AHR antagonist 8
AHR antagonist 8 (compound SG-02) is a regulator of utrophin, a homolog of dystrophin, and an AhR antagonist (Kd: 41.68 nM). Studies have shown that 800 nM of AHR antagonist 8 can upregulate utrophin by 2.7 times. AHR antagonist 8 also stimulates increased MyHC expression, suggesting that it has the potential to enhance myogenesis. After ADME evaluation, AHR antagonist 8 also has a certain oral bioavailability.
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- CAS No.: 3052113-26-2
- Formule: C16H14FN3O2S
- Masse moléculaire:331.36
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Activité biologique
Description
IC50 & Target
Chemical Information
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CAS No. 3052113-26-2
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Masse moléculaire 331.36
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Formule C16H14FN3O2S
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SMILES
O=S(C1=CC2=CN=C(NCC3=CC=C(F)C=C3)N=C2C=C1)(C)=O
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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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C2C12 myoblast-to-myotube differentiation
C2C12 cells are mouse myoblast-lineage cells that proliferate in growth conditions and differentiate after mitogen reduction into elongated, multinucleated myotubes; the differentiation readout is generated by morphology, myogenic marker expression, and immunofluorescent detection of myosin heavy chain-positive myotubes with nuclear counterstaining.
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Protocol for Pharmacokinetic Study
Pharmacokinetic studies quantify how an organism handles a drug over time through absorption, distribution, metabolism, and excretion, and the core experimental readout is the concentration-time profile of parent drug and, when relevant, metabolites in biological matrices such as plasma, whole blood, urine, bile, or tissue. Pharmacokinetic analysis links dose, route, exposure, clearance, half-life, distribution, bioavailability, and systemic exposure to drug efficacy and toxicity hypotheses rather than measuring a signaling pathway directly. The literature links pharmacokinetics to drug-development phenotypes by showing that drug metabolism and pharmacokinetics influence compound progression, exposure-response interpretation, safety margins, dosing strategy, and failure risk during discovery and development. DMPK science contributes to compound optimization by integrating physicochemical properties, in vitro metabolism, transporter behavior, in vivo exposure, and pharmacodynamic contex
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)