On August 30, 2017 Karyopharm Therapeutics Inc. (Nasdaq:KPTI), a clinical-stage pharmaceutical company, reported two upcoming poster presentations at the European Society of Medical Oncology (ESMO) (Free ESMO Whitepaper) 2017 Annual Meeting, taking place September 8-12, 2017 in Madrid, Spain (Press release, Karyopharm, AUG 30, 2017, View Source [SID1234520355]). One poster will describe Phase 1 data from an ongoing investigator-sponsored trial (IST) evaluating the safety and tolerability of the Company’s lead product candidate, selinexor (KPT-330), an oral Selective Inhibitor of Nuclear Export / SINE compound, in combination with paclitaxel and carboplatin in patients with advanced ovarian or endometrial cancers. The other poster will describe Phase 1 clinical data from an ongoing study evaluating the safety and tolerability of KPT-9274, Karyopharm’s oral, dual inhibitor of p21-activated kinase 4 (PAK4) and nicotinamide phosphoribosyltransferase (NAMPT) in patients with advanced solid malignancies or non-Hodgkin’s lymphoma (NHL).
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"We look forward to the presentations of the findings from both of these early-stage clinical trials at ESMO (Free ESMO Whitepaper) this year, the results of which will continue to inform and guide our ongoing clinical programs," said Sharon Shacham, PhD, MBA, President and Chief Scientific Officer of Karyopharm.
Details for the Poster Presentations at ESMO (Free ESMO Whitepaper) 2017:
Title: A Phase 1 Study of Selinexor (S) in Combination with Paclitaxel (P) and Carboplatin (C) in Patients (pts) with Advanced Ovarian (OC) or Endometrial Cancers (EC)
Presenter: Vicky Makker, Memorial Sloan Kettering Cancer Center, New York, New York, USA
Abstract code: 970P
Session: Poster Display Session
Location: Hall 8
Date and Time: Saturday, September 9, 2017 from 13:15 – 14:15 CET
Title: A First in Human Phase 1 Study of KPT-9274, a First in Class Dual Inhibitor of PAK4 and NAMPT, in Patients with Advanced Solid Malignancies or NHL
Presenter: Aung Niang, MD Anderson Cancer Center, Houston, Texas, USA
Abstract code: 374PD
Session: Poster Discussion Session — Developmental Therapeutics
Location: Alicante Auditorium
Date and Time: Saturday, September 9, 2017 from 16:30 – 18:00 CET
About Selinexor
Selinexor (KPT-330) is a first-in-class, oral Selective Inhibitor of Nuclear Export / SINE compound. Selinexor functions by binding with and inhibiting the nuclear export protein XPO1 (also called CRM1), leading to the accumulation of tumor suppressor proteins in the cell nucleus. This reinitiates and amplifies their tumor suppressor function and is believed to lead to the selective induction of apoptosis in cancer cells, while largely sparing normal cells. To date, over 2,100 patients have been treated with selinexor and it is currently being evaluated in several mid- and later-phase clinical trials across multiple cancer indications, including in multiple myeloma in a pivotal, randomized Phase 3 study in combination with Velcade (bortezomib) and low-dose dexamethasone (BOSTON), in combination with low-dose dexamethasone (STORM) and backbone therapies (STOMP), and in diffuse large B-cell lymphoma (SADAL), and liposarcoma (SEAL), among others. Additional Phase 1, Phase 2 and Phase 3 studies are ongoing or currently planned, including multiple studies in combination with one or more approved therapies in a variety of tumor types to further inform the Company’s clinical development priorities for selinexor. Additional clinical trial information for selinexor is available at www.clinicaltrials.gov.
About KPT-9274
KPT-9274 is a first-in-class, orally bioavailable, small molecule immunometabolic modulator that works through non-competitive dual inhibition of p21-activated kinase 4 (PAK4) and nicotinamide phosphoribosyltransferase (NAMPT). Co-inhibition of these targets is believed to lead to synergistic anti-tumor effects through suppression of ß-catenin by blocking PAK4, leading to both immune cell activation and inhibition of tumor growth, energy depletion through NAMPT inhibition, blockade of DNA repair, cell cycle arrest and ultimately apoptosis. KPT-9274 may therefore have both immune-activating and direct antitumor effects. In contrast, normal cells are less sensitive to inhibition by KPT-9274 due in part to their relative genomic stability and lower metabolic demands.