|OHSU and Aptose Present CG’806 Preclinical Data at ASH 59th Annual Meeting|
The poster CG’806, a First-in-Class Pan-FLT3/BTK Inhibitor, Exhibits Potent Growth Inhibition as a Single Agent and in Combination with a BET Bromodomain Inhibitor and a Bcl2 Inhibitor Against AML and CLL Patient Samples, evaluated the activity of CG’806 on various hematologic malignancy cell lines and patient primary bone marrow specimens through the Beat AML Initiative. CG’806 exhibited broad and potent activity against primary patient samples over a diverse range of hematologic malignancy subtypes, including AML, CLL, myelodysplastic syndromes/myeloproliferative neoplasms (MDS/MPN), and acute lymphoblastic leukemia (ALL).
The poster presentation can be accessed on the Events & Presentations section of the Aptose website at the following link.
“In patient samples and cultured cell lines, CG’806 demonstrated potent and broad inhibitory activity against hematologic malignancies alone and in combination,” said
OHSU researchers used an ex vivo drug sensitivity assay to determine the activity of CG’806 as a single agent and in combination with the
"Collaborating with OHSU and the Beat AML initiative has provided us an exceptional opportunity to explore the activity of CG‘806 against a large and diverse set of freshly isolated patient bone marrow samples from patients with AML, CLL and other hematologic malignancies,” commented
Separately, Aptose and The
In addition to the abstracts that were presented at ASH, two additional abstracts on CG’806 and two abstracts on APTO-253, Aptose’s small molecule c-Myc Inhibitor, have been published on the ASH abstracts site. All abstracts will become part of the permanent ASH and Blood abstracts archive.
For more information on Beat AML refer to https://www.lls.org/content/what-is-beat-aml.
CG‘806 is an oral, first-in-class pan-FLT3/pan-BTK inhibitor. This small molecule demonstrates potent inhibition of all wild type and mutant forms of FLT3 tested (including internal tandem duplication, or ITD, and mutations of the receptor tyrosine kinase domain and gatekeeper region), eliminates AML tumors in the absence of toxicity in murine xenograft models, and represents a potential best-in-class therapeutic for patients with FLT3-driven AML. Likewise, CG’806 demonstrates potent, non-covalent inhibition of the wild type and Cys481Ser mutant forms of the BTK enzyme, as well as other oncogenic kinases operative in B cell malignancies, suggesting CG’806 may be developed for CLL and MCL patients that are resistant/refractory/intolerant to covalent BTK inhibitors.
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