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December 8, 2013
21:06 EDTKPTIKaryopharm presents data for Selinexor at ASH
Karyopharm Therapeutics announced the oral presentation of clinical data from an ongoing Phase 1 clinical trial of its lead oral SINE compound, Selinexor, KPT-330, in patients with relapsed and/or refractory non-Hodgkin lymphoma, NHL, and chronic lymphocytic leukemia, CLL, at the 2013 American Society of Hematology, ASH, Annual Meeting and Exposition being held December 7-10 in New Orleans.The data indicate that, as of December 4, first-in-class oral Selinexor showed preliminary evidence of anti-cancer activity as a single agent in the majority of heavily pretreated relapsed and/or refractory NHL and CLL patients in the study cohort with progressive disease on study entry. In these NHL and CLL patients, Selinexor induced low levels of severe adverse events, and several of these patients have remained on study with Selinexor as their only anti-cancer treatment for more than 6-12 months.
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November 24, 2014
08:05 EDTKPTIKaryopharm presents data on oncology pipeline
Karyopharm Therapeutics announced the presentation of data describing its oncology product candidates at the 26th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapeutics in Barcelona, Spain held November 18-21. Data for its lead product candidate, Selinexor, a first-in-class, oral Selective Inhibitor of Nuclear Export / SINE compound, described its synergistic anti-tumor activity in combination with DNA damage-inducing treatments such as anthracyclines or radiation in a non-small cell lung cancer mouse model. In addition, a description of a newly developed pharmacodynamic assay designed to evaluate direct Selinexor binding to XPO1 in patients was presented. Finally, data describing the identification of novel mechanism PAK4 allosteric modulators and their ability to inhibit tumor cell growth and induce apoptosis were presented. In a poster entitled "Selective Inhibitors of Nuclear Export (SINE™) Block the Expression of DNA Damage Repair Proteins and Sensitize Cancer Cells to DNA Damage Inducing Agents," data demonstrated that Selinexor inhibited the DNA repair mechanisms in solid and hematological cancer cell lines and therefore, preventing the cancer cell recovery following treatment with agents that cause DNA damage, leading to increased cancer cell death.

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