Two small preliminary studies of JAK2 inhibitors CYT387 and SB1518 had encouraging results in patients with myelofibrosis, and these studies were reported in poster presentations at the Annual Meeting.^1,2 Both drugs reduced splenomegaly and achieved improvement in constitutional symptoms. SB1518 demonstrated an associated downmodulation in cytokines, and CYT387 was associated with an improvement in anemia.

“The JAK2 mutation as a potential cause of myelofibrosis is an important discovery,” said Olatoyosi Odenike, MD, University of Chicago Medical Center, who was the discussant for the two poster presentations. She said that a number of JAK inhibitor ATP mimetics are in clinical trials for myelofibrosis.

“There is a lack of effective therapy for patients with cytopenias, but JAK inhibitors achieve improvement in spleen size and constitutional symptoms. Novel agents are still desperately needed. We don’t quite understand how these agents are working, since responses are independent of JAK2 mutational status,” Dr. Odenike said. ■

Disclosure: Dr. Odenike has been a consultant or advisor for Amgen, Cephalon, Incyte, and MGI Pharma. She has received research funding from MGI Pharma/Eisai and Topotarget, and honoraria from Celgene and Genzyme.

References

1. Pardanani AD, Caramazza D, George G, et al: Safety and efficacy of CYT387, a JAK-1/2 inhibitor, for the treatment of myelofibrosis. 2011 ASCO Annual Meeting. Abstract 6514. Presented June 3, 2011.

2. Deeg HJ, Odenike O, Scott BL, et al: Phase II study of SB1518, an orally available JAK2 inhibitor, in patients with myelofibrosis. 2011 ASCO Annual Meeting. Abstract 6515. Presented June 3, 2011.