Completed preclinical proof-of-concept

One treatment.
No detectable infection.

Chronic wound biofilms are built to survive. In a three-species chronic wound model, one in which no clinical therapy works, AURAs wipe out all bacteria after a single local treatment.

Complete Bacterial Elimination- roughly a million-fold reduction in bacteria across an infection containing P. aeruginosa, S. aureus and A. baumannii.

Dual microscopy images showing before and after AURA treatment
100%

average reduction in bacterial burden.

1×

AURA-plus-ultrasound treatment produced the full response.

3

WHO priority pathogens together in one wound.

95%

of experimental treatments failed to resolve the infection.

Built to perform where treatment breaks down

We've only tested against the toughest models. Clinical bacteria, mixed-species, dense necrotic material, and resistance spreading inside the wound. Testing the limits of our treatment against the limits of biology.

Untreated and free-drug wounds stayed heavily infected. AURAs plus ultrasound did not.

AURAs plus ultrasound produced an average 99.9999% reduction in the number of bacteria with no bacterium left detected. Antibiotic alone, at the same dose, had little effect.

High burden
Untreated
High burden
Free drug
Below LoD
AURA + US
550×

Through the hard stuff

Inside a dense necrotic wound, AURAs plus ultrasound cut bacterial counts 550-fold compared with the same dose of free antibiotic.

Why this is a tougher test

Necrotic tissue and hard eschar can seal bacteria beneath a compact transport barrier. This model asks whether the treatment can work beyond the easy-to-reach wound surface.

99.99%

Resistance moved. The effect held.

Even after bacteria exchanged a resistance plasmid inside the wound, AURAs plus ultrasound delivered a 133-fold reduction at 24 hours and a 4-log reduction by 48 hours.

The hard comparator

A 100-fold higher encapsulated-drug concentration without effective ultrasound activation failed to clear the infection, which regrew by 48 hours.

24 h

Releasing the wound from immune gridlock

Once the biofilm was cleared, immune-cell and cytokine profiling showed the wound shifting away from the distorted inflammatory state associated with chronic infection.

How we measured it

The team used high-dimensional flow cytometry and local cytokine analysis to map how the wound's immune landscape changed after treatment.

Why antibiotics lose

Biofilms turn bacteria into a fortified ecosystem.

A biofilm is a living ecosystem built by bacteria. Its polymer-rich matrix slows antibiotics, shelters dormant persister cells, connects multiple species and creates a crowded arena where resistance genes can spread.

Diagram showing the mechanisms of biofilm resilience
01The matrix blocks the route in

The extracellular polymeric substance (EPS) can trap, bind, and slow antibiotics before they reach bacteria buried deep inside the community.

02Dormant cells wait out the attack

Many antibiotics work best on metabolically active cells. Persisters and viable-but-nonculturable cells can drop into low-activity states, survive treatment and restart the infection later.

03Mixed species make a tougher colony

Real chronic wounds contain an average of 5 species living together. Their shared chemistry and architecture can make the community more resilient than any one species grown alone.

04Resistance genes move through the crowd

Inside the dense community, neighbouring bacteria can exchange plasmids by horizontal gene transfer, passing resistance from one cell, and even one species, to another.

Peer-reviewed science

The platform does more than carry antibiotics. It changes where they go.

In a 2025 peer-reviewed study, four different types of AURAs with different antibiotic classes were tested against clinical isolates, mature biofilms and dormant persister cells. Ultrasound was the switch that converted delivery into potency.

44.4×

Less drug needed to eradicate mature biofilms

Across the tested drug–isolate combinations, ultrasound-activated AURAs cut the concentration required to eradicate culturable bacteria in mature biofilms by an average of 44.4-fold versus free drug.

25.5×

Less drug needed to eliminate persisters

AURAs plus ultrasound reduced the concentration needed to eliminate dormant persister populations by an average of 25.5-fold. Targeting the cells most likely to survive and cause recurrence.

11.1×

More antibiotic inside the bacterial cytoplasm

Subcellular analysis found 11.1-fold more antibiotic in where the drug needs to go than after treatment with unencapsulated drug.

We stress-tested the reasons chronic infections come back.

A powerful result is only useful if it survives harder questions. We asked whether the matrix physically breaks, whether treatment reaches dense necrotic material, whether resistance defeats it, whether clearance lasts and what happens to the wound's immune state afterwards.

Architecture

Did the biofilm actually break?

Confocal microscopy visualised the loss of mature biofilm architecture after ultrasound activation—direct evidence that the platform acts on the physical structure, not only the bacterial count.

Why the image matters

Counting bacteria tells us who survived. Confocal imaging tells us whether the fortress itself was dismantled.

Depth

Could it work beneath the surface?

A compact clot-transplant model created a dense, necrotic barrier. AURAs plus ultrasound produced a 4-log-scale response and a 550-fold advantage over dose-matched free drug.

Why depth changes the problem

Chronic infections are three-dimensional. Protected bacterial pockets can remain beneath the visible surface even when the top of a wound looks cleaner.

Resistance

What happens when bacteria share resistance?

AURAs retained strong log-reduction activity after bacteria exchanged a resistance plasmid inside the wound. High-dose encapsulated drug without effective activation failed to maintain clearance.

Inside the model

The consortium allowed A. baumannii to pass a resistance plasmid to P. aeruginosa, raising the antibiotic-resistance threshold while the infection was already established.

Durability

Did the infection rebound?

The resistant-infection model moved from a 133-fold reduction at 24 hours to a 4-log reduction at 48 hours, deepening the response instead of rebounding.

Why the second timepoint matters

Biofilms can regrow from a small surviving population. The 48-hour readout tests whether early killing holds once the immediate treatment window has passed.

Host response

What happened after the biofilm was cleared?

After treatment, immune profiling showed the wound moving away from the dysfunctional inflammatory state associated with chronic biofilm infection and towards a more repair-associated profile.

Chronic inflammatory signature
Reduced
Repair-associated profile
Increased

AURAs

Antibiotic-loaded ultrasound-responsive agents: proprietary particles that carry antibiotic and activate under ultrasound.

Biofilm

A structured community of microorganisms embedded in a self-produced polymer matrix.

Log reduction

A logarithmic measure of killing. Each log is a tenfold fall; 6 logs is approximately one million-fold.

Limit of detection

The smallest bacterial burden the assay can reliably measure. Below this point, no bacteria were recovered by the method used.