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tuspetinib
- Development stage
- Phase 2
- Lead developer
- Aptose Biosciences
- Modality
- Bivalent/Multivalent Binders → Multivalent & Scaffold-Based Small Molecules → Small Molecules, Orthosteric Ligands → Classical Binding Small Molecules → Small Molecules, Reversible Covalent Inhibitors → Covalent Small Molecules → Small Molecules, Allosteric Modulators → Classical Binding Small Molecules → Small Molecules, Irreversible Covalent Inhibitors → Covalent Small Molecules → Small Molecules, Fragment-Derived Small Molecules → Multivalent & Scaffold-Based Small Molecules → Small Molecules
- Administration
- Oral
01
Overview
Tuspetinib is a potent oral small molecule myeloid kinase inhibitor (MKI) in clinical development for the treatment of acute myeloid leukemia (AML). It is designed to simultaneously inhibit a select set of kinases that drive prosurvival and drug resistance pathways in myeloid malignancies. Tuspetinib targets key kinases including Spleen tyrosine kinase (SYK), wild-type and mutant forms of FMS-like tyrosine kinase 3 (FLT3), mutant Mast/stem cell growth factor receptor Kit (but not wild-type), Janus kinase 1/2, Ribosomal S6 kinase alpha-1/2 (RSK1/2), Mitogen activated protein kinase kinase kinase TAK1–TAB1 complex kinases, and indirectly suppresses MCL1 expression. This multikinase inhibition leads to suppression of multiple oncogenic signaling pathways such as STAT5, MEK/ERK, AKT/mTOR. Preclinical studies have shown that tuspetinib prolongs survival in AML models and demonstrates enhanced activity when combined with venetoclax or azacitidine. Clinical trials are ongoing for relapsed/refractory AML as monotherapy or in combination regimens[1][2][3][4][5][6][7][8].
- Other names
- tuspetinib
02
Targets
JAK2 (Janus kinase 2)FLT3 (Fms related receptor tyrosine kinase 3)KIT (c-KIT proto-oncogene receptor tyrosine kinase)TAB1 (Mitogen activated protein kinase kinase kinase TAK1-TAB1 complex)JAK1 (Janus kinase 1)RPS6KA3 (RSK2)SYK (Spleen Tyrosine Kinase)RPS6KA1 (Ribosomal S6 kinase Alpha-1)
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