Aptose spent a long time fruitlessly chasing the non-covalent BTK inhibitor leaders with its lead project, CG-806, but judging by this morning’s 60% share price uplift what it really needed was a rebrand. The asset now has an INN, luxeptinib, and – more importantly – a complete remission. This was seen not in a chronic lymphoblastic leukaemia/lymphoma study, where luxeptinib would be expected to hit BTK, but in an acute myelogenous leukaemia trial, relevant for its separate effect on Flt3. Aptose yesterday said the CR occurred in a patient given 450mg twice daily, but gave no details about the subject’s Flt3 status. However, it made much of pharmacology, saying the molecule inhibited Flt3 more potently than the marketed Flt3-targeted drugs Vanflyta, Xospata and Rydapt. With the non-covalent BTK space now the domain of efficacious Lilly and Merck & Co projects perhaps a mechanistic focus switcheroo to Flt3 was in order, but it did not end there: Aptose now calls luxeptinib a “cluster-selective” agent inhibiting “clusters of related kinases” including PDGFR-alpha, CSF1R, Akt, Ras, Erk, Stat and Syk. Amazingly there is no added toxicity, Aptose claims, saying luxeptinib is “not a dirty kinase inhibitor”.
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