Multitarget AD-IN-8
Multitarget AD-IN-8 is a blood-brain barrier-penetrant, orally active multitarget inhibitor. Multitarget AD-IN-8 inhibits abnormal Tau phosphorylation at Thr181 and Ser396 sites and attenuates NF-κB phosphorylation. Multitarget AD-IN-8 downregulates BACE1 expression to reduce Aβ production, inhibits the Bax/Bcl-2 pathway, and suppresses Caspase-1 activation. Multitarget AD-IN-8 attenuates p38, ERK1/2, and JNK phosphorylation and inhibits Aβ25-35-induced Apoptosis. Multitarget AD-IN-8 exhibits neuroprotective effects against Aβ25-35-induced injury, ameliorates learning and memory deficits in AD mouse models, and alleviates hippocampal neuronal pathological damage. Multitarget AD-IN-8 can be used for research on Alzheimer's disease.
For research use only. We do not sell to patients.
- Formula: C31H34N2O8
- Molecular Weight:562.61
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Caspase Isoforms
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Biological Activity
Description
IC50 & Target
[1]|
BACE1 |
Bax |
Bcl-2 |
Caspase-1 |
ERK1 |
ERK2 |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| PC-12 | EC50 |
1.24 μM
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Neuroprotective activity against Aβ25-35-induced injury in PC12 cells assessed as increase in cell viability incubated for 24 hrs by CCK-8 assay.
Neuroprotective activity against Aβ25-35-induced injury in PC12 cells assessed as increase in cell viability incubated for 24 hrs by CCK-8 assay.
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42628381 |
In Vitro
Multitarget AD-IN-8 (Compound S12) (20 μM) demonstrates potent neuroprotective activity against Aβ25-35 induced injury in PC12 cells with an EC50 of 1.24 μM[1].
Multitarget AD-IN-8 (5-20 μM; 1 h pretreatment and 24 h Aβ25-35 exposure) suppresses the aberrant phosphorylation of tau protein at Thr181 and Ser396 in PC12 cells[1].
Multitarget AD-IN-8 (5-20 μM; 1 h pretreatment and 24 h Aβ25-35 exposure) inhibits the Aβ25-35 induced activation of the NF-κB signaling pathway in PC12 cells[1].
Multitarget AD-IN-8 (5-20 μM; 1 h pretreatment and 24 h Aβ25-35 exposure) suppresses Aβ25-35 induced activation of the MAPK signaling pathway in PC12 cells[1].
Multitarget AD-IN-8 (5-20 μM; 1 h pretreatment and 24 h Aβ25-35 exposure) inhibits the production of BACE1 in PC12 cells induced by Aβ25-35[1].
Multitarget AD-IN-8 (5-20 μM; 1 h pretreatment and 24 h Aβ25-35 exposure) inhibits the activation of the Bax/Bcl-2 pathway and suppresses caspase-1 activation in PC12 cells[1].
Multitarget AD-IN-8 (20 μM; 24 h) effectively suppresses Aβ25-35 induced apoptosis in PC12 cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:PC12
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Concentration:5-20 μM
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Incubation Time:1 h (pretreatment); 24 h (Aβ25-35 exposure)
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Result:Markedly attenuated Aβ25-35 induced hyperphosphorylation of tau at Thr181 and Ser396 residues.
Inhibited the relative protein expression of p-Tau (Thr181)/Total-Tau and p-Tau (Ser396)/Total-Tau.\nAt a concentration of 20 μM, significantly attenuated Aβ25-35 induced phosphorylation of NF-κB.
Exhibited greater inhibitory activity than both donepezil and UA.\nAttenuated the Aβ25-35 induced upregulation of p-p38/p38, p-ERK1/2/ERK1/2, and p-JNK/JNK.\nMarkedly attenuated the Aβ25-35 induced BACE1 upregulation.\nAttenuated the Aβ25-35 induced upregulation of the Bax/Bcl-2 ratio and caspase-1 expression.
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Cell Line:PC12
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Concentration:20 μM
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Incubation Time:24 h
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Result:Reduced the percentage of apoptotic PC12 cells to 11%, compared to the Aβ25-35 group which had an apoptosis rate of 35.2%.
In Vivo
Multitarget AD-IN-8 (12.5-50 mg/kg; i.g.; daily; 20 consecutive days) exhibits no overt toxicity in major organs including the heart, liver, spleen, and kidneys in mice[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:ICR mice (Male, 20-25 g)[1]
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Dosage:12.5, 25, 50 mg/kg
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Administration:i.g.; daily; 21 consecutive days
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Result:Ameliorated the alternation behavior deficit in the Y-maze test.
Increased the discrimination index (DI) and preference index (PI) at 1 h and 24 h in the novel object recognition test.
Decreased escape latency and swimming distance in the Morris water maze, with the 50 mg/kg group differing significantly from the model group.
Increased time spent in and distance traveled within the target quadrant in the spatial probe test, with the 50 mg/kg group showing the most pronounced improvement.
Resulted in a more organized neuronal architecture and significantly attenuated neuronal damage in both the CA1 and CA3 regions.
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Animal Model:ICR mice (Male)[1]
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Dosage:12.5, 25, 50 mg/kg
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Administration:i.g.; daily; 20 consecutive days
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Result:No abnormal behavior, mortality, or clinically significant changes in body weight were observed.
HE staining of major organs (heart, liver, spleen, and kidney) showed no obvious pathological lesions in all groups.
- Western Blot
- RNA extraction experimental
- Annexin V plus membrane-impermeant dye apoptosis staining
- Protocol for Water Maze
- Research Protocol for Inflammation-related Diseases
- Alzheimer’s Disease Modeling
- Kinase activity and phosphorylation assays
- Protocol for Shuttle Box Test (TDPA)
- Detection of Apoptosis
- TUNEL staining for apoptotic DNA fragmentation
- Apoptosis Solutions
- Protocol for Kinase activity and phosphorylation assays
- Pyroptosis Solutions
Chemical Information
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Molecular Weight 562.61
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Formula C31H34N2O8
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SMILES
CC(C1=C(O)C(C)=C(O)C([C@@]2(C)C(/C3=C(NC4=CC=C(OC(N(CCC)CCC)=O)C=C4)/C)=O)=C1OC2=CC3=O)=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.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)