Study Highlights Momelotinib as a Promising Alternative for Myelofibrosis With Anemia
A real-world study highlights the benefits of momelotinib (MMB) as an effective treatment option for patients with myelofibrosis (MF) and anemia, particularly those who have received prior JAK inhibitor therapy. The findings suggest that MMB, a first-in-class inhibitor of activin A receptor type 1, JAK1, and JAK2, provides significant anemia improvements while also addressing disease-related symptoms and spleen enlargement.
The multicenter, observational, retrospective study, conducted in Spain, analyzed 154 patients with MF who received MMB through a managed-access program between March 2023 and July 2024. Among the participants, 26 received MMB as a first-line treatment, while the remaining 128 had previously received other therapies, including ruxolitinib (91%). The majority (93.5%) presented with MF-related symptoms, and 83% had splenomegaly at baseline.
The study found that MMB led to notable anemia improvement. Among 133 evaluable patients, the median hemoglobin increased from 8.0 to 8.9 g/dL, and 52% of transfusion-dependent patients achieved transfusion independence. This trend remained stable across follow-ups at 3, 6, 9, and 12 months. Additionally, 79% of patients reported symptom relief, and 50% to 57% of those with splenomegaly experienced spleen reduction.
In terms of safety, MMB was well tolerated, with the most common adverse events being diarrhea (11.7%), thrombocytopenia (10%), and infections (9%). At the last follow-up, 79% of patients remained on treatment.
These findings reinforce MMB’s role as a valuable option for patients with MF struggling with anemia and symptoms, particularly those transitioning from other JAK inhibitors.
Reference
Pérez-Lamas L, Segura Diaz A, García Delgado R, et al. Real-world outcomes of momelotinib as an alternative therapy to other JAK inhibitors in myelofibrosis patients with anemia. Presented at: 2024 ASH Annual Meeting & Exposition; December 7-10, 2024; San Diego, CA, and virtual; Abstract 634.
