ZMF-10
ZMF-10 is a highly potent PAK1 inhibitor, with IC50s of 174 nM, 1.038 μM and 1.372 μM for PAK1, PAK2 and PAK3, respectively. ZMF-10 can inhibit PAK1 activity to affect PAK1-regulated apoptosis, ER-Stress and migration in MDA-MB-231 cells. ZMF-10 can be used for researching anticancer.
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- CAS. Nr.: 2415295-37-1
- Formel: C19H17F6N7O
- Molecular Weight:473.37
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biologische Aktivität
Beschreibung
IC50 & Target
[1]|
PAK1 174 nM (IC50) |
PAK2 1.038 μM (IC50) |
PAK3 1.372 μM (IC50) |
In Vitro
ZMF-10 (0-10 μM; 48 hours) exhibits potent antiproliferative activity in a dose-dependent manner[1].
ZMF-10 (20 μM; 24 hours) suppresses the phosphorylation of PAK1 at Ser199 and Thr212[1].
ZMF-10 (10-40 μM; 24 hours) downregulates the expression of ERK, and suppresses the phosphorylation of c-Raf, MEK and ERK; up-regulates the expression of Bax and downregulates the expression of Bcl-2; induces apoptosis in a dose-dependent manner with the increase of early and late apoptotic cell population[1].
ZMF-10 (10-40 μM; 24 hours) inhibits the PI3K-AKT-mTOR signaling with the decreasing phosphorylation of AKT and mTOR; inhibits JNK1/2 and cells migration in MDA-MB-231 cells[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-231[1]
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Concentration:0-10 μM
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Incubation Time:48 hours
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Result:Exhibited potent antiproliferative activity in a dose-dependent manner with an IC50 value of 3.48 μM.
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Cell Line:MDA-MB-231[1]
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Concentration:20 μM
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Incubation Time:24 hours
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Result:Suppressed the phosphorylation of PAK1 at Ser199 and Thr212.
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Cell Line:MDA-MB-231[1]
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Concentration:10, 20 and 40 μM
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Incubation Time:24 hours
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Result:Downregulated the expression of ERK, and suppressed the phosphorylation of c-Raf, MEK and ERK; up-regulated the expression of Bax and downregulated the expression of Bcl-2.
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Cell Line:MDA-MB-231[1]
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Concentration:10, 20 and 40 μM
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Incubation Time:24 hours
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Result:Induced apoptosis in a dose-dependent manner with the increase of early and late apoptotic cell population.
Chemical Information
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CAS. Nr. 2415295-37-1
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Molecular Weight 473.37
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Formel C19H17F6N7O
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SMILES
O=C(NC1CCN(CC1)C2=C3C=NNC3=NC=N2)NC4=CC(C(F)(F)F)=CC(C(F)(F)F)=C4
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
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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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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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Cell migration
Cell migration is a method that plays an important role in wound healing, cell differentiation, embryonic development, etc.
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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
Reinheit & Dokumentation
Verweise
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)