MIC Testing Results Prove Consistent Efficacy Against Resistant Pathogens

We tested AvantGuard’s antiseptic compound, polyvantoin chlorine, against some of the most feared pathogens in modern medicine: pan-resistant Candida auris, multidrug-resistant ESKAPE bacteria, and a comprehensive panel of dangerous fungi. The results revealed something remarkable.

You might think that an antibiotic-resistant pathogen is somehow tougher and harder for any compound to kill. However, whether the pathogen was resistant or susceptible to a particular antibiotic, polyvantoin chlorine's minimum inhibitory concentration (MIC) remained virtually identical. For infectious disease specialists and infection prevention teams, this consistency represents something healthcare desperately needs: predictability. For patients, it could mean the difference between a preventable infection and a life-threatening one.

At AvantGuard, we believe this data tells a compelling story, not just about polyvantoin chlorine, but about a fundamentally different approach to fighting the antimicrobial resistance crisis.

Understanding MIC - The Universal Language of Antimicrobial Efficacy

Before we dive deeper, let's establish why MIC matters. Minimum inhibitory concentration (MIC) is the lowest concentration of an antimicrobial that prevents visible growth of a microorganism after a set incubation period. Think of it as the threshold dose needed to stop a pathogen in its tracks.

Lower MIC values correspond to higher potency, as a smaller amount of the substance is required to inhibit growth. Clinicians rely on MIC data to select effective treatments and determine appropriate dosing. It's the gold standard for comparing antimicrobial efficacy across different antibiotics and different pathogens.

Variability in MIC values creates real clinical uncertainty. When a patient presents with a suspected infection, clinicians often must make treatment decisions before they know the exact pathogen or its resistance profile to the available antibiotics. They're essentially making educated guesses, hoping the empiric therapy they choose will work.

Polyvantoin chlorine eliminates that uncertainty.

Testing Polyvantoin Chlorine Against The ESKAPE Pathogens

We wanted definitive proof that polyvantoin chlorine's efficacy wasn't affected by antibiotic resistance, so we started with the toughest challenge in bacterial medicine: the ESKAPE pathogens.

This acronym, coined by the Infectious Diseases Society of America (IDSA), encompasses six highly virulent bacteria that represent one of the most urgent threats to global public health: Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacter species.¹⁷ These pathogens are responsible for approximately two-thirds of all nosocomial infections worldwide and cause over 2 million illnesses and roughly 23,000 deaths annually in the United States alone.¹⁸

Their clinical importance is reflected in the World Health Organization's 2017 Priority Pathogens List, where Acinetobacter baumannii and carbapenem-resistant Enterobacterales are classified as "critical priority" threats—the highest level of concern.

We are grateful to the NIH’s National Institute of Allergy and Infectious Diseases (NIAID) Pre-Clinical Services group, which contracted Element Materials Technology (North Liberty, IA) to test polyvantoin chlorine against both antibiotic-resistant and non-resistant strains of the complete ESKAPE pathogen set. We included levofloxacin, a fluoroquinolone antibiotic often used as a last-resort option, as a comparison.

The results were striking. (Figure 1)

Figure 1

Levofloxacin showed dramatic variations in susceptibility across different ESKAPE pathogens and between resistant and susceptible strains of the same species. Some pathogens were inhibited at relatively low concentrations, while others required substantially higher doses or weren't inhibited at all. This variability perfectly illustrates the challenge infectious disease specialists face: without knowing the exact strain and its resistance profile, predicting which antibiotic will work is extraordinarily difficult.

Polyvantoin chlorine told a completely different story. Across all ESKAPE pathogens tested, whether antibiotic-resistant or susceptible, MIC values remained remarkably consistent. The compound that stopped methicillin-susceptible S. aureus was equally effective against MRSA. Carbapenem-resistant and carbapenem-susceptible strains showed virtually identical susceptibility.

This wasn't a marginal improvement. It was a fundamental difference in approach to killing pathogens.

Candida auris: Four Clades, One Consistent MIC

Since its first identification in 2009, Candida auris has been reported in over 30 countries worldwide, causing outbreaks in healthcare facilities and earning designation as an urgent threat by the CDC. What makes C. auris uniquely dangerous is its perfect storm of characteristics: it grows at human body temperature, thrives in saline conditions (enabling rapid skin colonization of immunocompromised patients), spreads easily between patients and throughout healthcare environments, and exhibits alarming drug resistance.

Among C. auris strains, 87-100% are resistant to fluconazole, 8-35% to amphotericin B, 0-8% to echinocandins, and over 40% show combined resistance to two or more antifungal classes.^19-21 When echinocandin resistance combines with resistance to azoles and amphotericin B, creating pan-resistance (resistance to all drug classes), clinicians essentially run out of treatment options.²⁰

C. auris can also become more resistant during the course of antifungal treatment, with approximately three times as many pan-resistant cases documented in 2021 compared to the previous two years combined.^22,23

C. auris exists in six distinct clades (I, II, III, IV, V, and VI), each with different geographic origins and different resistance profiles. This genetic diversity adds another layer of complexity to treatment decisions. 

We wanted to know: Would polyvantoin chlorine's efficacy be consistent across these different clades?

We partnered with iFyber (Ithaca, NY) to test representative strains from clades I, II, III, and IV. Clades V and VI were excluded since they are not prevalent in the US. The results showed minimal difference in MIC values between clades. (Figure 2) Whether the C. auris strain originated from South Asia, East Asia, Africa, or South America, regardless of its specific resistance profile, polyvantoin chlorine maintained consistent efficacy.

Beyond Candida auris: A Comprehensive Fungal Panel

To understand polyvantoin chlorine's full antifungal spectrum, we asked the NIAID PCS to expand our testing to include multiple Candida species and other clinically important fungi. The Fungus Testing Laboratory at the University of Texas Health Science Center (San Antonio, TX) conducted this testing according to rigorous CLSI M27 and M38 methodologies—the gold standards for antifungal susceptibility testing.

Once again, our polymer demonstrated remarkably consistent MIC values across the fungal species tested. (Figure 2) This consistency extended beyond just Candida species to include other pathogenic fungi that cause serious infections in immunocompromised patients.

Through three independent laboratories, multiple pathogen categories, resistant and susceptible strains, and different clades and species, the message was consistent: polyvantoin chlorine's efficacy doesn't depend on the pathogen's resistance profile.

Figure 2

The Nature-Inspired Science Behind Polyvantoin Chlorine

Your immune system has spent millions of years perfecting antimicrobial chemistry. When your neutrophils encounter invading microbes, they take chlorine from the salt in your bodily fluids and convert it into hypochlorous acid (HOCl). Some of that chlorine also attaches to an amino acid called taurine, producing taurine chloramine (TauCl).⁴

Both HOCl and TauCl are naturally occurring, broad-spectrum biocides that eliminate bacteria, fungi, and viruses by oxidizing the bonds holding a pathogen's cell wall together. This creates openings in the wall, causes cytoplasmic leakage, and leads to cell death.^5-7 Your body uses a carefully controlled chemical formulation to fight pathogens, making chlorine chemistry naturally biocompatible.

Unlike antibiotics that inhibit specific metabolic pathways (which pathogens can circumvent through genetic mutations), oxidative chemistry makes virtually no distinction between antibiotic-resistant and non-antibiotic-resistant pathogens.⁸ You can't easily evolve resistance to having your cell wall oxidized.

So why isn't everyone using TauCl or HOCl? The answer is stability. While TauCl can achieve high concentrations in solution and has shown success in human clinical trials for wound care and other indications, it requires constant refrigeration, making widespread use impractical. HOCl faces similar stability challenges at clinically relevant concentrations.^9,10

Polyvantoin Chlorine: Stabilized Oxidative Chemistry for Clinical Use

We start with a chloramine monomer, called Avantamine, that stabilizes chlorine, and then incorporate Avantamine into a polymeric delivery system to make polyvantoin chlorine. This reduces both skin irritation and neutralization in the presence of organic material compared to chlorine alone. Polyvantoin chlorine works through the same oxidative mechanism as HOCl and TauCl, and appears to preferentially oxidize negatively charged pathogenic cell walls over positively charged human cell membranes. But our polymer offers distinct advantages:

• Enhanced safety: It is not a skin irritant even at a 3.6% chlorine concentration

• Stability: It does not require refrigeration; it maintains efficacy over time

• Long-lasting activity: It provides residual protection on skin surfaces

• Format flexibility: It can be formulated as a liquid, as a solid in solution, or as a hydrogel at high concentrations

• Maintained efficacy: It demonstrates pathogen-killing activity nearly identical to bleach, without the toxicity

Addressing the Resistance Question

Given our MIC data, the obvious question arises: could pathogens eventually develop resistance to polyvantoin chlorine?

Based on the high in-use concentrations of polyvantoin chlorine and the complete absence of chlorine-resistant pathogens despite over a century of human use, we believe resistance development is highly unlikely. This isn't speculation; it's grounded in fundamental biology.

Bacteria can develop tolerance to oxidative stress through various mechanisms: efflux pumps, protein and nucleic acid repair systems, transcription factors, chaperones, detoxifying enzymes, and membrane modifications like downregulation of porins or increased hydrophobicity.^11-15 However, the oxidative potential of chlorine is so catastrophic to so many parts of a pathogen that resistance is unlikely, which is why our bodies chose this chemistry.

While some studies have shown potential for cross-resistance due to overexpression of efflux pumps,^12,15 a landmark study by Oggioni and colleagues is particularly instructive. They tested 1,632 clinical isolates of Staphylococcus aureus for the generation of cross-resistance by sodium hypochlorite. The conclusion? Cross-resistance generation was not concerning.¹⁶

The other tolerance mechanisms are relevant for low-concentration applications like water treatment, but they're rapidly overwhelmed by the higher concentrations used in antiseptic applications. This is a critical distinction that sets oxidative chemistry apart from traditional antibiotics.

More importantly, our consistent MIC data across resistant and susceptible strains provides evidence that existing resistance mechanisms don't protect pathogens from oxidative chemistry. Despite the presence of antibiotic resistance genes, efflux pumps, and other defense mechanisms, resistant strains show no increase in MIC values against our polymer.

The AMR Crisis: Why We Need a Different Approach

Antimicrobial resistance (AMR) is rapidly becoming one of the most pressing global health threats, driven by decades of antibiotic overuse and misuse.¹ True pan-resistant "superbugs" (pathogens resistant to every available antibiotic) have emerged in the United States with Candida auris and in Ukraine with Klebsiella pneumoniae.^2,3

Hospital-acquired infections cost the U.S. healthcare system over $41 billion annually in direct medical and societal costs. The WHO's 2025 Global Antimicrobial Resistance Surveillance report revealed that one in six laboratory-confirmed bacterial infections worldwide were resistant to antibiotic treatments.²⁴ The World Health Organization projects that by 2050, more people will die from drug-resistant pathogens than from cancer. Globally, antimicrobial resistance represents a $100 billion problem.

We desperately need new antibiotics, but we're confronting an uncomfortable truth: every new antibiotic will eventually fail, just as those before it have. Each new systemic antimicrobial creates evolutionary pressure on pathogens, driving resistance. It's not a question of if resistance will develop, but when.

In addition to new antibiotics, we need a fundamentally different approach. As Desiderius Erasmus observed in the 16th century: "Prevention is better than cure." Antiseptics can't treat systemic infections, but they can prevent infections from becoming systemic in the first place. 

The healthcare industry needs a better solution – one that's broad-spectrum, non-resistance-generating, long-lasting, and safe for repeated use on human skin. Our MIC data demonstrates that polyvantoin chlorine can be that solution.

Building a Future Where the Data Speaks for Itself

At AvantGuard, we believe in letting our science tell the story. The consistent MIC values across resistant and susceptible strains, across multiple pathogen categories, tested at three independent laboratories using rigorous methodologies—this data speaks to polyvantoin chlorine's potential more eloquently than any marketing claims could.

But data alone isn't enough. We need to translate scientific innovation into practical clinical solutions. We need to shift healthcare's approach from treating infections after they occur to preventing them before they start. We need to tackle the antimicrobial resistance crisis with tools that don't contribute to it.

That's why we developed polyvantoin chlorine. 

The question isn't whether we need new approaches to infection prevention; it's which approaches will prove effective, safe, and practical for widespread use. Our MIC data suggests our compound can be one of those groundbreaking approaches. 

The future of infection prevention is prevention itself. The future is here.

Contact AvantGuard

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References

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