Improved Iron Overload with Pegcetacoplan in Eculizumab-Experienced Patients with Paroxysmal Nocturnal Hemoglobinuria

Jamile Shammo1, Peter Hillmen2, Peter Blandino2

  • 1Feinberg School of Medicine, Northwestern University, Chicago, IL 60612, USA.

Complement factor 5 (C5) inhibitors for paroxysmal nocturnal hemoglobinuria (PNH) may cause iron overload due to residual intravascular hemolysis (IVH) and emergent extravascular hemolysis (EVH). In PEGASUS (phase 3; NCT03500549), adults with PNH with residual anemia (hemoglobin concentration < 10.5 g/dL) after ≥3 months of eculizumab received eculizumab and pegcetacoplan for 4 weeks and were then randomized (1:1) to eculizumab or pegcetacoplan monotherapy for 16 weeks; in the following 32-week, open-label period, patients either continued pegcetacoplan or switched from eculizumab to pegcetacoplan. This post hoc analysis reports PEGASUS transfusion-related data and iron-related biomarkers to evaluate pegcetacoplan's effects on iron regulation. Of 80 patients randomized in PEGASUS, 27 (33.8%) had baseline iron overload (serum transferrin saturation ≥ 50%). Iron overload resolved within 52 weeks of pegcetacoplan treatment in 16 of 22 patients (72.7%) with baseline and postbaseline data; 10 experienced resolution after 20 weeks. With pegcetacoplan, transfusion numbers decreased for patients with and without iron overload, hepcidin concentrations increased, and absolute reticulocyte counts (ARCs) decreased to normal range. Mean ferritin concentrations were above normal throughout the study, regardless of iron overload status. Pegcetacoplan improves iron overload-related biomarkers, including increased hepcidin concentrations and decreased ARCs, by blocking IVH and EVH and preventing anemia.

Related Concept Videos

Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers01:26

Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers

Receptor tyrosine kinase inhibitors (TKIs) and calcium channel blockers (CCBs) are two critical categories of drugs employed in the treatment of pulmonary artery hypertension (PAH). PAH is a disease that causes high blood pressure in the pulmonary arteries, resulting in chest pain, fatigue, and shortness of breath.
TKIs, such as imatinib (Gleevec), are particularly effective in tackling the growth and mitogenic factors that become upregulated in PAH patients. These factors contribute to the...
429
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists01:23

Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists

Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
452
Pulmonary Embolism II: Diagnostic Studies and Interprofessional Care01:29

Pulmonary Embolism II: Diagnostic Studies and Interprofessional Care

Diagnosing Pulmonary EmbolismDiagnosing pulmonary embolism (PE) involves clinical assessment and advanced imaging tests. The preferred diagnostic tool is the spiral (helical) CT scan or CT angiography (CTA), which uses intravenous contrast media to visualize the pulmonary vasculature and identify emboli.A ventilation-perfusion (V/Q) scan is an alternative for patients unable to receive contrast media. This scan includes both perfusion and ventilation scanning. Perfusion scanning involves...
308
Antiepileptic Drugs: Potassium Channel Activators01:20

Antiepileptic Drugs: Potassium Channel Activators

Ezocgabine or retigabine, an antiepileptic drug of remarkable efficacy, has revolutionized the management of seizures. It is a potassium channel activator, explicitly targeting the family of Q subtype potassium channels. It enhances the transmembrane potassium currents, regulating neuronal excitability. This action stabilizes the resting membrane potential, a pivotal factor in mitigating the hyperexcitability that characterizes epilepsy.
Ezogabine has gained approval as an adjunctive treatment...
624