Cat. No.: HY-N21694

Ciliatoside A

Ciliatoside A is a naturally bioactive compound that exhibits significant anti-inflammatory, antiviral, and neuroprotective activities. Ciliatoside A serves as a mitophagy inducer and NLRP3 inflammasome inhibitor, activating AMPK, SIRT1, and the PINK1/Parkin axis, and inhibiting pyroptosis and apoptosis. Ciliatoside A promotes autophagic flux, autophagosome-lysosome fusion, mTOR inhibition, and p62-dependent HBc degradation; reduces Aβ aggregation, plaque deposition, microglial/astrocyte activation, and bacterial load; and maintains neuronal integrity, mitochondrial membrane potential, and ATP production. Ciliatoside A is used in research on Alzheimer's disease, Klebsiella pneumoniae-induced pneumonia, hepatitis B virus infection, and inflammation.

For research use only. We do not sell to patients.

CAS No.: 303084-57-3
Formula: C₃₆H₄₀O₁₉
Molecular Weight:776.70

Storage:

Please store the product under the recommended conditions in the Certificate of Analysis.

Ciliatoside A Chemical Structure

CAS No.: 303084-57-3

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Use of MCE Products

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biological Activity
- Description
- Cellular Effect
- In Vitro
- In Vivo
Chemical Information
Purity & Documentation
References
Calculators
Help & FAQs
Classifications
Bioz

Biological Activity

Description

All NOD-like Receptor (NLR) Isoforms :

All AMPK Isoforms :

All Sirtuin Isoforms :

All mTOR Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
HepG2 2.2.15	CC₅₀	200 μM	Cytotoxicity against human HepG2.2.15 cells incubated for 72 h assessed by MTT, CCK-8, Alamar Blue, and flow cytometric apoptosis assays, with CC50 greater than 200 μM. Cytotoxicity against human HepG2.2.15 cells incubated for 72 h assessed by MTT, CCK-8, Alamar Blue, and flow cytometric apoptosis assays, with CC50 greater than 200 μM.	36496141
HepG2	CC₅₀	200 μM	Cytotoxicity against human HepG2 cells incubated for 72 h assessed by MTT, CCK-8, Alamar Blue, and flow cytometric apoptosis assays, with CC50 greater than 200 μM. Cytotoxicity against human HepG2 cells incubated for 72 h assessed by MTT, CCK-8, Alamar Blue, and flow cytometric apoptosis assays, with CC50 greater than 200 μM.	36496141
Huh-7	CC₅₀	200 μM	Cytotoxicity against human Huh-7 cells incubated for 72 h assessed by MTT, CCK-8, Alamar Blue, and flow cytometric apoptosis assays, with CC50 greater than 200 μM. Cytotoxicity against human Huh-7 cells incubated for 72 h assessed by MTT, CCK-8, Alamar Blue, and flow cytometric apoptosis assays, with CC50 greater than 200 μM.	36496141
RAW264.7	IC50	27.1 μM	Inhibition of lipopolysaccharide-induced nitrite accumulation in RAW 264.7 mouse macrophage-like cells, with 1 h pretreatment prior to LPS stimulation and total LPS incubation of 24 h, measured via Griess reaction with absorbance read at 550 nm. Inhibition of lipopolysaccharide-induced nitrite accumulation in RAW 264.7 mouse macrophage-like cells, with 1 h pretreatment prior to LPS stimulation and total LPS incubation of 24 h, measured via Griess reaction with absorbance read at 550 nm.	11087610

In Vitro

Innate ImmunityInflammasomePyroptosisOxidative StressMitochondrial FunctionAutophagyAnti-cancerBacterial InfectionApoptosisCytokines & ChemokinesViral InfectionLysosomal Metabolism

Innate Immunity

Inflammasome

Pyroptosis

Ciliatoside A (2.5-10 µM; 12 h) effectively inhibits NLRP3 inflammasome activation and suppresses pyroptosis in LPS (HY-D1056)/Nigericin (Nig) (HY-127019)-stimulated BV-2 microglial cells^[1].

Oxidative Stress

Mitochondrial Function

Ciliatoside A (10 µM; 12 h) effectively attenuates H₂O₂-induced oxidative stress, mitochondrial dysfunction, and cell death in BV-2 microglial cells^[1].

Autophagy

Ciliatoside A (2.5-10 µM; 6-24 h) activates autophagy and mitophagy in BV-2 microglial cells in a dose- and time-dependent manner through activation of AMPK/ULK1 and PINK1/Parkin signaling pathways, and reverses LPS/Nig-induced mitophagy impairment^[1].

Anti-cancer

Ciliatoside A (0.6-160 μM; 24 h) shows no cytotoxicity in A549 cells at concentrations up to 10 μM, but decreases cell viability at concentrations of 20 μM and higher after 24 h^[2].

Bacterial Infection

Ciliatoside A (2.5-10 μM; 24 h) inhibits the expression of KP resistance genes in Klebsiella pneumoniae (KP) bacteria and KP-infected A549 cells^[2].

Bacterial Infection

Anti-cancer

Ciliatoside A (2.5-10 μM; 24 h) protects A549 cells against KP-induced cytotoxicity, restoring cell viability and normal morphology^[2].
Ciliatoside A (2.5-10 μM; 24 h) activates the SIRT1/PINK1/Parkin pathway in KP-infected A549 cells^[2].

Bacterial Infection

Mitochondrial Function

Oxidative Stress

Anti-cancer

Ciliatoside A (2.5-10 μM; 24 h) attenuates KP-induced mitochondrial damage and oxidative stress in A549 cells by reducing mtROS, restoring MMP and ATP production, and modulating SOD/MDA levels^[2].

Bacterial Infection

Autophagy

Anti-cancer

Ciliatoside A (2.5-10 μM; 24 h) promotes autophagy and restores impaired autophagic flux in KP-infected A549 cells, reduces p62 accumulation, and simultaneously increases LC3-II levels and the number of autophagosomes^[2].

Bacterial Infection

Apoptosis

Inflammasome

Cytokines & Chemokines

Anti-cancer

Ciliatoside A (2.5-10 μM; 24 h) inhibits KP-induced apoptosis and NLRP3 inflammasome-mediated inflammatory cell death in A549 cells, reducing pro-inflammatory cytokine release and cell death^[2].

Viral Infection

Ciliatoside A (0-50 μM; 3 days) potently inhibits secreted HBsAg in HBV-infected HepG2-NTCP cells and primary human hepatocytes, with EC₅₀ values of 5.13 μM and 3.36 μM, respectively, without impairing the overall secretory function of the cells^[4].
Ciliatoside A (2.5-5 μM; 3-9 days) reduces intracellular HBsAg, secreted HBsAg, HBV RNA, and capsid-derived DNA in HBV-infected HepG2-NTCP cells in a time-dependent manner^[4].
Ciliatoside A (1-10 μM; 9 days) inhibits HBV cccDNA transcription, leading to dose-dependent reductions in HBV RNA, HBsAg, and capsid-derived DNA in HBV-infected HepG2-NTCP cells and primary human hepatocytes, without altering cccDNA levels or HBV RNA stability^[4].

Viral Infection

Lysosomal Metabolism

Autophagy

Ciliatoside A (2.5-5 μM; 3-6 days) induces autophagic flux and autolysosome formation in both HBV-infected and uninfected HepG2-NTCP cells, with a stronger late-stage autophagic response observed in HBV-infected cells^[4].
Ciliatoside A (5 μM) enhances the interaction between HBc and the autophagy cargo receptor p62 and accelerates the degradation of HBc protein in Huh-7 cells and HBV-infected HepG2-NTCP cells^[4].

Viral Infection

Autophagy

Ciliatoside A (0.5-10 μM; 6 days) activates the AMPK-ULK1-mTOR autophagy pathway in a dose-dependent manner in HBV-infected HepG2-NTCP cells, and its anti-HBV effect depends on AMPK activation^[4].

Innate Immunity

Ciliatoside A (3-30 μM; pretreatment for 1 h before LPS stimulation; total LPS incubation time of 24 h) potently inhibits LPS-induced nitrite accumulation in RAW 264.7 mouse macrophage-like cells in a concentration-dependent manner, with an IC₅₀ of 27.1 μM^[5].
Ciliatoside A (10-30 μM; 1 h pretreatment prior to LPS stimulation; total LPS incubation 24 h) exhibits weak inhibitory activity against nitrite accumulation in LPS/IFN-γ-stimulated N9 mouse microglial cells, with an inhibition rate of 26.1% at 30 μM^[5].

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

Cell Autophagy Assay^[1]

Cell Line:

BV-2 microglial cells
Concentration:

2.5, 5, 10 µM (dose-response for LC3 Western blot and GFP-LC3 puncta); 10 µM (time-course and Mito-QC experiments)
Incubation Time:

24 h (LC3 Western blot and GFP-LC3 puncta); 6, 12, 24 h (time-course); 12 h (pretreatment before LPS/Nig in Mito-QC experiments)
Result:

Induced a notable and dose-dependent elevation in GFP-LC3 puncta formation in BV-2 cells.
Elevated LC3-II accumulation with both dose- and time-dependent increases in LC3-I to LC3-II conversion as shown by Western blot analysis.
Augmented autophagic flux at 6, 12, and 24 h as confirmed by the ptfLC3 assay.
Further increased GFP-LC3 puncta and LC3-II levels when co-treated with bafilomycin A1, confirming autophagy activation rather than blockade of autophagosome degradation.
Effectively reversed the impaired autophagic flux caused by LPS/Nig in LPS/Nig-stimulated BV-2 cells transfected with ptfLC3.
Enhanced mitophagy and reversed LPS/Nig-induced mitophagy impairment in BV-2 cells transfected with the Mito-QC plasmid at 10 µM.

Western Blot Analysis^[1]

Cell Line:

BV-2 microglial cells
Concentration:

2.5, 5, 10 µM (Western blotting; co-treatment with CC or AC220 (HY-13001) for GFP-LC3 assay)
Incubation Time:

24 h (Western blotting; GFP-LC3 assay)
Result:

Increased phosphorylation of AMPK and ULK1, while mTOR phosphorylation levels remained unchanged.
Induced a dose-dependent increase in PINK1 expression and Parkin phosphorylation.
Induced GFP-LC3 puncta formation that was attenuated by co-treatment with the AMPK inhibitor CC or the Parkin inhibitor AC220, indicating that both AMPK and PINK1/Parkin activation are essential for Ciliatoside A-induced autophagy.

Cell Viability Assay^[2]

Cell Line:

A549 human lung cancer cells
Concentration:

0.6, 1.25, 2.5, 5, 10, 20, 40, 80, 160 μM
Incubation Time:

24 h
Result:

Showed no considerable impact on A549 cell viability at concentrations of 0.6-10 μM.
Significantly reduced A549 cell viability at concentrations of 20, 40, 80, and 160 μM.

Real Time qPCR^[2]

Cell Line:

Klebsiella pneumoniae (KP)-infected A549 cells and KP bacteria
Concentration:

2.5, 5, 10 μM (added after 24 h KP infection)
Incubation Time:

24 h
Result:

Effectively downregulated RmpA, Acr AB, bla OXA-48, and TEM mRNA levels in both KP bacteria and KP-infected A549 cells.

Cell Viability Assay^[2]

Cell Line:

KP-infected A549 cells
Concentration:

2.5, 5, 10 μM (added after 24 h KP infection)
Incubation Time:

24 h
Result:

Reversed KP-induced A549 cell swelling and irregular deformation, restoring normal cell size and clear intercellular boundaries.
Effectively reversed KP-induced reduction in A549 cell viability and significantly improved cell viability.

Cell Autophagy Assay^[2]

Cell Line:

KP-infected A549 cells
Concentration:

2.5, 5, 10 μM (added after 24 h KP infection)
Incubation Time:

24 h
Result:

Further increased autophagosome numbers and significantly alleviated KP-induced mitochondrial structural damage (swelling, cristae disruption) as observed by transmission electron microscopy.
Markedly reduced p62 protein levels while further increasing LC3 protein levels in KP-infected cells as measured by Western blot.
Further amplified the KP-induced increase in GFP-LC3 spots as shown by GFP-LC3 spot formation assay.
Effectively restored KP-blocked autophagy flow and promoted the degradation of autophagic substrates as revealed by GFP-mRFP-LC3 dual-fluorescence experiments.

Apoptosis Analysis^[2]

Cell Line:

KP-infected A549 cells
Concentration:

2.5, 5, 10 μM (added after 24 h KP infection)
Incubation Time:

24 h
Result:

Markedly reduced the KP-induced apoptosis rate in A549 cells.
Effectively reversed KP-induced BAX upregulation and BCL-2 downregulation.
Effectively suppressed KP-induced release of pro-inflammatory cytokines IL-1β, TNF-α, and IL-6.
Markedly reduced NLRP3 fluorescence intensity and downregulated NLRP3, ASC, and Cleaved-IL-1β/IL-1β protein levels, confirming inhibition of NLRP3 inflammasome activation.
Effectively suppressed the KP-induced increase in PI/Hoechst fluorescence intensity, indicating reduced inflammatory cell death.

ELISA Assay^[4]

Cell Line:

HBV-infected HepG2-NTCP cells and primary human hepatocytes (PHHs)
Concentration:

0, 0.39, 0.78, 1.6, 3.1, 6.25, 12.5, 25, 50 μM
Incubation Time:

3 days
Result:

Decreased secreted HBsAg levels in a dose-dependent manner in both HBV-infected cell models.
Had an EC₅₀ for HBsAg inhibition of 5.13 μM in HepG2-NTCP cells and 3.36 μM in PHHs, corresponding to selectivity indices greater than 38.99 and 59.52 respectively.
Did not affect albumin or apolipoprotein B secretion even at 50 μM, ruling out a general blockade of cellular secretion pathways.

In Vivo

Aβ/Tau/α-Synuclein AggregationInnate ImmunityInflammasomeAutophagyOxidative StressBacterial InfectionApoptosisViral Infection

Aβ/Tau/α-Synuclein Aggregation

Innate Immunity

Inflammasome

Autophagy

Ciliatoside A (0.5-2 mg/kg; i.p.) improves cognitive function, reduces Aβ plaque deposition, alleviates neuroinflammation, and preserves neuronal integrity in 3xTg-AD mice by enhancing mitophagy and inhibiting NLRP3 inflammasome activation^[1].

Aβ/Tau/α-Synuclein Aggregation

Oxidative Stress

Autophagy

Ciliatoside A (50-200 μM; administered in nematode growth medium; L3/L4 stage) exerts neuroprotective effects in transgenic C. elegans AD models by reducing Aβ aggregation, decreasing oxidative stress, and enhancing autophagy and mitophagy^[1].

Innate Immunity

Bacterial Infection

Apoptosis

Ciliatoside A (2 mg/kg; i.p.; once daily; 2 days) alleviates Klebsiella pneumoniae-induced pneumonia in mice by activating the SIRT1/PINK1/Parkin pathway, reducing pulmonary edema, inflammatory cell infiltration, apoptosis, and bacterial load^[2].

Viral Infection

Autophagy

Ciliatoside A (0.5 mg/kg; i.p.; every 2 days; 20 days) reduces serum HBsAg by 174.3 IU/mL and serum HBV DNA by 2.15 log₁₀ in an HBV recombinant-cccDNA mouse model, without affecting cccDNA levels and via AMPK-mediated autophagy^[4].

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

Animal Model:

3xTg-AD (male; 6 months of age)^[1]
Dosage:

0.5 mg/kg; 1 mg/kg; 2 mg/kg
Administration:

i.p.
Result:

Reduced total swimming distance and shortened escape latency over 6 training days in the Morris Water Maze test, while average swimming speed remained unchanged.
Reduced Aβ plaque deposition in the hippocampal CA3 region.
Decreased microglial activation (Iba1) and astrocyte activation (GFAP) in the hippocampal CA3, CA1, and dentate gyrus regions.
Preserved neuronal integrity, as indicated by increased numbers of NeuN-positive cells in the hippocampus.
Increased co-localization of LC3 with NLRP3 in the cerebral cortex.
Increased PINK1 expression alongside decreased Iba1 expression in the hippocampus.

Animal Model:

Multiple transgenic (CL4176, CL2006, CL2331, CL2122, CL2355, DA2123, BC12921, IR1631)^[1]
Dosage:

50 μM; 100 μM; 150 μM; 200 μM
Administration:

administered in nematode growth medium; L3/L4 stage
Result:

Dose-dependently reduced Aβ-induced paralysis in CL4176 worms.
Prolonged lifespan in CL2006 worms.
Substantially reduced Aβ aggregation in both CL4176 and CL2331 worms.
Improved movement rates in CL2122 and CL2355 strains.
Significantly decreased ROS levels in CL4176 worms.
Enhanced autophagic activity in DA2123 worms, as shown by increased GFP::LGG-1 puncta formation and elevated PE-GFP::LGG-1 expression.
Reduced GFP::p62 expression in BC12921 worms, indicating enhanced autophagic flux.
Decreased the GFP/DsRed ratio in IR1631 worms, indicating enhanced mitophagy.

Animal Model:

C57BL/6 (6 weeks old; 15-18 g; both sexes)^[2]
Dosage:

2 mg/kg
Administration:

i.p.; once daily; 2 days
Result:

Increased SIRT1, PINK1, and Parkin protein levels in mouse lung tissue.
Reduced the lung wet/dry weight ratio.
Alleviated KP-induced pulmonary pathological damage including alveolar septal edema, thickened alveolar walls, and inflammatory cell infiltration.
Decreased the proportion of TUNEL-positive cells in lung tissue.
Lowered total protein levels in bronchoalveolar lavage fluid.
Reduced IL-1β, IL-6, and TNF-α levels in BALF.
Decreased neutrophil counts in lung tissue.
Reduced myeloperoxidase activity.
Reduced KP bacterial load in lung tissue.

Animal Model:

Alb-cre transgenic (male; 4-5 weeks of age; HBV recombinant-cccDNA model via hydrodynamic injection of 4 μg precursor plasmid rcccDNA)^[4]
Dosage:

0.5 mg/kg
Administration:

i.p.; every 2 days; 20 days
Result:

Reduced serum HBsAg by 174.3 IU/mL compared with the vehicle group.
Reduced serum HBV DNA by 2.15 log10 compared with the vehicle group.
Potently decreased intrahepatic total HBV RNAs, intrahepatic 3.5-kb RNA, intrahepatic HBV DNA, and intrahepatic HBsAg protein levels.
Did not affect intrahepatic cccDNA levels.
Strongly elevated LC3 and Beclin-1 levels in liver tissue.
Increased levels of phosphorylated AMPK and ULK1 in liver tissue.
Reduced levels of phosphorylated mTOR in liver tissue.

Related Protocols :

Chemical Information

CAS No. 303084-57-3
Molecular Weight 776.70
Formula C₃₆H₄₀O₁₉
SMILES

O=C1C2=C(C=3C(C(O[C@H]4[C@H](O[C@H]5[C@H](O)[C@@H](O)[C@@H](O)CO5)[C@](CO[C@H]6[C@H](O)[C@@H](O)[C@H](O)CO6)(O)CO4)=C2CO1)=CC(OC)=C(OC)C3)C=7C=C8C(=CC7)OCO8
Structure Classification
- Phenylpropanoids
- Lignans
Initial Source
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

Purity & Documentation

Handling Instructions (2659 KB)

References

[1]. Guo M, et al. Ciliatoside A attenuates neuroinflammation in Alzheimer's disease by activating mitophagy and inhibiting NLRP3 inflammasome activation. Phytomedicine : international journal of phytotherapy and phytopharmacology. 2025 Sep;145:156928.

[2]. Zhu J, et al. Ciliatoside A Improves Klebsiella pneumoniae-Induced Pneumonia by Modulating Mitochondrial Autophagy via the SIRT1/PINK1/Parkin Pathway. Clinical and experimental pharmacology & physiology. 2026 May;53(5):e70125. [Content Brief]

[3]. Day SH, et al. Potent cytotoxic lignans from Justicia procumbens and their effects on nitric oxide and tumor necrosis factor-alpha production in mouse macrophages. Journal of natural products. 2002 Mar;65(3):379-81. [Content Brief]

[4]. Fang R, et al. Ciliatoside A, isolated from Peristrophe japonica, inhibits HBsAg expression and cccDNA transcription by inducing autophagy. Antiviral research. 2023 Jan;209:105482.

[5]. Day SH, et al. New lignan glycosides with potent antiinflammatory effect, isolated from Justicia ciliata. Journal of natural products. 2000 Nov;63(11):1560-2. [Content Brief]

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1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

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Ciliatoside A

All NOD-like Receptor (NLR) Isoforms

All AMPK Isoforms

All Sirtuin Isoforms

All mTOR Isoforms