FAK-IN-9
FAK-IN-9 (Compound 8f) is a potent and orally active FAK inhibitor with an IC50 of 27.44 nM. FAK-IN-9 induces triple-negative breast cancer (TNBC) cell apoptosis.
For research use only. We do not sell to patients.
- CAS No.: 2911655-93-9
- Formula: C36H38ClN7O8S
- Molecular Weight:764.25
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
IC50: 27.44 nM (FAK)[1]
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| MCF-10A | IC50 |
2.401 μM
Compound: 8f
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Cytotoxicity against human MCF-10A cells assessed as inhibition of cell proliferation incubated for 72 hrs by MTT assay
Cytotoxicity against human MCF-10A cells assessed as inhibition of cell proliferation incubated for 72 hrs by MTT assay
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[PMID: 36801517] |
| MDA-MB-157 | IC50 |
0.167 μM
Compound: 8f
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Antiproliferative activity against human MDA-MB-157 cells assessed as inhibition of cell proliferation incubated for 72 hrs by MTT assay
Antiproliferative activity against human MDA-MB-157 cells assessed as inhibition of cell proliferation incubated for 72 hrs by MTT assay
|
[PMID: 36801517] |
| MDA-MB-231 | IC50 |
0.126 μM
Compound: 8f
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Antiproliferative activity against human MDA-MB-231 cells assessed as inhibition of cell proliferation incubated for 72 hrs by MTT assay
Antiproliferative activity against human MDA-MB-231 cells assessed as inhibition of cell proliferation incubated for 72 hrs by MTT assay
|
[PMID: 36801517] |
| MDA-MB-453 | IC50 |
0.159 μM
Compound: 8f
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Antiproliferative activity against human MDA-MB-453 cells assessed as inhibition of cell proliferation incubated for 72 hrs by MTT assay
Antiproliferative activity against human MDA-MB-453 cells assessed as inhibition of cell proliferation incubated for 72 hrs by MTT assay
|
[PMID: 36801517] |
In Vitro
FAK-IN-9 (Compound 8f; 72 h) shows antiproliferative activity with IC50s of 0.167±0.025, 0.126±0.012 and 0.159±0.017 μM against MDA-MB-157, MDA-MB-231 and MDA-MB-453 cells, respectively[1].
FAK-IN-9 (1-4 μM; 72 h) leads to relatively high levels of NO production in a dose-dependent manner in MDA-MB-231 cells[1].
FAK-IN-9 (1-4 μM; 48 h) inhibits invasion and migration of MDA-MB-231 cells[1].
FAK-IN-9 (1-4 μM; 72 h) efficiently blocks FAK mediated-signaling pathways[1].
FAK-IN-9 (4 μM; 72 h) inhibits the formation of focal adhesions (FAs) and stress fibers (SFs) in MDA-MB-231 cells[1].
FAK-IN-9 (1-4 μM; 72 h) induces MDA-MB-231 cell apoptosis[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:MDA-MB-157, MDA-MB-231, MDA-MB-453 and MCF10A
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Concentration:
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Incubation Time:72 h
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Result:Inhibited proliferation with IC50s of 0.167±0.025, 0.126±0.012, 0.159±0.017 and 2.401±0.131 μM against MDA-MB-157, MDA-MB-231, MDA-MB-453 and MCF10A, respectively.
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Cell Line:MDA-MB-231 cells
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Concentration:1, 2 and 4 μM
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Incubation Time:48 h
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Result:The numbers of invasive MDA-MB-231 cells were reduced dose-dependently.
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Cell Line:MDA-MB-231 cells
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Concentration:1, 2 and 4 μM
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Incubation Time:48 h
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Result:Remarkably block the migration of MDA-MB-231 cells in a dose-dependent manner.
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Cell Line:MDA-MB-231 cells
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Concentration:1, 2 and 4 μM
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Incubation Time:72 h
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Result:Potently suppressed the autophosphorylation of Y397 in a dose-dependent manner. Decreased the levels of p-AKT, MMP-2 and MMP-9 dose dependently.
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Cell Line:MDA-MB-231 cells
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Concentration:1, 2 and 4 μM
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Incubation Time:72 h
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Result:The percentage of apoptotic MDA-MB-231 cells gradually increased ranging from 19.06% to 77.66% at 4 μM.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c nude mice, MDA-MB-231 experimental pulmonary metastasis model[1]
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Dosage:15 or 30 mg/kg
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Administration:Oral, once daily for 30 days
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Result:Potently reduced the numbers of lung tumor nodules dose-dependently.
Chemical Information
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CAS No. 2911655-93-9
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Molecular Weight 764.25
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Formula C36H38ClN7O8S
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SMILES
CNC(C1=C(C=CC=C1)NC2=C(C=NC(NC3=CC=C(C=C3)CC(OCCCCCCCCOC4=NO[N+]([O-])=C4S(=O)(C5=CC=CC=C5)=O)=O)=N2)Cl)=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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Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
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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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Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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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.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)