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(CAS: 1429515-49-0 )

Suppliers of LT-106-175

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Background Information of LT-106-175

LT-106-175, a multiple kinases inhibitor, shows potent inhibitory activities against CDKs and FLT3 with IC50s of 0.60±0.11 nM, 3.33±0.25 nM, and 9.10±0.16 nM for FLT3, CDK6, and CDK2, respectively. Fms-like tyrosine kinase 3 (FLT3) is among the most frequently mutated protein in acute myeloid leukemia (AML), which has been confirmed as an important drug target for AML chemotherapy.

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Mechanism and Indications

Signaling Pathways Protein Tyrosine Kinase/RTK Cell Cycle/DNA Damage
Target CDK FLT3
Research Area Cancer

Clinical Information

Product Name Sponsor & Collaborators Indications Start Date End Date Phase

Chemical Information

M.Wt Formula CAS No. Synonyms
448.54 C22H24N8OS 1429515-49-0

Structure Information of LT-106-175

Smiles N1(C)CCN(CC2C=CC(NC(=O)C3=NNC=C3NC3N=CN=C4SC=CC=34)=CC=2)CC1
InChI InChI=1S/C22H24N8OS/c1-29-7-9-30(10-8-29)13-15-2-4-16(5-3-15)26-21(31)19-18(12-25-28-19)27-20-17-6-11-32-22(17)24-14-23-20/h2-6,11-12,14H,7-10,13H2,1H3,(H,25,28)(H,26,31)(H,23,24,27)

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[1].Zhi Y, et al. Discovery of the selective and efficacious inhibitors of FLT3 mutations. Eur J Med Chem. 2018 Jun 5;155:303-315.
Fms-like tyrosine kinase 3 (FLT3) is among the most frequently mutated protein in acute myeloid leukemia (AML), which has been confirmed as an important drug target for AML chemotherapy. Starting from the lead compound LT-106-175, a series of 1-H-pyrazole-3-carboxamide derivatives were synthesized to improve the FLT3 inhibitory potency and selectivity. Among them, compound 50 was identified as a highly potent and selective FLT3 inhibitor (IC50 = 0.213 nM), which showed equal activities against various mutants of FLT3 including FLT3 (ITD)-D835V and FLT3 (ITD)-F691L that is resistant to quizartinib. Compound 50 also exhibited efficacy against the human AML cell line MV4-11 (IC50 = 16.1 nM) harboring FLT3-ITD mutants. Inversely, compound 50 displayed no cytotoxicity to FLT3-independent cells, and the biochemical analyses showed that its effects were related to the inhibition of FLT3 signal pathways. Additionally, compound 50 induced apoptosis in MV4-11 cell as demonstrated by flow cytometry. Moreover, compound 50 showed enhanced metabolic stability. Altogether, it was concluded that compound 50 could be a promising FLT3 inhibitor for further developing therapeutic remedy of AML.

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