Plumericin
Plumericin is an anti-inflammatory, antioxidant, and antibacterial agent. Plumericin reduces Apoptosis, promotes Nrf-2 and inhibits NF-κB and AhR activation, blocks STAT3 signaling. Plumericin inhibits Mycobacterium tuberculosis growth. Plumericin can be used for the research of chronic kidney disease, vascular diseases, inflammatory bowel diseases, peritonitis, and tuberculosis.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- CAS. Nr.: 77-16-7
- Formel: C15H14O6
- Molecular Weight:290.27
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biologische Aktivität
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STAT3 |
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Cell Line
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Type | Value | Description | References |
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| Cancer cell lines | ED50 |
0.1 μg/mL
Compound: 5
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Cytotoxicity against human colon cancer cells
Cytotoxicity against human colon cancer cells
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[PMID: 1965200] |
Plumericin (0.5-2 μM; 1 h pre-incubation, then 24 h co-incubation with IS) significantly reduces IS-induced apoptosis, decreases Bax expression, and increases Bcl-2 expression in IEC-6 cells[1].
Plumericin (0.5-2 μM; 1 h pre-incubation, then 24 h co-incubation with IS) significantly inhibits IS-induced expression of iNOS, COX-2, and caspase-1, as well as IL-1β production, in IEC-6 cells[1].
Plumericin (0.3-3 μM; 30 min pre-incubation, 24 h serum-stimulated) inhibits serum-induced proliferation of primary rat aortic VSMC with an IC50 of 1.11 μM, as measured by BrdU incorporation following 30 min pre-incubation and 24 h serum stimulation[2].
Plumericin (0.5-2 μM; 24 h) does not reduce proliferation of rat intestinal epithelial IEC-6 cells[3].
Plumericin (0.3-10 μM; 30 min pretreatment + 4 h incubation) potently inhibits TNF-α-induced and constitutively active IKK-β-induced NF-κB pathway activation in HEK293/NF-κB-luc cells, with an IC50 of 1.07 μM for TNF-α-induced transactivation, and does not alter basal NF-κB activity[4].
Plumericin (0.5-2 μM; 24 h) significantly increases migration speed in LPS + IFN-stimulated IEC-6 cells, promoting intestinal epithelial wound restitution[5].
Plumericin (serial dilutions; 5 days for MIC, 6 weeks for MBC) inhibits the growth of pan-sensitive Mycobacterium tuberculosis H37Rv with an MIC of 2.1 ± 0.12 μg/mL and reduces viable bacterial counts by ≥99% at an MBC of 3.6 ± 0.22 μg/mL[6].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:IEC-6 rat intestinal epithelial cells
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Concentration:0.5-2 μM
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Incubation Time:1 h pre-incubation, then 24 h co-incubation with IS
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Result:Significantly reduced IS-induced apoptosis at all tested concentrations.
Significantly decreased pro-apoptotic Bax expression at all tested concentrations compared to IS-only treated cells.
Significantly increased anti-apoptotic Bcl-2 expression at all tested concentrations compared to IS-only treated cells.
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Cell Line:IEC-6 rat intestinal epithelial cells
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Concentration:1 μM
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Incubation Time:1 h before IS
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Result:Significantly reduced IS-induced nuclear translocation of NF-κB p65, decreasing nuclear NF-κB p65 fluorescence intensity compared to IS-only treated cells.
Plumericin (3 mg/kg; i.p.; twice) statistically significantly reduces thioglycollate-induced neutrophil recruitment to the peritoneal cavity of mice (P < 0.001)[4].
Plumericin (3 mg/kg; i.p.; once daily; 4 days) significantly alleviates colonic inflammation, PARP activation, and apoptotic damage in DNBS-induced mouse colitis models[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:CD1 mice (male, 20-25 g, DNBS-induced colitis)[3]
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Dosage:3 mg/kg
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Administration:i.p.; daily; 4 days
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Result:Significantly reduced body weight loss compared to DNBS-only mice.
Prevented colon shortening relative to DNBS-only mice.
Significantly reduced macroscopic colon damage scores.
Reduced histological signs of colon injury, including decreased cellular infiltration, edema, and inflammatory lesions.
Significantly reduced colon TNF-α levels (P < .001 vs DNBS group).
Inhibited DNBS-induced IκB-α degradation and NF-κB p65 nuclear translocation.
Significantly reduced colon malondialdehyde (MDA) levels (P < .001 vs DNBS group).
Reduced nitrotyrosine immunoreactivity in colon tissue (P < .001 vs DNBS group).
Significantly increased colon Nrf2 and superoxide dismutase (SOD) expression.
Significantly reduced colon IL-1β levels (P < .001 vs DNBS group).
Reduced colon caspase-1 expression.
Chemical Information
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CAS. Nr. 77-16-7
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Molecular Weight 290.27
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Formel C15H14O6
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SMILES
C(\C)=C/1\[C@]2([C@]3([C@@]4([C@](C=C3)(C(C(OC)=O)=CO[C@@]4(O2)[H])[H])[H])OC1=O)[H]
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Structure Classification
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Initial Source
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Reinheit & Dokumentation
Verweise
[1]. Rispoli RM, et al. Plumericin Modulates the AhR-NFκB-Nrf2 Signaling Network to Counteract Indoxyl Sulfate-Induced Intestinal Epithelial Cells Impairment. Int J Mol Sci. 2025;27(1):293. Published 2025 Dec 27. [Content Brief]
[2]. Heiss EH, et al. Plumericin inhibits proliferation of vascular smooth muscle cells by blocking STAT3 signaling via S-glutathionylation. Sci Rep. 2016;6:20771. Published 2016 Feb 9. [Content Brief]
[3]. Rapa SF, et al. Plumericin prevents intestinal inflammation and oxidative stress in vitro and in vivo. FASEB J. 2020;34(1):1576-1590. [Content Brief]
[4]. Fakhrudin N, et al. Identification of plumericin as a potent new inhibitor of the NF-κB pathway with anti-inflammatory activity in vitro and in vivo. Br J Pharmacol. 2014;171(7):1676-1686. [Content Brief]
[5]. Rapa SF, et al. Plumericin Protects against Experimental Inflammatory Bowel Disease by Restoring Intestinal Barrier Function and Reducing Apoptosis. Biomedicines. 2021;9(1):67. Published 2021 Jan 12. [Content Brief]
[6]. Kumar P, et al. Anti-mycobacterial activity of plumericin and isoplumericin against MDR Mycobacterium tuberculosis. Pulm Pharmacol Ther. 2013;26(3):332-335. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)