Jacqueline S. Garcia, MD,discusses how navitoclax differs from other agents in primary or secondary myelofibrosis.
Jacqueline S. Garcia, MD, instructor in Medicine, Department of Medical Oncology, Harvard Medical School, and physician, Dana-Farber Cancer Institute, discusses how navitoclax differs from other agents in primary or secondary myelofibrosis.
Navitoclax is an oral BH3 memetic that targets cells that are dependent on BCL-XL and not as dependent on BCL-2 and BCL-W, explains Garcia. This therapy shows that myelofibrosis cells undergo apoptotical priming, and there’s evidence for the activity of BCL-XL inhibition in reversing fibrosis and causing apoptosis, says Garcia.
In preclinical models, there has also been activity with BCL-XL inhibition and JAK2-mutant and -resistant models, according to Garcia. There is evidence of synergy when BCL-XL inhibitors and JAK2 inhibitors, such as ruxolitinib, are combined. Additionally, navitoclax as an oral therapy makes the combination interesting, concludes Garcia.