Seattle, WA

Making new drugs for bad bugs.

Developing next-generation antimicrobials.

Drug-resistant infections are making routine surgeries, cancer treatments, and minor injuries dangerous again. Marva Labs develops therapies that speak bacteria's native language and signal them to self-destruct.

See the science Request executive summary

Making new drugs for bad bugs · Developing next-generation antimicrobials · Making new drugs for bad bugs · Developing next-generation antimicrobials ·

Redefining infection control as negotiation instead of warfare. Marva Labs is pioneering cooperative biology: the foundation of post-antibiotic medicine.

The problem

Antimicrobial resistance is the single greatest threat to humanity.

1.27M

Deaths directly attributed to AMR worldwide in 2019. Nearly 5M more deaths were associated with drug-resistant infections.

2.8M+

AMR infections occur annually in the U.S. alone, resulting in more than 35,000 deaths.

$4.6B

Spent each year in U.S. healthcare costs treating just six of the most concerning AMR threats.

$159B

Projected additional global healthcare costs annually by 2050 if current AMR trends continue.

By 2050, unless something changes

4.71M deaths / year linked to drug-resistant infections

Up 75% from 4.71M in 2021. Deaths directly attributable to resistance climb too, from 1.14M to 1.91M annually.

Source: Naghavi et al., The Lancet, 2024

How resistance happens

Bacteria have always won this arms race.

Every antibiotic creates selective pressure, and bacteria have spent billions of years evolving ways around it. Five mechanisms do most of the work, and one of them, biofilms, makes all the others worse.

Mutation & selection

Random mutations let a few cells survive exposure. Those survivors multiply while the drug clears out everything else.

Gene transfer

Resistant bacteria hand off their defenses directly to neighboring cells, even across different species.

Efflux pumps

Molecular pumps in the cell membrane physically eject the antibiotic before it reaches a lethal concentration.

Drug inactivation

Enzymes chemically disarm the antibiotic itself, breaking it apart before it can do any damage.

Target modification

Bacteria subtly reshape the exact molecule a drug is designed to bind to, so the drug simply doesn't fit anymore.

Biofilms

Bacteria build a shared protective matrix that blocks drug penetration, shelters dormant "persister" cells, and speeds up gene sharing between neighbors, compounding every mechanism above. This is where Marva Labs focuses.

Our thesis

We're not racing to build a better weapon.

The consensus

Invent new antibiotics: new chemistries, new targets, fast enough to outrun resistance.

Our belief

Bacteria already have the machinery to coordinate growth and death. We hijack it instead of out-inventing it.

Platform

At Marva Labs, we signal bad bugs to self-destruct.

The failure point

Biofilms are why antibiotics stop working.

80%+ of microbial infections in the body involve a biofilm

78.2% of chronic wounds have an associated biofilm

$5T+ in annual global economic impact from biofilm-related failure

Source: Cámara et al., NPJ Biofilms and Microbiomes, 2022

At Marva Labs, we're pioneering a novel antimicrobial platform that exploits bacterial communication systems to induce self-destruction. Our flagship product, EndoVox™, uses death-phase extracellular vesicles (D-EVs) to deliver native microbial signals that trigger ferroptosis, an iron-dependent oxidative death pathway. The name comes from endo-, meaning "within," and vox, meaning "voice." Unlike conventional antibiotics, which the biofilm matrix physically blocks, D-EVs are built from the same material as the biofilm itself, giving them privileged access other drugs don't have. It's a Trojan horse: the pathogen's own communication system, turned against it from within.

Native signaling

D-EVs deliver a pathogen's own death-phase signals back to it, including deep inside biofilm colonies where conventional antibiotics can't reach.

Redox disruption

Silences quorum sensing while enhancing reactive oxygen species (ROS) production, destabilizing the pathogen's redox balance from within.

Self-destruction

Triggers ferroptosis, an iron-dependent oxidative death pathway that causes the pathogen to dismantle itself from within.

Pipeline

One platform. Every biofilm battleground.

One EV delivery platform, deployed differently for every biofilm we target: from EndoVox™'s native signaling to Xanthos™'s targeted antibiotic delivery. Here's where each program stands today.

Chronic Wounds & Diabetic Foot Ulcers Discovery Lead candidate Preclinical Phase 1 Phase 2 Phase 3

EndoVox™ was validated in vivo: >3.5-log bacterial reduction and >30% improved wound healing in a murine model. Advancing toward IND-enabling studies.

Surgical Site Infections (SSI) Discovery Lead candidate Preclinical Phase 1 Phase 2 Phase 3

Introducing Xanthos™, our second platform product: bacterial EVs loaded with conventional antibiotic payloads, restoring their efficacy through direct, site-specific delivery to topical infections and sparing patients the side effects of systemic antibiotics.

Cystic Fibrosis (CF) Discovery Lead candidate Preclinical Phase 1 Phase 2 Phase 3

Early exploration of D-EV delivery against chronic P. aeruginosa biofilms colonizing the CF airway.

Candida auris & Fungal Biofilms Discovery Lead candidate Preclinical Phase 1 Phase 2 Phase 3

Early-stage work applying native signaling against drug-resistant fungal biofilms, including Candida auris. We're also now extracting fungal-derived EVs directly, extending the platform beyond bacterial vesicles.

Bacterial Canker (Agriculture) Discovery Lead candidate Preclinical Phase 1 Phase 2 Phase 3

Testing the EV platform as a foliar spray for high-value perennial stone fruit crops, where bacterial canker causes significant yield loss. It's an extension of Marva's platform from human health into agriculture.

Traction