6-K – Report of foreign issuer [Rules 13a-16 and 15d-16]

On November 5, 2015 Aptose Biosciences Inc. (NASDAQ:APTO) (TSX:APS), a clinical-stage company developing targeted agents and molecular diagnostics to treat the underlying mechanisms of cancer, reported that preclinical data for its lead investigational anticancer therapeutic APTO-253 will be presented at the 57th American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting and Exposition being held December 5-8, 2015, in Orlando, FL (Filing, 6-K, Aptose Biosciences, NOV 5, 2015, View Source [SID:1234508000]).

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Researchers from the Knight Cancer Institute at Oregon Health & Science University (OHSU) will present data demonstrating the ability of APTO-253 to kill acute myeloid leukemia (AML) cells in the majority of patient samples, with a trend toward correlation with baseline KLF4 expression level. Moreover, APTO-253 demonstrated enhanced killing ability of AML cells in patient samples when combined with either the BET inhibitor JQ1 or with the FLT3 inhibitor quizartinib. The studies were led by OHSU Knight Cancer Institute researcher Jeffrey Tyner, Ph.D., an assistant professor in the Department of Cell, Developmental & Cancer Biology in the OHSU School of Medicine. Beat AML is a collaborative research initiative spearheaded by the OHSU Knight Cancer Institute and The Leukemia & Lymphoma Society.

"These findings further support the ability of APTO-253, a first-in-class KLF4 inducer, to serve as a targeted treatment for AML," commented William G. Rice, Ph.D., Chairman and Chief Executive Officer of Aptose. "Indeed, this emboldens our clinical efforts to develop APTO-253 for use as a single agent and in combination therapies to treat AML and other hematologic malignancies and achieve favorable outcomes with lesser side effects."

The abstract is also available in the online edition of Blood, the official Journal of the American Society of Hematology (ASH) (Free ASH Whitepaper) and on the ASH (Free ASH Whitepaper) conference website:

Abstract Details

Title: "Broad Activity of Apto-253 in AML and Other Hematologic Malignancies Correlates with KLF4 Expression Level"
Date/Time: Saturday, December 5, 2015, 5:30-7:30 p.m.
Location: Orange County Convention Center, Hall A
Abstract #: 83676
Session: 616. Acute Myeloid Leukemia: Novel Therapy, excluding Transplantation: Poster I

Additional Abstract

An additional abstract describingthe favorable pharmacokinetics and safety profile of APTO-253 was accepted for publication in the ASH (Free ASH Whitepaper) online conference materials, in the December 3 edition of Blood and in the ASH (Free ASH Whitepaper) and Blood abstract archive.

Title: "Clinical Pharmacokinetics of APTO-253 Support its Use as a Novel Agent for the Treatment of Relapsed or Refractory Hematologic Malignancies"
Abstract #: 4934
Location: Publication

About APTO-253

APTO-253 is a clinical-stage small molecule targeted agent that acts through induction of the innate tumor suppressor gene Krüppel-like factor 4 (KLF4). Suppression of KLF4 gene expression has been reported as a key driver in the leukemogenesis of AML and subsets of other hematologic diseases. Aptose researchers have reported the ability of APTO-253 to upregulate KLF4 expression and induce cell death, or apoptosis, in multiple blood cancer cell lines including AML, as well as in vitro synergy with various classes of conventional approved therapies for AML or myelodysplastic syndromes (MDS).

At last year’s ASH (Free ASH Whitepaper) meeting, Aptose presented data that demonstrated APTO-253’s robust safety profile and potent activity as a single agent and administered in combination with the chemotherapeutic drug azacitadine. In a prior single-agent, Phase 1 clinical study, APTO-253 demonstrated antitumor activity and a robust safety profile in patients with solid tumors.

APTO-253 is currently being evaluated in an ongoing open-label, single-agent, dose-escalating Phase 1b clinical trial in patients with relapsed or refractory hematologic malignancies, including AML and high-risk MDS.