Deltafluorine
Deltafluorine is a phosphodiesterase delta (PDEδ) inhibitor with an IC50 of 27 nM, a KD of 148 nM. Deltafluorine covalently modifies the specific glutamate residue p.E88 in the ligand binding site of PDEδ, interfering with its chaperone function. Deltafluorine inhibits signaling through the MAPK and Akt-mTOR pathway, reduces ERK1/2 expression. Deltafluorine reduces tumor volume in an autochthonous mouse model of Kras-driven lung adenocarcinoma. Deltafluorine can be used for the research of lung adenocarcinoma.
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- Formule: C33H42ClFN4O4S2
- Masse moléculaire:677.29
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Activité biologique
Description
IC50 & Target
[1]|
PDEδ 27 nM (IC50) |
PDEδ 148 nM (Kd) |
ERK1 |
ERK2 |
In Vitro
Deltafluorine (Compound 22a) (60 μM; 0-7 days) covalently modifies purified PDEδ at residue p.E88 with >85% efficiency over 7 days in vitro, with a second-order rate constant of 5.4 M−1 s−1[1].
Deltafluorine (10 μM; 2 h) induces significant thermal stabilization of PDEδ in Jurkat cells with a ΔTm of 16.6 ± 3.2 °C[1].
Deltafluorine (5 μM; 0.25-4 h) reduces phosphorylation of ERK1/2 and S6 in PA-TU-8902 cells[1].
Deltafluorine (5 μM; 0-120 h) inhibits the proliferation of PA-TU-8902 cells with 84 ± 2% growth inhibition[1].
Deltafluorine (5 μM; 2 h) inhibits the MAPK and Akt-mTOR pathways in PA-TU-8902 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:PA-TU-8902 cells
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Concentration:5 μM
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Incubation Time:0.25, 0.5, 1, 2, 4 h
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Result:Reduced phosphorylation of ERK1/2 (Thr202/Tyr204) and S6 (S235/236) in PA-TU-8902 cells over the time course.
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Cell Line:PA-TU-8902 cells
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Concentration:5 μM
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Incubation Time:4 h treatment + 20 h wash-out regimen over 4 days
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Result:Inhibited growth of PA-TU-8902 cells with 84 ± 2% growth inhibition under wash-out conditions.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:KrasLSL.G12D/wt; Trp53fl/fl (KP mice; autochthonous lung adenocarcinoma model induced by intratracheal Adeno-CMV-Cre instillation)[1]
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Dosage:15 mg/kg
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Administration:I.p.; daily; 21 days
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Result:Reduced tumor load by 42% compared to untreated controls.
Lowered lung tumor volume occupancy to 21.6% versus 47.5% in untreated controls.
Chemical Information
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Masse moléculaire 677.29
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Formule C33H42ClFN4O4S2
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SMILES
CC1=NC(C)=C(CF)C=C1CN(S(=O)(C2=CC=C(S(=O)(N(C3CCCC3)CC4=CC=C(Cl)C=C4)=O)C=C2)=O)CC5CCNCC5
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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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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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
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)