The Science of DH2

THE PROBLEM

Ischemia-Reperfusion Injury

To transplant an organ, the blood flow must be stopped. When blood flow is restored, the tissue is overwhelmed and produces toxins that injure the tissue. IRI is the leading cause of organ failure, dysfunction, and discarding in transplantation.

TREATMENT APPROACH

DIATOMIC HYDROGEN THERAPY

DH2 delivers a proprietary dissolved hydrogen based gaseous mix directly to the organ during preservation and transport. Hydrogen neutralizes the main toxin produced by IRI, the hydroxyl radical.

CLINICAL EVIDENCE

PRECLINICAL STUDY RESULTS

DH2 has been demonstrated to be superior to standard therapy in sponsored large animal studies at the Texas Heart Institute at Baylor College of Medicine and the Center for Translational Transplant Studies at Western University, with results presented at international meetings and published in peer-reviewed literature.

the problem

ischemia-reperfusion injury

Ischemia-reperfusion injury (IRI) occurs when blood flow is restored to an oxygen-deprived organ. The reintroduction of oxygen triggers a cascade of oxidative damage that can compromise or destroy the tissue being preserved. IRI affects every transplanted organ, including those from otherwise healthy donors.

It is the primary cause of primary graft failure, early graft dysfunction, and organ discard, and a significant contributor to long-term transplant complications. Current preservation solutions were developed in the 1980s and do not address IRI directly.

 OXIDATIVE STRESS

Reperfusion triggers a surge of reactive oxygen species, particularly the hydroxyl radical, which overwhelms the organ's antioxidant defenses and damages cell membranes, proteins, and DNA.

 INFLAMMATION      

Oxidative stress activates downstream inflammatory pathways, increasing cytokine expression and immune cell recruitment that compound the initial injury.

 CELL DEATH  

Sustained oxidative and inflammatory insult triggers apoptosis and necrosis within the graft, reducing organ viability and increasing the risk of long-term dysfunction.

The Scope of the Problem
103,223
Patients currently awaiting a transplant in the US
1.5M+
Patients with end-stage organ failure not yet on the waitlist
62%
Of donated organs discarded, frequently due to ischemia-reperfusion injury
20 / day
People who die each day while waiting for a transplant
40+ Yrs
Since the last major innovation in organ preservation solutions
$3.15B
Projected global IRI therapeutics market by 2030

TREATMENT APPROACH

DIATOMIC HYDROGEN PRESERVATION

Diatomic DH2 is an organ preservation additive that delivers dissolved diatomic hydrogen (H₂) directly to the organ during the standard flushing and preservation process performed at organ recovery. It is formulated to be added to existing preservation solutions already used in standard transplant protocols.

DH2 is compatible with all organ types and all preservation methods, including static cold storage and hypothermic machine perfusion. It does not require new equipment or changes to the surgical team's existing workflow.

Preservation solutions have remained largely unchanged since the introduction of UW and HTK solutions in the 1980s. DH2 is designed to address the mechanism of injury those solutions do not target.

Mechanism of Action

How DH2 Works

Diatomic hydrogen (H₂) is the smallest known molecule. Its size allows it to diffuse rapidly across cell membranes and reach intracellular targets, including mitochondria, more efficiently than conventional antioxidants.

Step 1 – Trigger
OH•

Reperfusion generates a surge of hydroxyl radicals, the primary mediator of oxidative injury in IRI.

→
Step 2 – Delivery
H₂

DH2 delivers dissolved diatomic hydrogen to the organ during preservation and transport.

→
Step 3 – Reaction
H₂O

H₂ enters the mitochondria, reacts with hydroxyl radicals, and forms water as a byproduct.

→
Outcome
IRI Reduced

The oxidative cascade is interrupted, reducing injury to the graft during reperfusion.

Key Properties
Selective H₂ reacts preferentially with hydroxyl radicals without disrupting other physiological redox processes.
Highly Permeable As the smallest known molecule, H₂ crosses cell membranes and reaches mitochondria rapidly.
Anti-Inflammatory Modulates NF-kB signaling and reduces downstream cytokine expression.
Anti-Apoptotic Attenuates pro-apoptotic signaling pathways activated by oxidative stress.
Diagram illustrating the mechanism of action of diatomic hydrogen in organ preservation
Preclinical Evidence – Cardiac

Cardiac Preservation Study

Research conducted at the Texas Heart Institute at Baylor College of Medicine, Houston, TX. Large animal model: 6 porcine heart transplants. Control: HTK Solution (current standard of care for cardiac preservation).

The heart is the most time-sensitive organ in transplantation. Standard cold storage limits safe ischemic time to approximately four hours, constraining both geography and donor eligibility. This study evaluated DH2 at seven hours of cold storage, beyond the current practical limit.

Ejection Fraction

Left ventricular ejection fraction is a primary measure of cardiac function. Hearts preserved with HTK solution showed approximately 50% reduction in ejection fraction following transplantation, consistent with ischemia-reperfusion injury.

Hearts preserved with DH2 maintained ejection fraction within normal range at seven hours of cold ischemia.

Wall Motion Assessment

Echocardiographic assessment showed extensive regions of microvascular dysfunction and wall thickening in HTK-preserved hearts, consistent with reperfusion injury affecting multiple myocardial segments.

DH2-preserved hearts showed uniform wall motion with no significant regional abnormalities.

Histological Analysis

HTK-preserved hearts showed contraction band necrosis and myocyte dissolution on histological review, findings consistent with severe, irreversible reperfusion injury and elevated risk of primary graft failure.

DH2-preserved hearts showed minimal histological injury, with myocardial architecture preserved throughout.

Preclinical Evidence – Renal

Kidney Preservation Study

Research conducted at the Center for Translational Transplant Studies, Western University, London, Ontario. 12 porcine kidneys. Ex-vivo hypothermic machine perfusion system. Control: UW Solution (current standard of care for kidney preservation).

Kidneys donated after cardiac death (DCD) represent a high-risk subgroup in transplantation. Reperfusion injury following DCD procurement is a significant contributor to delayed graft function, increased rejection risk, and higher post-transplant care costs. This study evaluated DH2 against UW solution under these conditions.

Post-Reperfusion Kidney Function

URINE PRODUCTION (mL) 0 500 1000 1500 2000 2500 3000 3500 4000 4500 p<0.01 UW DH2 CREATININE CLEARANCE (mL/min) 0 2 4 6 8 10 12 p<0.01 UW DH2

Four hours post-reperfusion, urine production and creatinine clearance are established early indicators of kidney graft function.

Kidneys preserved with UW solution (standard of care) showed low output on both measures, caused by severe ischemia-reperfusion injury.

Kidneys preserved with DH2 showed significantly higher urine output and creatinine clearance than UW controls, indicating prevention of ischemia-reperfusion injury.

Acute Tubular Necrosis and Inflammation

Acute tubular necrosis (ATN) is a direct histological consequence of ischemia-reperfusion injury and a primary pathological driver of delayed graft function. UW-preserved kidneys showed severe ATN on histological review.

DH2-preserved kidneys showed only minor, focal tubular injury. Immunohistochemical analysis also demonstrated significantly reduced expression across multiple inflammatory and oxidative stress markers:

IL-6 CD68 MPO MDA TUNEL
Histological images comparing kidney tissue in UW vs. DH2 preserved kidneys

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