MAPK-IN-6
For research use only. We do not sell to patients.
- Formula: C21H24O10
- Molecular Weight:436.41
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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
- Purity & Documentation
- References
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Help & FAQs
All Caspase Isoforms
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Biological Activity
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p38 |
ERK1 |
ERK2 |
Caspase 3 |
MAPK-IN-6 (Compound 116B) binds tightly to p38-MAPK with a predicted binding energy of -9.2 kcal/mol[1].
MAPK-IN-6 (10 nM-200 μM; 24 h) exhibits cytocompatibility with SH-SY5Y neuronal cells at concentrations up to 100 μM, and maintains over 90% cell viability[1].
MAPK-IN-6 (10 nM-50 μM; 24 h) exhibits significant neuroprotective activity and preserves cell membrane integrity in H2O2 (400 μM)-stressed SH-SY5Y neuronal cells, and significantly reduces the release of lactate dehydrogenase (LDH)[1].
MAPK-IN-6 (1 μM; 24 h) promotes cell survival, reduces the level of total intracellular reactive oxygen species (ROS), decreases mitochondrial superoxide accumulation, stabilizes mitochondrial membrane potential, maintains mitochondrial morphology, preserves nuclear integrity, inhibits apoptosis, blocks the MAPK cascade, and downregulates the expression of pro-inflammatory factors and enzymes in H2O2 (400 μM)-stressed SH-SY5Y neuronal cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:SH-SY5Y cells
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Concentration:10 nM, 50 nM, 100 nM, 200 nM, 500 nM, 1.0 μM, 5 μM, 10 μM, 50 μM, 100 μM, 200 μM
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Incubation Time:24 h
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Result:Demonstrated excellent cytocompatibility.
The cell survival rate remained above 90% even at a high concentration of 100 μM.
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Cell Line:SH-SY5Y cells
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Concentration:10 nM, 50 nM, 100 nM, 200 nM, 500 nM, 1.0 μM, 5 μM, 10 μM, 50 μM
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Incubation Time:Pretreatment for 24 h, followed by co-incubation with 400 μM H2O2 for 2 h
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Result:Effectively rescued cells from oxidative stress-induced death.
A dose of 1 μM restored cell viability to approximately 89.4%.
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Cell Line:SH-SY5Y cells
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Concentration:1 μM
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Incubation Time:Pretreatment for 24 h, followed by H2O2 exposure
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Result:Significantly suppressed the expression of pro-apoptotic proteins (Caspase 3, Cleaved Caspase 3, Bax).
Significantly upregulated the level of the anti-apoptotic protein (BCL-XL).
significantly attenuated the signal activation induced by oxidative stress.
Markedly reduced the phosphorylation levels of ERK1/2, p38, and JNK kinases.
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Cell Line:SH-SY5Y cells
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Concentration:1 μM
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Incubation Time:Pretreatment for 24 h, followed by H2O2 exposure
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Result:Exerted broad anti-inflammatory effects at the transcriptional level.
Significantly downregulated the mRNA expression of TNF-α, IL-1β, IL-6, iNOS, and COX-2.
MAPK-IN-6 (5 mg/kg; i.p.; single administration) exhibits the ability to successfully cross the blood-brain barrier (BBB) and reach effective concentrations in brain tissues in normal rat models[1].
MAPK-IN-6 (1-10 mg/kg; i.p.; single administration; 3 days) exhibits excellent in vivo safety in normal rat models, causing no observable organ toxicity or structural abnormalities in the liver, kidney, or spleen[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Transient bilateral common carotid artery occlusion reperfusion (tBCCAO/R) rat model. Bilateral common carotid arteries were sequentially occluded for 30 minutes, followed by a 5-minute interruption of blood flow, two additional 3-second clamping cycles, and subsequent reperfusion[1]
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Dosage:5 mg/kg
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Administration:i.p.; single dose
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Result:Reduced the cerebral infarct volume and effectively decreased the modified neurological severity scores (mNSS).
Improved ischemia-induced motor incoordination, reducing the number of falls in the rotarod test and shortening the completion time in pole and balance beam tests.
Alleviated post-stroke anxiety and depressive-like behaviors by increasing time spent in the central zone during the open field test and enhancing sucrose consumption in the sucrose preference test.
Preserved neuronal morphology in the cortex and striatum, reduced pyknosis and neurodegeneration, and largely increased the ratio of surviving neurons.
Suppressed the pathological activation of astrocytes (GFAP, S100β) and microglia (IBA1) in cortical and striatal regions, reversing their transition into hypertrophic or amoeboid forms.
Upregulated the gene expression of endogenous antioxidant enzymes (SOD1, CAT, GPx4) in the cortex and striatum, reversing oxidative stress injury.
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Animal Model:Normal healthy rat model[1]
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Dosage:5 mg/kg
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Administration:i.p.; single dose
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Result:Successfully penetrated the blood-brain barrier, exhibiting a distinct mass spectrometry peak in brain extracts with an estimated penetration concentration of 3.68 μM.
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Animal Model:Normal healthy rat model[1]
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Dosage:1 mg/kg, 5 mg/kg, 10 mg/kg
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Administration:i.p.; single dose; 3 days
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Result:Caused no morphological damage or tissue necrosis to the kidneys, liver, and spleen, demonstrating excellent in vivo organ compatibility.
Chemical Information
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Molecular Weight 436.41
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Formula C21H24O10
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SMILES
O=C1C2=C(C=CO2)C3=C(OC)C(O[C@H]4[C@H](O)[C@@H](O)[C@H](O)[C@@H](CO)O4)=C(OC)C=C3CC1
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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.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
MAPK-IN-6 Related Classifications
HY-180807 Related Classifications
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