FLT3-IN-6
99%
- Product Code: 189920
CAS:
2377141-31-4
| Molecular Weight: | 419.48 g./mol | Molecular Formula: | C₂₃H₂₅N₅O₃ |
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| Density: | Storage Condition: | -20°C |
Product Description:
FLT3-IN-6 is a potent and selective inhibitor of FMS-like tyrosine kinase 3 (FLT3), particularly effective against both wild-type and internal tandem duplication (ITD) mutant forms of the receptor. It is primarily used in research settings to study signaling pathways involved in acute myeloid leukemia (AML). Due to its high selectivity, it helps suppress the proliferation of leukemia cells that depend on FLT3 activity for survival and growth.
In preclinical studies, FLT3-IN-6 has shown strong anti-leukemic effects, making it a valuable tool compound for evaluating targeted therapies in FLT3-driven cancers. It is often used in cell-based assays and animal models to assess the efficacy of FLT3 inhibition, apoptosis induction, and downstream pathway modulation, such as suppression of STAT5 and MAPK signaling. Its application supports the development of new therapeutic strategies aimed at overcoming drug resistance in AML patients with FLT3 mutations.
Sizes / Availability / Pricing:
| Size | Availability | Price | Quantity |
|---|---|---|---|
| 5mg | 10-20 days | $1,472.90 |
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FLT3-IN-6
FLT3-IN-6 is a potent and selective inhibitor of FMS-like tyrosine kinase 3 (FLT3), particularly effective against both wild-type and internal tandem duplication (ITD) mutant forms of the receptor. It is primarily used in research settings to study signaling pathways involved in acute myeloid leukemia (AML). Due to its high selectivity, it helps suppress the proliferation of leukemia cells that depend on FLT3 activity for survival and growth.
In preclinical studies, FLT3-IN-6 has shown strong anti-leukemic effects, making it a valuable tool compound for evaluating targeted therapies in FLT3-driven cancers. It is often used in cell-based assays and animal models to assess the efficacy of FLT3 inhibition, apoptosis induction, and downstream pathway modulation, such as suppression of STAT5 and MAPK signaling. Its application supports the development of new therapeutic strategies aimed at overcoming drug resistance in AML patients with FLT3 mutations.
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