SAP2-IN-1
SAP2-IN-1 is a secreted aspartic protease 2 (SAP2) inhibitor and has potent SAP2 inhibitory activity with an IC50 value of 0.92 μM. SAP2-IN-1 also is a virulence factor inhibitor and is inactive in vitro. SAP2-IN-1 can be used for the research of infection.
商品は「研究用試薬」です。人や動物の医療用・臨床診断用・食品用の製品ではありません。
研究用途以外に使用した場合、当社は一切の責任を負いかねます。
- CAS 番号: 2512847-37-7
- 分子式: C34H29NO7
- 分子量:563.60
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保管条件:
Please store the product under the recommended conditions in the Certificate of Analysis.
生物活性
製品説明
IC50 & Target
IC50: 0.92 μM (SAP2)[1]
体外実験
SAP2-IN-1 (compound 24a) (100 μM) shows potent SAP2 inhibitory activity with an IC50 value of 0.92 μM[1].
SAP2-IN-1 (100 μM) has not inhibit the growth of C. albicans and inactive in vitro[1].
SAP2-IN-1 (64 μg/mL) blocks fungi biofilm and hypha formation by down-regulating the expression of genes SAP2, ECE1, ALS3 and EFG1[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:C. albicans cells
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Concentration:64 μg/mL
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Incubation Time:
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Result:Inhibited hypha growth through the cAMP-dependent pathway.
体内実験
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:a murine model of invasive candidiasis[1]
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Dosage:10 mg/kg
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Administration:intraperitoneally administration, once daily, for four days
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Result:Significantly reduced the fungal burden in the kidney.
化学情報
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CAS 番号 2512847-37-7
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分子量 563.60
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分子式 C34H29NO7
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SMILES
CC1=CC=C(C2=CC=C(/C(C3=O)=C\C4=CC=C(OCC(O)=O)C=C4OCC(O)=O)C(N3CC5=CC=C(C)C=C5)=C2)C=C1
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
プロトコル
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Research Protocol for Infectious Diseases
Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.
純度とドキュメンテーション
参考文献
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)