MAPK-IN-9
MAPK-IN-9 is a ERK MAPK-MCL-1 inhibitor. MAPK-IN-9 activates caspase-7 and caspase-3, and cleaves poly (ADP-ribose) polymerase (PARP) to induce apoptosis. MAPK-IN-9 inhibits the clonogenic capacity of non-small cell lung cancer cells. MAPK-IN-9 can be used in research related to non-small cell lung cancer.
For research use only. We do not sell to patients.
- Formula: C21H14BrN5O3
- Molecular Weight:464.27
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
[1]|
Caspase-3 |
Caspase-7 |
Mcl-1 |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| H1975 | IC50 |
1.055 μM
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Inhibition of cell viability against human H1975 non-small cell lung cancer cells incubated for 24 hrs by Cell Counting Kit-8 assay.
Inhibition of cell viability against human H1975 non-small cell lung cancer cells incubated for 24 hrs by Cell Counting Kit-8 assay.
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42456857 |
In Vitro
MAPK-IN-9 (Compound PPC-15) (1-20 μM; 7 days) potently inhibits the colony-forming ability of H1975 non-small cell lung cancer cells[1].
MAPK-IN-9 (0.1-20 μM; 24 h) inhibits the viability of H1975 non-small cell lung cancer cells, with an IC50 of 1.055 μM after 24 h of treatment[1].
MAPK-IN-9 (10 μM; 24 h) induces significant cell death in H1975 non-small cell lung cancer cells, reducing the viable cell population by more than 48%[1].
MAPK-IN-9 (10 μM; 18 h) induces apoptotic cell death in H1975 non-small cell lung cancer cells after 18 h of treatment, as evidenced by nuclear fragmentation and an increased population of Annexin V-positive cells[1].
MAPK-IN-9 (1-20 μM; 6-24 h) induces apoptosis in H1975, PC-9, HCC827 and A549 non-small cell lung cancer cells by downregulating MCL-1 expression and activating caspase-7, caspase-3 and PARP, which is associated with the selective inhibition of ERK phosphorylation[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:H1975 non-small cell lung cancer cells
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Concentration:0.1, 1, 10, 20 μM
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Incubation Time:24 h
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Result:Reduced cell viability in a dose-dependent manner, with a half-maximal inhibitory concentration (IC50) of 1.055 μM.
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Cell Line:H1975 non-small cell lung cancer cells
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Concentration:10 μM
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Incubation Time:18 h
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Result:Induced nuclear condensation and fragmentation, characteristic of apoptosis.
Increased the proportion of early apoptotic PI-negative/Annexin V-positive cells from 3% to 25%.
Increased late apoptotic/necrotic PI-positive/Annexin V-positive cells from 5% to 75%.
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Cell Line:H1975, PC-9, HCC827, and A549 non-small cell lung cancer cells
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Concentration:1, 10, 20 μM (H1975 dose-dependent); 10 μM (H1975, PC-9, HCC827, A549 time-dependent)
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Incubation Time:24 h (H1975 dose-dependent); 6, 12, 24 h (H1975, PC-9, HCC827, A549 time-dependent)
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Result:Reduced MCL-1 expression and increased cleavage of caspase-7, caspase-3, and PARP in H1975 cells in both dose- and time-dependent manners.
Selectively reduced ERK phosphorylation in H1975 cells in a time-dependent manner, with no significant effect on AKT or MEK phosphorylation.
Reduced ERK phosphorylation, reduced MCL-1 expression, and increased caspase-7 and PARP cleavage in PC-9, HCC827, and A549 cells.
Chemical Information
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Molecular Weight 464.27
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Formula C21H14BrN5O3
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SMILES
N#CC1=C2N=CC(C(C3=CC(Br)=CC=C3O)=O)=CN2N=C1NC4=CC=CC(OC)=C4
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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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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
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
MAPK-IN-9 Related Classifications
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