PRESERVE THE TISSUE. PROTECT WHAT MATTERS.

The science of preserving tissue during ischemia reperfusion injury

Waventra develops long half-life HGF mimetics designed to preserve microvascular integrity, stabilize stressed tissue and reduce ischemia reperfusion injury when administered early in acute care.

WHY ISCHEMIA REPERFUSION INJURY MATTERS

Ischemia damage

Reduced blood flow deprives tissue of oxygen and nutrients, causing metabolic stress and cellular injury

Reperfusion injury

Reperfusion restores oxygen but can also trigger endothelial dysfunction, capillary obstruction, inflammation and microvascular collapse that extend tissue injury beyond the initial ischemic event.

Why infarct size matters

Larger infarcts are strongly associated with heart failure, arrythmias, hospitalization and mortality

HGF AS A SURVIVAL SIGNAL

Hepatocyte growth factor is the natural ligand for c-MET that mobilizes endogenous survival pathways to protect, stabilize and restore tissue

Preserves endothelial barrier integrity

Supports microvascular survival and perfusion

Limits inflammatory amplification and reperfusion mediated injury signaling

Promotes survival and regenerative programs

PI3K PATHWAY

Survival – cytoprotection – metabolism

STAT3 PATHWAY

Anti-inflammation – angiogenesis – tissue repair

HGF signaling is protective but transient.WAV-301 is engineered for durability and early action.

HOW WAV-301 WORKS

INTERVENE DURING TISSUE SALVAGE WINDOW

Administer WAV-301 during evolving ischemic injury and before reperfusion

STABILIZE THE MICROVASCULATURE

Activate c-MET signaling to support endothelial integrity, perfusion and survival pathways

REDUCE SECONDARY TISSUE LOSS

Limit reperfusion related injury progression, infarct expansion and downstream remodeling

Administered before PCI, WAV-301 protects the endothelium and arrests the wavefront of reperfusion injury before it spreads. Preserve more now; improve recovery later.

PROTECTS THE MICROVASCULATURE

Preserve endothelial integrity and capillary perfusion to reduce no-reflow and microvascular obstruction after reperfusion

CONTROLS PROGRAMMED CELL DEATH

Limits apoptosis and necrosis in stressed but salvageable cells.

REDUCES REMODELING AND FIBROSIS

Mitigates adeverse remodeling and preerves long term organ function.

EXTENDS THE THERAPEUTIC WINDOW

Long half-life molecules provide sustained activity during the critical period of tissue recovery.

Much of the tissue at risk during acute ischemia is stressed but not yet irreversibly lost

Early targeted intervention can preserve what matters most

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