Acremonamide
Acremonamide is a cyclic pentapeptide lactone discovered from the marine-derived Acremonium strain CNQ-049, possessing wound healing activity. Acremonamide upregulates the expression of COL1A2 and ACTC1 genes and enhances the motility of keratinocytes and fibroblasts. Acremonamide promotes wound healing in mouse skin wound models. Acremonamide can be used in research related to skin wound healing.
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- CAS 番号: 2855099-87-3
- 分子式: C33H44N4O6
- 分子量:592.74
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保管条件:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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生物活性
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化学情報
- プロトコル
- 純度とドキュメンテーション
- 参考文献
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Help & FAQs
Endogenous Metabolite アイソフォーム固有の製品をすべて表示
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生物活性
製品説明
体外実験
Acremonamide regulates the expression of wound healing-related genes (ACTC1, COL1A2) in HaCaT cells[2].
Acremonamide (5 µM; 24-48 h) reduces the mRNA expression of β-catenin downstream target genes in A549, AGS, and Caco-2 cells[3].
Acremonamide (5 µM) decreases Hes-1 mRNA expression in AGS, A549, and Caco-2 cells[3].
Acremonamide (1-5 µM; three weeks) significantly inhibits the tumorigenicity of A549, AGS, and Caco-2 cells[3].
Acremonamide (1-5 µM; 24 h) decreases the protein levels of KITENIN and Cleaved Notch1 in A549, AGS, and Caco-2 cells; it decreases the protein level of β-catenin in AGS and Caco-2 cells, but not in A549 cells[3].
Acremonamide (1-5 µM) decreases the mRNA expression of KITENIN and KAI1 in A549, AGS, and Caco-2 cells[3].
Acremonamide (1-5 µM) reduces β-catenin-mediated TOPFLASH activity in HEK293T cells[3].
Acremonamide (5 µM) decreases the nuclear-to-cytoplasmic ratio of β-catenin in A549 cells without affecting total β-catenin levels[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:Caco2, HaCaT, NIH3T3
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Concentration:3.12, 6.25, 12.5, 25, 50 μM
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Incubation Time:48 h
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Result:Did not affect Caco2 cell viability at tested concentrations.
Marginally increased the viability of HaCaT and NIH3T3 cells.
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Cell Line:HaCaT, NIH3T3
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Concentration:12.5 μM
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Incubation Time:24 h
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Result:Increased HaCaT and NIH3T3 cell invasion by approximately 50%.
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Cell Line:HaCaT, NIH3T3
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Concentration:12.5 μM
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Incubation Time:24 h
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Result:Increased HaCaT and NIH3T3 cell migration by approximately 50%.
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Cell Line:A549, AGS, and Caco-2
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Concentration:10, 25, 50, 100 μM
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Incubation Time:48 h
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Result:Decreased the viability of AGS and Caco-2 cells significantly at concentrations of 50-100 μM.
Did not affect the viability of A549 cells at concentrations of 10-50 μM.
Decreased the viability of A549 cells marginally at 100 μM.
Did not decrease the viability of AGS and Caco-2 cells at concentrations of 10-25 μM.
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Cell Line:A549, AGS, and Caco-2
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Concentration:1, 2.5, 5 μM
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Incubation Time:24 h
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Result:Displayed a dose-dependent inhibitory effect on the migration of all three cell types at concentrations from 1 to 5 µM.
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Cell Line:A549, AGS, and Caco-2
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Concentration:1, 2.5, 5 µM
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Incubation Time:24 h
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Result:Displayed dose-dependent inhibition of invasion by each cell type by up to ~45% at 5 µM concentrations.
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Cell Line:A549, AGS, and Caco-2
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Concentration:1, 2.5, 5 µM
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Incubation Time:three weeks
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Result:Dose-dependently decreased the colony formation of A549, AGS, and Caco-2 cells.
Significantly decreased the tumorigenicity of A549, AGS, and Caco-2 cells at 5 µM.
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Cell Line:A549, AGS, and Caco-2
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Concentration:1, 2.5, 5 µM
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Incubation Time:24 h
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Result:Decreased the protein level of KITENIN in A549, AGS, and Caco-2 cells.\nDecreased the protein level of β-catenin in AGS and Caco-2 cells.
Did not significantly affect the protein level of β-catenin in A549 cells.\nDecreased the level of Cleaved Notch1 in A549, AGS, and Caco-2 cells.
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Cell Line:A549
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Concentration:5 µM
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Incubation Time:24 h
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Result:Did not affect the level of total β-catenin.
Decreased the β-catenin nuclear to cytoplasmic ratio remarkably.
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Cell Line:A549, AGS, and Caco-2
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Concentration:5 µM
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Incubation Time:24 h; 48 h
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Result:Suppressed the mRNA expression of cyclin-D1 in A549 and CD44 in Caco-2 at 24 h.
Suppressed the mRNA expression of c-Myc and CD44 in AGS cells at 24 h.
Suppressed the mRNA expression of c-Myc, CD44, and cyclin-D1 in AGS cells at 48 h.
Suppressed the mRNA expression of cyclin-D1 and CD44 in A549 at 48 h.
Suppressed the mRNA expression of CD44 in Caco-2 cells at 48 h.
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:BALB/C (male, six-week-old, 19 g)[2]
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Dosage:100 μM
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Administration:topical; immediately after surgery and after 24 h
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Result:Reduced wound area by approximately 25% at day 6 compared to vehicle control.
化学情報
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CAS 番号 2855099-87-3
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分子量 592.74
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分子式 C33H44N4O6
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SMILES
C([C@H]1C(=O)N[C@@H](CC2=CC=CC=C2)C(=O)N(C)[C@@H](C)C(=O)O[C@H]([C@H](C)C)C(=O)N[C@@H](C(C)C)C(=O)N1C)C3=CC=CC=C3
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Structure Classification
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Initial Source
marine-derived fungus
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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.
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)
Acremonamide 関連分類
HY-N15490 関連分類
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