2. Apoptosis NF-κB PI3K/Akt/mTOR Epigenetics Autophagy Anti-infection
  3. Apoptosis NF-κB Keap1-Nrf2 AMPK Autophagy SARS-CoV DNA Methyltransferase
  4. Panduratin A

Panduratin A is an orally active natural compound with multiple pharmacological activities. By specifically inhibiting the NF-κB signaling pathway, Panduratin A exerts potent anti-inflammatory and antioxidant effects in intestinal and vascular inflammation models. Panduratin A exerts a definite protective effect against Colistin (HY-113678)-induced nephrotoxicity by alleviating oxidative stress, improving mitochondrial dysfunction and inhibiting cell apoptosis. Panduratin A activates autophagy via an AMPK-dependent pathway and exhibits anti-tuberculosis activity. Panduratin A exerts antiviral effects by inhibiting the methyltransferase (DNA Methyltransferase) of SARS-CoV-2.

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Panduratin A

Panduratin A Chemical Structure

CAS No. : 89837-52-5

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Panduratin A Related Antibodies

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Description

Panduratin A is an orally active natural compound with multiple pharmacological activities. By specifically inhibiting the NF-κB signaling pathway, Panduratin A exerts potent anti-inflammatory and antioxidant effects in intestinal and vascular inflammation models. Panduratin A exerts a definite protective effect against Colistin (HY-113678)-induced nephrotoxicity by alleviating oxidative stress, improving mitochondrial dysfunction and inhibiting cell apoptosis. Panduratin A activates autophagy via an AMPK-dependent pathway and exhibits anti-tuberculosis activity. Panduratin A exerts antiviral effects by inhibiting the methyltransferase (DNA Methyltransferase) of SARS-CoV-2[1][2][3][4][5].

Cellular Effect
Cell Line Type Value Description References
Vero C1008 CC50
14.71 μM
Compound: 94
Cytotoxicity against African green monkey Vero E6 cells assessed as reduction in cell growth incubated for 24 hrs by WST-8 assay
Cytotoxicity against African green monkey Vero E6 cells assessed as reduction in cell growth incubated for 24 hrs by WST-8 assay
[PMID: 37597436]
In Vitro

Panduratin A alleviates tert-butyl hydroperoxide-induced oxidative damage in human hepatocellular carcinoma (HepG2) cells[1].
Panduratin A inhibits the production of inflammatory mediators TNF-α, NO and PGE2 in vitro[1].
Panduratin A inhibits mast cell degranulation and cytokine expression in rat basophilic leukemia mast cells[1].
Panduratin A (0.5-10 μM; 48 h) shows no toxicity to HMEC-1 human endothelial cells, and the cell viability remains above 90% at concentrations up to 4 μM (48 h treatment)[2].
Panduratin A (2-4 μM; 27 h) reduces the secretion levels of IL-6 and MCP-1 in TNF-α-stimulated human endothelial cell line HMEC-1 in a dose-dependent manner, with the strongest effect observed at 4 μM[2].
Panduratin A (4 μM; 24 h) inhibits TNF-α-induced upregulation of VCAM-1 and ICAM-1 in human endothelial cell line HMEC-1, while preserving cell morphology and cytoskeletal structure[2].
Panduratin A (4 μM; 24 h) significantly reduces the adhesion of THP-1 human monocytes to TNF-α-stimulated HMEC-1 human endothelial cells[2].
Panduratin A (2-4 μM; 3.5 h) dose-dependently inhibits TNF-α-induced phosphorylation of NF-κB and degradation of IκB in human endothelial cell line HMEC-1, with the most potent effect observed at 4 μM[2].
Panduratin A (2-4 μM; 3.5 h) dose-dependently inhibits TNF-α-induced NF-κB nuclear translocation and maintains the cytoplasmic IκB level in HMEC-1 human endothelial cells[2].
Panduratin A (50 μM; 4 h) induces autophagosome formation in RAW264.7 macrophages[3].
Panduratin A (0.048-50 μM; 2 h) acts as an autophagy inducer in RAW264.7 macrophages, with an EC50 of 12.55 μM; this is evidenced by the dose-dependent increase in the LC3-II/actin ratio and the dose-dependent decrease in the p62/actin ratio[3].
Panduratin A (25 μM; 4 h) induces complete autophagic flux in RAW264.7 macrophages, which is characterized by increased numbers of both autophagosomes and autolysosomes, as well as regulation of autophagic marker protein levels[3].
Panduratin A (25 μM; 4 h) induces autophagy in RAW264.7 macrophages via activating AMPK, independent of the inhibitory effect on the mTOR signaling pathway[3].
Panduratin A (25 μM; 2-24 h) does not induce TFEB nuclear translocation in RAW264.7 macrophages, which is consistent with mTOR-independent autophagy induction[3].
Panduratin A (1.5625-50 μM; 24 h) inhibits the survival of Mtb within RAW264.7 macrophages in a dose-dependent manner via a host-mediated mechanism rather than direct mycobactericidal activity, and this effect is significant when treated at 25 and 50 μM for 24 h[3].
Panduratin A (25 μM; 24 h) inhibits Mtb survival in RAW264.7 macrophages in a Beclin-1-dependent manner, suggesting that it mediates bacterial clearance via autophagy[3].
Panduratin A (25 μM; 4 h) enhances the sequestration of Mtb into autophagosomes in RAW264.7 macrophages[3].
Panduratin A (25 μM; 4 h) promotes autophagy-dependent trafficking of Mtb to lysosomes in RAW264.7 macrophages[3].
Panduratin A (1-5 μM) protects RPTEC/TERT1 cells against polymyxin-induced toxic damage by increasing cell viability, reducing apoptosis and reactive oxygen species (ROS) production, maintaining mitochondrial membrane potential, upregulating the anti-apoptotic protein Bcl-2, and downregulating the pro-apoptotic protein cytochrome c and activated caspase-3, with the most significant effect observed at the concentration of 5 μM[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Panduratin A Related Antibodies

Cell Cytotoxicity Assay[2]

Cell Line: HMEC-1 human endothelial cells
Concentration: 0.5, 1, 2, 3, 4, 5, 6, 7, 8, 9, 10 μM
Incubation Time: 48 h
Result: Reduced HMEC-1 cell viability/proliferation to below 90% at concentrations above 4 μM.
Maintained cell viability/proliferation at ≥ 90% at concentrations of 0.5, 1, 2, 3, 4 μM.

ELISA Assay[2]

Cell Line: TNF-α-stimulated HMEC-1 human endothelial cells
Concentration: 2, 3, 4 μM
Incubation Time: 3 h (pre-incubation); 24 h (co-incubation with TNF-α)
Result: Reduced TNF-α-induced IL-6 levels from ~300 pg/mL to ~270 pg/mL (2 μM), ~240 pg/mL (3 μM), and ~100 pg/mL (4 μM).
Reduced TNF-α-induced MCP-1 levels from ~6000 pg/mL to ~6300 pg/mL (2 μM), ~5300 pg/mL (3 μM), and ~2700 pg/mL (4 μM).

Immunofluorescence[2]

Cell Line: TNF-α-stimulated HMEC-1 human endothelial cells
Concentration: 4 μM
Incubation Time: 24 h (co-incubated with TNF-α)
Result: Reduced the surface expression of TNF-α-induced VCAM-1 and ICAM-1 on HMEC-1 cells.
Did not alter cell morphology or the arrangement of filamentous actin, α-tubulin, β-catenin, or vimentin.

Western Blot Analysis[2]

Cell Line: TNF-α-stimulated HMEC-1 human endothelial cells
Concentration: 2, 3, 4 μM
Incubation Time: 3 h (pre-incubation); 30 min (co-incubation with TNF-α)
Result: Reduced TNF-α-induced pNF-κB levels from ~6-fold (basal) to ~3-fold (4 μM), ~4-fold (3 μM), and ~5-fold (2 μM).
Inhibited TNF-α-induced IκB degradation, restoring IκB levels to ~0.8-fold (4 μM), ~0.7-fold (3 μM), and ~0.6-fold (2 μM) of the untreated control level.
Left total NF-κB levels unchanged.\nHad no inhibitory effect on TNF-α-induced phosphorylation of p38.
Did not alter basal phosphorylation levels of AKT, ERK1/2, or JNK in HMEC-1 cells.

Cell Autophagy Assay[3]

Cell Line: RAW264.7 macrophages
Concentration: 50 μM
Incubation Time: 4 h
Result: Increased the number of LC3+ puncta per cell by at least 3 SEM above the mean value of DMSO-treated controls.

Western Blot Analysis[3]

Cell Line: RAW264.7 macrophages
Concentration: 0.048-50 μM
Incubation Time: 2 h
Result: Dose-dependently increased LC3-II/Actin ratios while decreasing p62/Actin levels.
Reduced p62/Actin ratio to 0.877 at 12.5 μM and 0.476 at 50 μM compared to DMSO-treated controls.
Increased LC3-II/Actin ratio to 2.650 at 12.5 μM and 4.380 at 50 μM compared to DMSO-treated controls.
Achieved an EC50 of 12.55 μM for autophagy induction, calculated from LC3-II/Actin dose-response curve.

Cell Autophagy Assay[3]

Cell Line: RAW264.7 macrophages
Concentration: 25 μM
Incubation Time: 4 h
Result: Significantly increased both autophagosome and autolysosome numbers compared to DMSO-treated controls.
Reduced p62/Actin ratio to 0.683 and increased LC3-II/Actin ratio to 4.295 compared to DMSO-treated cells.
Elevated LC3-II/Actin ratio to 4.852 and p62/Actin ratio to 1.080 in the presence of bafilomycin A1, indicating proper autophagic flux.

Western Blot Analysis[3]

Cell Line: RAW264.7 macrophages
Concentration: 25 μM
Incubation Time: 4 h
Result: Increased phospho-AMPKα/AMPKα ratio to 1.741 without affecting phospho-mTOR/mTOR ratio (0.968) or phospho-4E-BP1/4E-BP1 ratio (1.004) compared to DMSO-treated controls.
Reduced p62/Actin ratio to 0.543 and increased LC3-II/Actin ratio to 1.741 compared to DMSO-treated controls.

Immunofluorescence[3]

Cell Line: RAW264.7 macrophages
Concentration: 25 μM
Incubation Time: 2 h, 4 h, 24 h
Result: Did not alter TFEB nuclear localization at any time point tested, with no significant difference in the percentage of cells with TFEB nuclear translocation compared to DMSO-treated controls.

Immunofluorescence[3]

Cell Line: RAW264.7 macrophages
Concentration: 25 μM
Incubation Time: 4 h
Result: Significantly increased Mtb-LC3 colocalization compared to DMSO-treated controls, with colocalization further increased upon bafilomycin A1 addition.\nSignificantly increased Mtb-Cathepsin D colocalization compared to DMSO-treated controls.
Reversed the increase in colocalization upon bafilomycin A1 treatment.
Abolished the increase in Mtb-Cathepsin D colocalization in Beclin-1-deficient macrophages.
In Vivo

Panduratin A (3-18 mg/kg; p.o.; daily; 14 days) dose-dependently mitigates DSS (HY-116282C)-induced ulcerative colitis in male mice[1].
Panduratin A reduces SARS-CoV-2 viral burden and lung inflammation in infected Golden Syrian hamsters[3].
Panduratin A (2.5-25 mg/kg; i.p.; daily; 7 days) exerts dose-dependent nephroprotective effects against Colistin-induced acute kidney injury by reducing oxidative stress, renal tubular damage, and renal cell apoptosis[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Male mice (20-24 grams; DSS-induced acute colitis)[1]
Dosage: 3 mg/kg; 6 mg/kg; 18 mg/kg
Administration: p.o.; daily; 14 days
Result: Produced dose-dependent improvements in colitis symptoms.
Significantly reversed DSS-induced body weight loss, colonic length shortening, and DAI increase at 18 mg/kg, with effects comparable to sulfasalazine.
Mitigated DSS-induced histopathological damage at all tested doses, preserving colonic architecture and goblet cells, with the 18 mg/kg dose showing the most pronounced improvement.
Significantly reduced DSS-elevated levels of myeloperoxidase (MPO), malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β).
Inhibited DSS-induced NF-κB activation by reducing phosphorylation of P65 and IκBα.
Enhanced expression of Nrf2 and HO-1 proteins, with the 18 mg/kg dose matching sulfasalazine's efficacy in these molecular effects.
Animal Model: C57BL/6 (male, 6-8 weeks of age, 20-22 g, acute kidney injury induced by intraperitoneal injection of 15 mg/kg colistin once daily for 7 days)[5]
Dosage: 2.5 mg/kg; 25 mg/kg
Administration: i.p.; daily; 7 days (administered 30 minutes before Colistin)
Result: Attenuated colistin-induced elevations in blood urea nitrogen (BUN) levels.
Significantly reduced colistin-induced increases in renal injury markers Tim-1 and Ngal, carbonyl protein, cytochrome c, and cleaved-caspase 3 at 2.5 mg/kg dose, and showed a trend toward increasing anti-apoptotic Bcl-2 expression.
Produced more pronounced reductions in renal injury, oxidative stress, and apoptotic markers (with lower p-value for significance compared to 2.5 mg/kg dose) and increased Bcl-2 expression at 25 mg/kg dose.
Significantly suppressed colistin-induced renal tubular damage (reduced semi-quantitative scores) at both doses.
Decreased the number of TUNEL-positive apoptotic renal cells at both doses.
Molecular Weight

406.51

Formula

C26H30O4
CAS No.
Appearance

Solid

Color

White to light yellow

SMILES

O=C(C1=C(C=C(C=C1O)OC)O)[C@H]2[C@H](C3=CC=CC=C3)CC=C([C@H]2C/C=C(C)\C)C
Structure Classification
Initial Source
Shipping

Room temperature in continental US; may vary elsewhere.
Storage
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
Purity & Documentation
References
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Panduratin A Related Classifications

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Keywords:

Panduratin A89837-52-5ApoptosisNF-κBKeap1-Nrf2AMPKAutophagySARS-CoVDNA MethyltransferaseNuclear factor-κBNuclear factor-kappaBAMP-activated protein kinaseSARS coronavirusDNMTsDNA MTasesNrf2HMEC-1 human endothelial cellsGolden Syrian hamstersRAW264.7 macrophagesDSS-induced colitisRPTEC/TERT1 cellsBeclin-1Mycobacterium tuberculosisSARS-CoV-2 2'-O-methyltransferaseInhibitorinhibitorinhibit

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