FLT3/D835Y-IN-1
FLT3/D835Y-IN-1 (compound 13a) is a orally active, potent and selective FLT3 and FLT3/D835Y inhibitor, with IC50 values of 0.26 nM and 0.18 nM, respectively. FLT3/D835Y-IN-1 also blocks tumor growth, has anticancer efficacy, and can be used to research for AML (acute myeloid leukemia).
For research use only. We do not sell to patients.
- CAS No.: 2648799-49-7
- Formula: C22H21N5O3
- Molecular Weight:403.43
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
FLT3/D835Y|
FLT3/D835Y 0.18 nM (IC50) |
In Vitro
FLT3/D835Y-IN-1 (compound 13a) (100 nM, 3 h) potently inhibits Ba/F3-FLT3-ITD, Ba/F3-FLT3-ITD/D835Y, Ba/F3-FLT3-ITD-F691L cell lines, and AML cells proliferation[1].
FLT3/D835Y-IN-1 (3-30 nM, 16 h) significantly inhibit FLT3, AKT, ERK, and STAT5 pathways[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:Ba/F3-FLT3-ITD, Ba/F3-FLT3-ITD/D835Y, and Ba/F3-FLT3-ITD-F691L cell lines, AML cells[1]
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Concentration:100 nM
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Incubation Time:3 h
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Result:Inhibited Ba/F3-FLT3-ITD, Ba/F3-FLT3-ITD/D835Y, Ba/F3-FLT3-ITD-F691L, MV4-11, MOLM14, and MOLM14-ITD/D835Y proliferation, with GI50 values of 0.59, 0.73, 5.54, 1.30, 6.20, and 4.58 nM, respectively.
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Cell Line:MOLM14-ITD/D835Y and MOLM14-ITD/F691L cells[1].
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Concentration:3, 10, and 30 nM
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Incubation Time:16 h
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Result:Significantly inhibited the FLT3, AKT, ERK, and STAT5 pathways at lower dosages.
In Vivo
FLT3/D835Y-IN-1 (10 mg/kg, IV or Orally, single) displays extremely low AUC and high clearance[1].
Pharmacokinetic Parameters of FLT3/D835Y-IN-1 in ICR mice[1].
| Parameters | 13a |
| AUClast (ng*h/mL) | 1360 ± 110 |
| CL (L/h/kg) | 6.96 ± 0.66 |
| Vss (L/kg) | 14.8 ± 0.7 |
| T1/2 (h) | 1.5 ± 0.1 |
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:NOD/SCID mice (6 weeks, male, nine mice per group)[1]
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Dosage:10 mg/kg
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Administration:IP, daily, 6 days per week, from day 7 to day 29
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Result:Significantly suppressed tumor growth.
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Animal Model:ICR mice (7–8 weeks, male)[1]
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Dosage:10 mg/kg, dissolved in a solution (10% DMSO, 40% PEG400, and 50% PBS)
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Administration:IV or Orally, single (Pharmacokinetic Analysis)
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Result:Displayed extremely low AUC and high clearance.
Chemical Information
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CAS No. 2648799-49-7
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Molecular Weight 403.43
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Formula C22H21N5O3
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SMILES
O=C1NC2=C(C=CC=C2)/C1=C3NC4=C(C=CC=C4)C/3=N\OCC(N5CCNCC5)=O
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Patient-Derived Xenograft (PDX)
Patient-derived xenograft (PDX) models are generated by engrafting primary human tumor tissue directly into immunodeficient mice, allowing in vivo propagation of patient tumor biology without initial in vitro adaptation. These models are used to preserve key histopathological and molecular characteristics of the original tumor and enable assessment of tumor growth dynamics and therapeutic response in a living organism. The biological readout is tumor engraftment and subsequent growth in the murine host, which reflects the ability of human tumor cells to survive, vascularize, and expand in an immunocompromised microenvironment.
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Patient-Derived Orthotopic Xenograft (PDOX)
Patient-derived orthotopic xenograft (PDOX) modeling implants fresh patient tumor tissue or patient-derived tumor cells into the anatomically corresponding organ or tissue site of immunodeficient mice, usually by surgical orthotopic implantation, to preserve patient tumor histology, local microenvironmental context, invasion, metastatic behavior, and treatment-response features better than subcutaneous implantation. PDOX readouts include tumor engraftment, orthotopic tumor growth, local invasion, metastasis, recurrence after resection, histologic similarity to the donor tumor, biomarker retention, molecular concordance, survival, and response or resistance to therapy. PDOX models are used for preclinical drug testing and individualized therapy evaluation, but engraftment success varies by tumor type and specimen quality.
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Subcutaneous Cell-Line-Derived Xenograft
Subcutaneous cell-line-derived xenograft (CDX) models are established by implanting cultured human cancer cell lines into immunodeficient mice, where the injected cells form localized tumors that can be monitored in vivo as a measure of tumorigenic potential, growth kinetics, and treatment response. These models are widely used in oncology research because they allow reproducible tumor formation and enable comparative assessment of tumor growth between different cell lines or genetic manipulations in a controlled in vivo microenvironment. Subcutaneous implantation of cancer cells in immunodeficient mice is a standard approach for evaluating tumor growth behavior and therapeutic response across multiple cancer types, including prostate, esophageal, pancreatic, and colon cancer models.
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Orthotopic Cell-Line Xenograft
Orthotopic cell-line xenograft models involve implantation of human cancer cell lines into the anatomically corresponding organ of immunodeficient mice to reproduce tumor growth within a native microenvironment, enabling more clinically relevant tumor behavior compared with subcutaneous models. These models are widely used because orthotopic placement better recapitulates tumor progression, including invasion and metastatic spread, which are often underrepresented in heterotopic implantation systems. Compared with conventional xenografts, orthotopic implantation is described as more technically complex but provides improved simulation of tumor-microenvironment interactions and metastatic behavior, making it particularly valuable for translational oncology research. Surgical orthotopic implantation approaches have been emphasized as enabling faithful reproduction of clinical cancer features, including metastasis and disease progression patterns that align with the tumor’s organ of origi
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)