1. MAPK/ERK Pathway Apoptosis Metabolic Enzyme/Protease Immunology/Inflammation NF-κB Epigenetics Cell Cycle/DNA Damage
  2. p38 MAPK Bcl-2 Family Caspase Reactive Oxygen Species (ROS) PARP Apoptosis
  3. MAPK-IN-5

MAPK-IN-5 is a potent MAPK inhibitor with an IC50 of 1.35 μM against HeLa cells. MAPK-IN-5 inhibits HeLa cell proliferation by inducing ROS-mediated DNA damage and mitochondrial apoptosis via the MAPK pathway. MAPK-IN-5 significantly inhibits colony formation, reduces the number of live cells, suppresses cell migration, and causes cell cycle arrest in the G2/M phase in HeLa cells. MAPK-IN-5 can be used for the study of cervical cancer.

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MAPK-IN-5

MAPK-IN-5 Chemical Structure

CAS No. : 2579683-39-7

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Description

MAPK-IN-5 is a potent MAPK inhibitor with an IC50 of 1.35 μM against HeLa cells. MAPK-IN-5 inhibits HeLa cell proliferation by inducing ROS-mediated DNA damage and mitochondrial apoptosis via the MAPK pathway. MAPK-IN-5 significantly inhibits colony formation, reduces the number of live cells, suppresses cell migration, and causes cell cycle arrest in the G2/M phase in HeLa cells. MAPK-IN-5 can be used for the study of cervical cancer[1].

IC50 & Target[1]

p38

 

Caspase-3

 

Caspase-9

 

Bcl-2

 

PARP-1

 

In Vitro

MAPK-IN-5 (Compound 3h) (5-10 μM, 48 h) significantly inhibits the colony formation of HeLa cells and increases the number of dead cells[1].
MAPK-IN-5 (5-10 μM, 0-48 h) has a pronounced inhibitory effect on the migration of HeLa cells[1].
MAPK-IN-5 (5-10 μM, 24 h) induces G2/M phase arrest in HeLa cells[1].
MAPK-IN-5 (5-10 μM, 48 h) induces apoptosis in HeLa cells, and the activation of the mitochondrial apoptosis pathway is involved[1].
MAPK-IN-5 (5-10 μM, 48 h) promotes ROS generation, triggers DNA damage and modulates the MAPK signaling pathway in HeLa cells[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Immunofluorescence[1]

Cell Line: HeLa cells
Concentration: 5 and 10 μM
Incubation Time: 48 h
Result: Gradually decreased the number of live cells, while the number of dead cells increased.
Dose-dependently increased the intracellular ROS level.
Increased the fluorescence intensity of γ-H2AX in the nuclei of HeLa cells.

Cell Cycle Analysis[1]

Cell Line: HeLa cells
Concentration: 5 and 10 μM
Incubation Time: 24 h
Result: Gradually decreased the proportion of cells in the G1 phase, while the proportion of cells in the G2/M phase significantly accumulated.

Cell Migration Assay [1]

Cell Line: HeLa cells
Concentration: 5 and 10 μM
Incubation Time: 0, 24, 48 h
Result: Reduced the migration rate of HeLa cells was to 20.75% at 10 μM.

Apoptosis Analysis[1]

Cell Line: HeLa cells
Concentration: 5 and 10 μM
Incubation Time: 48 h
Result: Increased the total apoptosis rate of HeLa cells by 37.63% at 10 μM.
Caused cell shrinkage, intensified nuclear staining, and even apoptotic features such as nuclear condensation and fragmentation were observed.

Western Blot Analysis[1]

Cell Line: HeLa cells
Concentration: 5 and 10 μM
Incubation Time: 48 h
Result: Decreased the levels of Bcl-2, Caspase-3, Caspase-9, and PARP-1.
Increased the levels of Bax and Cleaved PARP-1.
Dose-dependently inhibited the levels of phosphorylated ERK1/2 (p-ERK1/2) and phosphorylated JNK (p-JNK), while upregulating the phosphorylation of p38.
Had no effect on the total protein levels of ERK1/2, JNK, and p38.
Molecular Weight

594.58

Formula

C30H29F3N6O4

CAS No.
SMILES

COCCOC(C=C1N=CN=C2NC3=CC(C(N=N4)=CN4CC5=CC=C(C(F)(F)F)C=C5)=CC=C3)=C(C=C12)OCCOC

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Please store the product under the recommended conditions in the Certificate of Analysis.

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MAPK-IN-5
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HY-175175
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