Breaking the building blocks fungi depend on.

MycaZED targets chitin synthesis — a structural pathway fungi use to construct and reinforce their cell walls, and one current systemic antifungals do not target.

MURINE + CANINE EFFICACY
HUMAN SAFETY · 40 VOLUNTEERS
PHASE 2 DEVELOPMENT PATH
01 · The clinical need

Modern medicine extends survival. It also expands vulnerability to severe fungal disease.

An estimated 6.5 million invasive fungal infections occur each year. As more patients survive life-threatening illness and intensive treatment, more live with the immune compromise, damaged lungs, and physiologic vulnerability that serious fungi exploit. Resistance, toxicity, drug interactions and limited treatment options can then turn fungal infection into a major complication of already complex care.

ONCOLOGY & HEMATOLOGY
TRANSPLANTATION
CHRONIC LUNG DISEASE
CRITICAL ILLNESS
02 · The treatment gap

Different drugs. Too few targets.

Azoles

Block ergosterol synthesis. Foundational therapy, with clinically important resistance in major pathogens.

Polyenes

Bind fungal membrane sterols. Broad activity, but toxicity can constrain use.

Echinocandins

Target β-glucan synthesis. Important agents, but not a complete answer across yeasts and moulds.

Emerging agents

Add needed options, while serious fungal disease still depends on a relatively narrow set of biological pathways.

Resistance can compromise drugs within a class — and some pathogens arrive resistant to multiple classes. At the same time, antifungal development has lagged the growing clinical need, leaving a narrow therapeutic toolbox for increasingly complex patients.

That gap is attracting renewed attention from specialist developers, public-health programs and non-dilutive funding channels.

03 · The mechanism

Disrupt the fungal wall at its scaffold.

Fungi use chitin to construct and reinforce their cell walls. MycaZED inhibits the enzyme that synthesizes this structural scaffold — a target humans do not possess and current systemic antifungals do not use. Disrupting it weakens the fungal wall and creates a mechanistically distinct route to antifungal activity.

Stable fungal cell wall
Intact chitin scaffold
→
Disrupted fungal cell wall
Disrupted chitin scaffold
Orthogonal, fungal-specific target
Immune clearance via fungicidal activity*
*Demonstrated in the lead Valley Fever evidence package.
04 · Platform maturity

Twenty years of de-risking. A platform already expanding.

Animal efficacyMurine and naturally infected canine evidence in the lead program.
Human safetySingle- and multiple-dose Phase 1 safety/PK studies completed in 40 volunteers.
Regulatory progressOrphan drug and QIDP designations support the lead Valley Fever development path.

One differentiated antifungal mechanism, advancing across multiple serious fungal pathogens.

ProgramRole in the platformEvidence positionStageNext value inflection
Valley Fever / CoccidioidomycosisMost mature translational proof for the platform.Animal efficacy; human safety/PK; established regulatory history.Clinical-stageGenerate human efficacy data in the lead indication.
Invasive AspergillosisExpansion into high-need invasive mould disease.Mechanistic and preclinical evidence.PreclinicalComplete IND-enabling and regulatory work.
Invasive Candidiasis / C. aurisExpansion into invasive yeast disease and multidrug resistance.Preclinical program; evidence strength varies by species and model.PreclinicalPrioritize indication and build the translational package.
Platform extensionsAdditional fungal diseases where chitin biology and unmet need align.Evidence mapping and prioritization.ResearchSelect programs with a defensible biological and development rationale.

The platform is being advanced indication by indication, matching biological evidence with clinical need and a credible development path.

05 · Development milestones

Advance the programs. Expand the platform.

The next stage converts prior safety and translational work into two meaningful value inflections: human efficacy in the lead program and IND readiness for the first invasive-fungal expansion. Together, those milestones strengthen the platform for strategic and non-dilutive development partnerships.

Lead program

Human efficacy

Move the most mature program from completed Phase 1 work toward a controlled clinical efficacy readout.

Platform expansion

Aspergillus IND readiness

Complete the preclinical, regulatory, and product-development work required to define a credible clinical path in invasive aspergillosis.

Follow-on leverage

Partnerable milestones

Use clearer clinical and regulatory evidence to support larger non-dilutive programs and strategic development discussions.

06 · Collaboration

Different partners solve different development constraints.

MycaZED is building relationships around defined clinical and regulatory milestones — not a generic ecosystem story.

Institutional investors

Capital matched to clinical and regulatory value inflections.

Patient advocacy groups

Patient priorities, disease awareness, and trial-community engagement.

Fungal care centers & hospitals

Clinical expertise, trial sites, and access to difficult-to-treat populations.

Strategic & non-dilutive partners

Translational collaboration, grant-supported development, and downstream partnering.

07 · Team

Antifungal science, clinical development, and regulatory execution.

David Larwood, PhD JD MBA

Founder & CEO

Twenty years advancing the asset through NIH-funded development, formulation, and regulatory strategy.

John Galgiani, MD

Co-founder

Founder of the University of Arizona Valley Fever Center for Excellence and a leading coccidioidomycosis authority.

Roger Echols, MD FIDSA

Chief Medical Officer

Anti-infective clinical and regulatory experience across 15 drug approvals.

Lucia Mokres

Operating & clinical leadership

Senior pharmaceutical operating and clinical leadership.

MycaZED Therapeutics

Moving antifungal treatment from suppression toward resolution.

A distinct antifungal target. A human-tested lead program. A platform advancing across serious fungal disease.