Karyopharm Therapeutics Inc. (NASDAQ:KPTI), a commercial-stage pharmaceutical company pioneering novel cancer therapies, today announced that its late-breaking abstract was accepted for an oral presentation at the 2026 European Hematology Association (EHA) Congress, taking place June 11 to 14 in Stockholm, Sweden. The SENTRY presentation was selected by EHA's Scientific Program Committee as one of the six best abstracts to be presented during the Late-Breaking Oral Session on Sunday, June 14th. The oral presentation will feature results from the Phase 3 SENTRY trial, a randomized, double-blind, placebo-controlled trial of 60 mg selinexor in combination with ruxolitinib in myelofibrosis.

This abstract highlights the combination of selinexor plus ruxolitinib's ability to enable rapid, deep and sustained spleen volume reductions; similar symptom improvement; a promising signal of overall survival; more patients achieving ≥20% reductions in variant allele frequency (VAF) as early as week 24; and a manageable safety profile. In addition, new data will highlight a post-hoc analysis of 24 patients from the Phase 1 portion of the SENTRY trial which indicates that achieving a spleen volume reduction of 35% or more (SVR35) may predict overall survival, consistent with a similar analysis from the Phase 3 SENTRY trial.

"The SENTRY results are an important development for patients with myelofibrosis, with the combination of selinexor plus ruxolitinib showing a promising overall survival signal supported by rapid, deep and sustained spleen volume reduction and the potential for disease modification with lower levels of VAF," said Dr. Claire Harrison, Professor of Myeloproliferative Neoplasms at Guy's and St. Thomas' NHS Foundation Trust in the United Kingdom. "JAK inhibitors have transformed the treatment landscape over the past 15 years, but there remains a significant need for novel therapies that can build upon their foundation and target additional biological pathways driving disease progression. XPO1 inhibition represents a differentiated mechanism with the potential to extend the benefits of therapy beyond JAK inhibition alone, including the potential to extend overall survival which remains the ultimate objective for patients living with myelofibrosis."