50% inhibition of EBV growth at non-toxic concentrations, compared to acyclovir, which showed no measurable effect.

The potential for an oral health product like a mouth rinse or toothpaste to interrupt EBV transmission could be transformative for public health—possibly representing the first real tool against this silent and widespread pandemic.

What’s Next?

This promising preclinical data propels us one step closer to:

  • Preventing the spread of EBV in the population

  • Potentially targeting and eradicating dormant EBV in the body

  • Delivering safe, affordable and shelf-stable solutions for global health

  • Developing Claromer®-based consumer and clinical products, starting with oral hygiene innovations and progressing to treatments that may directly address EBV’s hidden reservoirs in the body.

Read the full press release: Maxwell Biosciences’ Claromers Destroy Epstein-Barr.

Partner With Us

Maxwell Biosciences is actively seeking sponsorships, strategic partnerships and funding opportunities to create a therapeutic for Epstein-Barr virus and other challenging pathogens. Together, we can build a healthier future.

Contact us at partnerships@maxwellbiosciences.com.

Maxwell Biosciences—delivering immune-inspired solutions for a healthier planet.

EPSTEIN-BARR STUDY RESULTS

Milestone 1: Cytotoxicity Testing

Graph comparing OD560 levels vs. concentration of test claromeres and acyclovir in 293T cells, with two panels showing different data sets and treatment conditions.
Line graphs showing OD560 values versus concentration of test compounds in SVK-CR2 cells, comparing the effects of Acyclovir and DMSO. The left graph displays multiple test compounds, while the right graph shows the Acyclovir and DMSO control.
Table showing CC50 values for test claromeres and a Cyclovir in 293T and SVK-CR2 cells, with sample IDs and numerical data for each drug.

Milestone 2: Antiviral Testing

Table showing the summary of % viability and % inhibition data for different samples with varying concentrations.
Graph comparing percent viability versus concentration of test claromers and acyclovir in 293T cells, with two panels showing different data sets labeled with legend keys.
Graph showing percent viability versus concentration of test compounds in SVK-CR2 cells, with two plots: (A) multiple test compounds with different data series, and (B) Acyclovir and DMSO comparison.

MTT assay was performed to evaluate the cytotoxic effects of the test Claromers®. All plates passed the plate level acceptance criteria (Table A1). Figures 1- 4 show the cytotoxicity results for test Claromers (A) and acyclovir and DMSO (B) in 293T and SVK-CR2 cells. OD560 versus Claromer concentration plots and the normalized % viability data versus concentration plots were used to represent the cytotoxicity of these test Claromers in 293T (Figure 1 and 2) and SVK-CR2 cells (Figure 3 and 4). CC50 values of all the test Claromers in 293T and SVK-CR2 cells were calculated and reported in Table 1.

Table showing cytotoxicity testing plate level acceptance criteria with columns for Cell Plate ID, Sample ID, Cell Type, and Plate Level Acceptance Criteria. The data includes cell identifiers, sample identifiers, cell types such as 293T and SVK-CR2, and acceptance criteria indicating 'Pass, no contamination'.
Graph showing FFU/mL versus concentration of test claromers in SVK-CR2 cells, with two panels labeled (A) and (B). Panel (A) has multiple trend lines representing different MXB strains, with a legend identifying each. Panel (B) shows a single trend line for Acyclovir with error bars.
A table titled 'Antiviral testing plate level acceptance criteria' that lists three plates with their respective sample IDs, viral titers (VC FFU/mL), percent value of contamination, and contamination status, all indicating no contamination.

Conclusions

Graph showing percentage inhibition versus concentration of test claromeres in SVK-CR2 cells, with two panels labeled A and B. Panel A displays multiple lines representing different test compounds with their respective IC50 values, while Panel B shows a line for Acyclovir.

FFA-based antiviral testing was performed in SVK-CR2 cells to evaluate the inhibitory effect of test Claromers on EBV-GFP replication. Plate-level acceptance criteria were met for all plates (Table A2). Figure 5 shows the change in viral replication (FFU/mL) vs test Claromer concentration. Figure 6 illustrates the percent inhibition of EBV-GFP replication vs Claromer concentration. An IC50 value was not generated for any of the test Claromers due to the absence of a complete linear inhibition range with the Claromer concentrations used. Therefore, a comparative analysis was performed for the % inhibition values observed at the two highest testing concentration against the % viability data to assess the antiviral effects (Table 2). 

Cytotoxicity Testing 
293T cells – 
MXB-24, 656, MXB-27,369 and MXB-25,605 - CC50 <32 μg/mL 
MXB-22,510 and MXB-25,739 - CC50 < 64ug/ml. 
MXB-24,816 - CC50 > 64ug/ml. 

SVK-CR2 cells – 
MXB-24,656, MXB-22,510 and MXB-25,605 - CC50 < 32ug/ml 
MXB-27,369, MXB-24,816, and MXB-25,739 - CC50 < 64ug/ml. 

Acyclovir treatment did not induce any significant cytotoxicity in either 293T or SVK-CR2 cells. 

Antiviral Testing 
SVK-CR2 cells – 
MXB-24,816 and MXB-25,739 - >50% inhibition of the EBV-GFP infection at 32 μg/mL (CC50 >32 μg/mL). 

MXB-24,656 and MXB-22,510 - >50% inhibition of the EBV-GFP infection at 32 μg/mL (CC50 <32 μg/mL). 

MXB-27, 369 and MXB-25, 605 did not show significant inhibition at the tested concentration range. 

Acyclovir treatment was not cytotoxic but did not show any inhibition against EBV in SVK-CR2 cells at the concentrations tested.