HER2-IN-9
HER2-IN-9 is an orally active HER2 inhibitor, with an IC50 value of 0.03 μM. HER2-IN-9 inhibits HER-2 positive breast cancer cells proliferation and migration. HER2-IN-9 can be used in the research of breast cancers.
For research use only. We do not sell to patients.
- Formula: C19H14BrF3N2O
- Molecular Weight:423.23
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All EGFR Isoforms
More
Biological Activity
Description
IC50 & Target
[1]|
HER2 0.03 μM (IC50) |
In Vitro
HER2-IN-9 (24 h) shows anti-proliferation activities against cancer cells (A549, HEPG2, MCF7, SKBR3)[1].
HER2-IN-9 (0-60 nM, 24 h) inhibits the migration of SKBR3 cells[1].
HER2-IN-9 (0-60 nM, 24 h) increases E-cadherin levels and decreases N-cadherin levels in SKBR3 cells[1].
HER2-IN-9 (0-60 nM, 24 h) suppresses the expression of p-HER-2, further inhibits the activation of the EMT signal pathway to inhibit the migration of SKBR3 cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
-
Cell Line:Cancer cells (A549, HEPG2, MCF7, SKBR3), normal cells (Beas2b, LO2, MCF-0A)
-
Concentration:0.05-30 μM approximately
-
Incubation Time:24 h
-
Result:Inhibited cancer cell proliferation with IC50s of 0.05-12.17 μM.
Inhibited noamal cell proliferation with IC50s of 15.4- 26.95 μM.
-
Cell Line:SKBR3 cells
-
Concentration:0, 20, 40, 60 nM
-
Incubation Time:24 h
-
Result:Inhibited HER-2 phosphorylation with no significant change in total HER-2 protein levels.
Down-regulated β-catenin, snail, and Vimentin level.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Animal Model:SKBR3 orthotopic xenograft model[1]
-
Dosage:30 mg/kg
-
Administration:Oral administration, every two days.
-
Result:Inhibited the growth of cancer cells in vivo without noticeable toxic effects.
Increased the level of cleaved-caspase 3 implicated in cell death pathways (immunohistochemistry assay in tumor).
Chemical Information
-
Molecular Weight 423.23
-
Formula C19H14BrF3N2O
-
SMILES
FC(F)(C1=CC=C(C=C1)/C=C/C2=COC(CNC3=CC=C(C=C3)Br)=N2)F
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
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.
-
Cell migration
Cell migration is a method that plays an important role in wound healing, cell differentiation, embryonic development, etc.
-
Breast Cancer Modeling
Breast cancer is a heterogeneous cancer, and it has been distinguished into four subtypes: luminal A, luminal B, HER2-positive and basal-like. Molecular mutations, epigenetic alterations, hormone exposure and immune microenvironment are related to the progression of breast cancer.
-
Cell Viability Determination by MTT Colorimetric Assay
The following protocol uses the MTT colorimetric assay as a classic literature-established method for assessing cell viability/metabolic activity in cultured mammalian cells. MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] is reduced by metabolically active cells to a colored formazan product; the amount of formazan is quantified spectrophotometrically and provides an indirect measure of metabolically active viable cells. Importantly, MTT reduction reflects cellular oxidoreductase/metabolic activity rather than an absolute direct count of living cells, so changes in cellular metabolism can alter the signal independently of cell number.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)