FOCUSED ON THE DEVELOPMENT OF TRANSFORMATIVE THERAPIES FOR THE TREATMENT OF :
Worsening heart failure
Hyponatremic acute heart failure
Worsening heart failure
Worsening heart failure
Worsening heart failure
AVP
Biology
Elevated circulating vasopressin has been reported in heart failure (HF) patients and in preclinical HF models. High vasopressin levels contribute to
- Deterioration of cardiac function through V1a receptor
- Systemic congestion and hyponatremia through V2 receptor
- Glucose metabolism impairment and increased sympathetic tone through its third receptor V1b.
Strategy
In order to inhibit the full spectrum of vasopressin activity, its 3 receptors (V1a, V1b and V2) should be equally blocked to avoid the overstimulation of an unblocked receptor subtype. This has not been achieved with small molecule receptor antagonist approach. The alternative strategy we are pursuing is to selectively neutralize vasopressin with a human monoclonal antibody that will suppress activation of the 3 receptor subtypes. The expected rapid benefit would be the restoration of normal natremia in these AHF patients with the reduction of intravascular and tissue congestion.
