flt3/btk

BTK-IN-24 is a Bruton's tyrosine kinase (BTK) inhibitor with potential anticancer activity, and it can be used in the study of myeloproliferative disorders.

RSH-7 is a potent dual inhibitor of BTK and FLT3, with IC50s of 47 and 12 nM, respectively.RSH-7 has antiproliferative and antitumor activities, inducing apoptosis and inhibiting BTK and FLT3 signaling.

AZ7550, an active metabolite of AZD9291, inhibits the activity of IGF1R (IC50: 1.6 μM).

AZ7550 hydrochloride (AZ7550 hydrochloride ), an active metabolite of AZD9291, inhibits the activity of IGF1R (IC50: 1.6 μM).

AZ7550 trimesylate salt (AZ7550 Mesylate) is the active metabolite of ositinib, AZ7550 trimesylate salt inhibits IGF1R activity and can be used in the study of non-small cell lung cancer.

JAK3-IN-1 is an orally active, selective and potent JAK3 inhibitor that can be used to study immune system diseases.

TL12-186 is a Cereblon-dependent kinase degrader that degrades CDK, BTK, FLT3, Aurora and other kinases.TL12-186 inhibits CDK2 cyclin A and CDK9 cyclin T1 with IC50s of 73 and 55 nM, respectively.

Luxeptinib (CG-806) is a novel pan-FLT3 pan-BTK inhibitor that is administered orally. It exhibits potent and reversible inhibition of these enzymes, acting through a non-covalent mechanism. Luxeptinib effectively induces cell cycle arrest, apoptosis, or autophagy in acute myeloid leukemia cells [1][2][3][4].

Abivertinib, also known as AC0010 and Avitinib, is a third-generation EGFR tyrosine kinase inhibitor and BTK Inhibitor that demonstrated clinical efficacy and manageable adverse events (AEs). Abivertinib inhibits cell proliferation, reduces colony-forming capacity, and induces apoptosis and cell cycle arrest in AML cells, especially those harboring FLT3-ITD mutations. Abivertinib was also found to be more sensitive than ibrutinib in treating AML. Abivertinib may be a promising novel agent for AML, with potential for combination treatment with HHT.