Disease Domain | Count |
---|---|
Endocrinology and Metabolic Disease | 4 |
Hemic and Lymphatic Diseases | 2 |
Nervous System Diseases | 1 |
Top 5 Drug Type | Count |
---|---|
Biological products | 2 |
Fc fusion protein | 2 |
Recombinant protein | 2 |
Antibody | 1 |
Target |
Mechanism ACVR2A modulators |
Active Org. |
Originator Org. |
Active Indication |
Inactive Indication |
Drug Highest PhasePhase 3 |
First Approval Ctry. / Loc.- |
First Approval Date- |
Target |
Mechanism ACVR2B modulators [+1] |
Active Org. |
Originator Org. |
Active Indication |
Inactive Indication |
Drug Highest PhasePhase 2 |
First Approval Ctry. / Loc.- |
First Approval Date- |
Target |
Mechanism Activin A inhibitors [+2] |
Active Org. |
Originator Org. |
Active Indication |
Inactive Indication- |
Drug Highest PhasePhase 1 |
First Approval Ctry. / Loc.- |
First Approval Date- |
Start Date01 Jun 2025 |
Sponsor / Collaborator |
Start Date14 Nov 2024 |
Sponsor / Collaborator |
Start Date20 Jun 2024 |
Sponsor / Collaborator |
Cardiac complications, including myocardial injury and dysfunction, are common in severe viral respiratory infections (VRI) and are associated with increased mortality1–3. The pathophysiology of VRI-induced myocardial injury is multifactorial, but frequently involves structural damage to the heart’s microvascular network that leads to subsequent myocardial ischemia and dysfunction4–6. Currently, there are no targeted therapies available to prevent or attenuate VRI-associated myocardial injury. Moreover, the molecular mechanisms driving the cardiac microvascular pathology in severe VRI are largely unclear. In this study, we identify increased endothelial cell (EC) activin type IIA receptor (ActRIIA) signaling as a key mediator of cardiac microvascular injury and pathologic remodeling in severe VRI. We show that genetic deletion of EC ActRIIA is sufficient to mitigate EC death and myocardial capillary loss in a murine model of severe influenza infection, which results in improved myocardial perfusion, cardiac function, and survival. We then provide proof-of-concept evidence for two novel pharmacological approaches to target EC ActRIIA pathophysiology in the treatment of VRI-induced cardiac dysfunction.
Drug(Targets) | Indications | Global Highest Phase |
---|---|---|
Elritercept ( ACVR2A ) | Myelodysplastic Syndromes More | Phase 3 |
KER-065 ( Activin A x MSTN x TGF-β ) | Obesity More | Phase 1 |
RKER-216 ( ALK2 ) | Iron-Refractory Iron Deficiency Anemia More | Preclinical |
Musculoskeletal(Keros Therapeutics) | Musculoskeletal Diseases More | Preclinical |
KER-034 ( Activin A x TGF-β ) | Obesity More | Preclinical |