Aptose Biosciences will co-develop CrystalGenomics’ preclinical cancer drug candidate CG026806, the companies said today, under an exclusive global option and license agreement that could generate up to $303 million-plus for CrystalGenomics.

Aptose said it expects to undertake IND-enabling studies immediately, and, if it exercises an option under the agreement, to launch a Phase I clinical trial by mid-2017. Upon exercise of that option, Aptose will own global rights to develop and commercialize CG026806 outside of South Korea and China.

“We are impressed by the ability of once-daily oral dosing of CG026806 to demonstrate tumor eradication in the absence of toxicity in murine xenograft models of human hematologic malignancies,” William G. Rice, Ph.D., Aptose’s Chairman, President and CEO, said in a statement.

The companies said their deal was valued at $303 million, with Aptose agreeing to pay CrystalGenomics payments tied to achieving development, regulatory, and commercial-based milestones. CrystalGenomics is also eligible to receive a single-digit royalty on sales worldwide except China and South Korea.

CG026806 is a first-in-class, noncovalent, small molecule inhibitor of Bruton’s tyrosine kinase (BTK), FMS-like tyrosine kinase 3 (FLT3), and Aurora kinases (AURK). The candidate is CrystalGenomics’ lead compound among BTK/FLT3/AURK inhibitors.

Oncology is one of CrystalGenomics’ therapeutic areas, along with infectious disease and inflammation. The company won approval in February from the Korean Ministry of Food and Drug Safety (MFDS) for its osteoarthritis drug Acelex® (polmacoxib). Aptose specializes in cancer drugs and diagnostics.

The companies envision CG026806 fighting multiple forms of cancer, particularly those resistant to current BTK inhibitors or those that possess the FLT3-internal tandem duplication (ITD) alteration.

BTK plays a key role in B-cell hematologic malignancies, such as chronic lymphocytic leukemia and mantle cell lymphoma, as well as some autoimmune diseases.  FLT3, including the ITD, a mutation of the FLT3 gene, occurs in approximately 30–35% of patients with acute myeloid leukemia. AURK participate in the epigenetic phosphorylation of histones and are key drivers in a series of hematologic malignancies and solid tumors.








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