PDE2-IN-1
PDE2-IN-1 is a potent and orally active PDE2 inhibitor with an IC50 of 0.6 μM, demonstrating neuroprotective effects. PDE2-IN-1 modulates the PKA/CREB/BDNF signaling pathway by inhibiting PDE2. PDE2-IN-1 improves memory deficits and cognitive impairment in an okadai acid (OKA)-induced Alzheimer’s disease (AD) mouse model. PDE2-IN-1 can be used for the research of AD.
For research use only. We do not sell to patients.
- Formula: C18H19F3N4O3
- Molecular Weight:396.36
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
PDE2 0.6 μM (IC50) |
In Vitro
PDE2-IN-1 (compound 14c) (0-50 μM; 24 h) shows no cytotoxicity in neuronal cells (U251, SY5Y, and HMC3 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:U251, SY5Y, and HMC3 cell lines
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Concentration:0, 1.5625, 3.125, 6.25, 12.5, 25, 50 μM
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Incubation Time:24 h
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Result:Showed no effects on U251, SY5Y, and HMC3 cell survival rates.
Parmacokinetics
| Species | Dose | Route | AUC0-t | AUC0-∞ | MRT0-t | MRT0-∞ | T1/2 | Tmax | Vz-F_obs | CL/F | Cmax | F |
|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Rat[1] | 2 mg/kg | i.v. | 3540.2 μg/L·h | 3560.228 μg/L·h | 4.292 h | 4.481 h | 4.437 h | 0.083 h | 3.493 L/kg | 0.584 L/h/kg | 1519.1 μg/L | / |
| Rat[1] | 20 mg/kg | p.o. | 34006.498 μg/L·h | 34057.752 μg/L·h | 7.856 h | 7.916 h | 4.418 h | 2.167 h | 3.748 L/kg | 0.598 L/h/kg | 3547.8 μg/L | 95.66 % |
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6 mice (20-30 g) bilateral intracerebroventricularly injected with OKA[1]
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Dosage:10 and 30 mg/kg
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Administration:i.p., daily for 14 days
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Result:Had a negligible effect on the mean daily bodyweight profile in OKA-induced AD mice.
Showed no obvious changes of the levels of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), carbamide (UREA), creatinine (CREA) and AST/ALT ratio in OKA-induced AD group and different doses group.
Led to minimal injury to hippocampal neurons.
Showed beneficial effects to ameliorate the memory and cognitive impairment in OKA-induced AD mice.
Ameliorated OKA-induced memory and cognitive impairment via PKA/CREB/BDNF pathway.
Alleviated synaptic impairments in OKA-induced AD mice.
Chemical Information
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Molecular Weight 396.36
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Formula C18H19F3N4O3
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SMILES
O=C1C2=NN(CCO)C(C(NC(C3=CC=C(C(F)(F)F)C=C3)C)=O)=C2CCN1
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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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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Alzheimer’s Disease Modeling
Alzheimer’s Disease (AD) is a neurodegenerative disorder characterized by a progressive decline in cognitive functions and loss of specific types of neurons and synapses. Alzheimer's symptoms can be simulated in mice by injecting drugs (such as Aβ) or genetically modified.
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How to Choose the Right Model Animal
Choosing the right model animal is a validity-driven decision in which the species, strain, sex, age, genetic background, disease-induction method, outcome measures, and welfare burden must match the scientific question rather than laboratory tradition or convenience. A model should be selected by judging face validity, construct validity, and predictive validity: whether it resembles the human phenotype, whether it reproduces relevant mechanisms, and whether results are likely to predict human biology or treatment response. Animal studies often fail to translate because of species differences, weak disease resemblance, poor experimental design, inadequate reporting, publication bias, and underuse of randomization, blinding, and sample-size justification. Unresolved questions include how to rank competing models objectively, how much human-disease complexity must be reproduced for a given objective, and when non-animal systems such as organoids, ex vivo tissue, or computational models
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)