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Addressing Life-Threatening Diseases

Sepsis is the leading cause of death worldwide, affecting 49 million patients and claiming the lives of 11 million people each year. Eliaz Therapeutics aims to keep families together and transform outcomes through targeted innovation.

THE PROBLEM

Sepsis is the #1 Cause of
ICU Death Worldwide

And there are currently no approved, effective therapeutic interventions – yet.

High ICU
Prevalence

Sepsis affects 30-50% of all patients in intensive care units.

The Fatal
Complication

Sepsis-induced Acute Kidney Injury (SA-AKI) doubles mortality rates to over 50%.

Global 

Mortality

Sepsis kills 11 million each year – and the numbers are rising.

Economic 

Burden

Sepsis costs the US healthcare system over $62B annually in direct medical cost alone.

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Supportive Care is not Effective Enough

Patients with sepsis face estimated mortality rates of up to 30%, rising to over 60% in critically-ill patients requiring dialysis — yet current treatments are limited to primarily managing symptoms with fluids and antibiotics.

Galectin-3: A Key Driver of Life-Threatening Disease

Galectin-3 is a protein naturally produced by the body in response to injury, but in critical conditions, becomes a "master switch" that drives systemic inflammation and organ failure.

Galectin-3
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From Protective to Pathologic
Galectin-3 supports normal immune response, but at elevated levels becomes a driver of uncontrolled inflammation.
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Systemic Impact in Sepsis
Sustained activation contributes to vascular damage, organ failure, and rapid clinical deterioration.
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Unaddressed Root Cause
Current treatments manage symptoms but do not remove Galectin-3.
Introducing A Different Approach:

The XGAL-3® device

Targeted Removal

Designed to selectively remove Galectin-3

Therapeutic Apheresis

Blood is processed outside the body and returned to circulation

Proprietary Resin

Antibody-based resin engineered to bind Galectin-3

How it Works

Mechanism of Action
XGal-3® in Treatment

1

Blood Extraction

Blood enters the apheresis device circuit from the patient via a central line or dialysis access.

2

Galectin-3 Binding

XGal-3® binds circulating Galectin-3 within the device column.

3

Filtered Blood Return

Filtered blood returns to the patient with reduced levels of circulating Galectin-3.

Mechanism of Action XGal-3® in Treatment

Broader Technology
Potential

XGal-3® is designed as a platform technology for the selective removal of circulating Galectin-3, which is implicated in multiple inflammatory and fibrotic processes.*

Galectin-3
Galectin-3
Fibrosis
Drives fibrotic pathways in multiple organs
Sepsis
Amplifies inflammation and immune dysregulation
Cancer
Promotes tumor progression, immune evasion and metastasis
Heart Disease
Associated with cardiac fibrosis, remodeling and heart failure
Acute Kidney Disease
Linked to inflammation, fibrosis and poor outcomes

How XGal-3® Compares to Pharmacologic Intervention 

Pharmacologic Intervention
XGal-3® Apheresis*

Acts through systemic pharmacologic mechanisms

Extracorporeal removal of circulating Galectin-3

Systemic exposure 
(potential for off-target effects)

No systemic drug 
exposure

Effects depend on 
pharmacokinetics and dosing

Direct removal during the apheresis procedure

Onset may vary

Reduction occurs during the procedure

*XGal-3® is an investigational device and has not been evaluated in human interventional clinical trials. Comparisons are based on general characteristics of pharmacologic therapies and extracorporeal approaches and do not imply clinical outcomes.

Program Status

clinical development

Regulatory

Regulatory

FDA Breakthrough Device Designation (Awarded 2025).

Technical

Technical

Functional prototype completed; Verification & Validation (V&V) in progress.

Clinical

Clinical

Observational diagnostic clinical study enrolling; Preparation for GLP safety studies and First-in-Human evaluation.