Agrimonolide
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Agrimonolide is a phenethyl isocoumarin compound discovered from Agrimonia pilosa, exhibiting anti-inflammatory, antioxidant, and anticancer activities. Agrimonolide inhibits NF-κB, MAPK, and TLR4-mediated neuroinflammatory signaling, suppresses Notch and JAK2/STAT3 signaling to modulate Th17/Treg balance and maintain the intestinal barrier. Agrimonolide decreases HIF1A expression, inhibits glycolysis, and induces ferroptosis and cell cycle arrest via the mTOR pathway in tumor models, thereby suppressing cancer cell viability, proliferation, and metastasis. Agrimonolide exerts hepatoprotective and anti-fibrotic effects by regulating bile acid transporter expression and reducing hepatic bile acid accumulation. Agrimonolide is used for research on ulcerative colitis, ovarian cancer, non-small cell lung cancer, cholestatic liver injury, and neuroinflammation.
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- Pureté : 98%
- CAS No.: 21499-24-1
- Formule: C18H18O5
- Masse moléculaire:314.33
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Stockage:Powder -20°C, 3 years ; In solvent -80°C, 6 months , -20°C, 1 month
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Activité biologique
Description
Agrimonolide is a phenethyl isocoumarin compound discovered from Agrimonia pilosa, exhibiting anti-inflammatory, antioxidant, and anticancer activities. Agrimonolide inhibits NF-κB, MAPK, and TLR4-mediated neuroinflammatory signaling, suppresses Notch and JAK2/STAT3 signaling to modulate Th17/Treg balance and maintain the intestinal barrier. Agrimonolide decreases HIF1A expression, inhibits glycolysis, and induces ferroptosis and cell cycle arrest via the mTOR pathway in tumor models, thereby suppressing cancer cell viability, proliferation, and metastasis. Agrimonolide exerts hepatoprotective and anti-fibrotic effects by regulating bile acid transporter expression and reducing hepatic bile acid accumulation. Agrimonolide is used for research on ulcerative colitis, ovarian cancer, non-small cell lung cancer, cholestatic liver injury, and neuroinflammation[1][2][3][4][5][6].
In Vitro
Adaptive ImmunityCytokines & ChemokinesAnti-cancerCarbohydrate MetabolismCell Cycle RegulationFerroptosisInnate ImmunityLipid Inflammatory Mediators
Adaptive Immunity
Cytokines & Chemokines
Agrimonolide (10-20 μM; 4 days) inhibits Th17 cell differentiation from naïve CD4+ T cells isolated from C57BL/6J mice, as shown by reduced CD4+IL-17A+ cell frequency and lower RORγt mRNA expression[1].
Agrimonolide (10-20 μM; 4 days) promotes Treg cell differentiation from naïve CD4+ T cells isolated from C57BL/6J mice, as shown by increased CD4+CD25+Foxp3+ cell frequency and higher Foxp3 mRNA expression[1].
Agrimonolide (10-20 μM; 4 days) promotes Treg cell differentiation from naïve CD4+ T cells isolated from C57BL/6J mice, as shown by increased CD4+CD25+Foxp3+ cell frequency and higher Foxp3 mRNA expression[1].
Anti-cancer
Network pharmacology analysis identifies HIF1A as a key core target of Agrimonolide in ovarian cancer, with significant enrichment of the HIF-1 signaling pathway[2].
Agrimonolide (10-40 μM; 0-3 days) inhibits viability of SKOV3 and A2780 ovarian cancer cells[2].
Agrimonolide (10-40 μM; 14 days) suppresses colony formation of SKOV3 and A2780 ovarian cancer cells[2].
Agrimonolide (10-100 μM; 24 h) exhibits no significant cytotoxicity in BV2 microglial and Neuro-2a neuronal cells at concentrations below 100 μM[6].
Agrimonolide (10-40 μM; 0-3 days) inhibits viability of SKOV3 and A2780 ovarian cancer cells[2].
Agrimonolide (10-40 μM; 14 days) suppresses colony formation of SKOV3 and A2780 ovarian cancer cells[2].
Agrimonolide (10-100 μM; 24 h) exhibits no significant cytotoxicity in BV2 microglial and Neuro-2a neuronal cells at concentrations below 100 μM[6].
Anti-cancer
Carbohydrate Metabolism
Agrimonolide (10-40 μM; 48 h) reduces glucose uptake and lactate production in SKOV3 and A2780 ovarian cancer cells[2].
Agrimonolide (20-40 μM) decreases extracellular acidification rate, indicating reduced glycolytic activity, in SKOV3 and A2780 ovarian cancer cells[2].
Agrimonolide (10-40 μM) decreases protein expression of HIF1A, HK2, and LDHA in SKOV3 and A2780 ovarian cancer cells[2].
Agrimonolide (40 μM) has inhibitory effects on glycolysis and HK2 expression in A2780 ovarian cancer cells that are reversed by overexpression of HIF1A, confirming that Agrimonolide attenuates glycolysis through modulation of HIF1A[2].
Agrimonolide (20-40 μM) decreases extracellular acidification rate, indicating reduced glycolytic activity, in SKOV3 and A2780 ovarian cancer cells[2].
Agrimonolide (10-40 μM) decreases protein expression of HIF1A, HK2, and LDHA in SKOV3 and A2780 ovarian cancer cells[2].
Agrimonolide (40 μM) has inhibitory effects on glycolysis and HK2 expression in A2780 ovarian cancer cells that are reversed by overexpression of HIF1A, confirming that Agrimonolide attenuates glycolysis through modulation of HIF1A[2].
Anti-cancer
Cell Cycle Regulation
Ferroptosis
Agrimonolide (10-40 μM) inhibits malignant progression and induces ferroptosis in A549 non-small cell lung cancer cells by blocking the mTOR signaling pathway[3].
Innate Immunity
Agrimonolide does not show significant inhibitory activity against LPS-induced NO production in BV2 microglial cells at the tested concentrations, as it is not among the five active compounds identified in the assay[5].
Agrimonolide (10-50 μM; 2 h pre-incubation before LPS stimulation) dose-dependently inhibits LPS-induced P65 phosphorylation in BV2 cells with an IC50 of 20.3 μM[6].
Agrimonolide (10-50 μM; 2 h pre-incubation before LPS stimulation) dose-dependently inhibits LPS-induced phosphorylation of JNK and P38 in BV2 microglial cells[6].
Agrimonolide (10-50 μM; 2.5 h pre-incubation before LPS stimulation) dose-dependently inhibits LPS-induced nuclear translocation of the NF-κB subunit P50 in BV2 cells[6].
Agrimonolide (10-50 μM; pre-incubated before LPS stimulation) inhibits LPS-induced activation of NF-κB and MAPK signaling pathways in primary mouse astrocytes[6].
In silico molecular docking predicts that agrimonolide binds with high affinity to TLR4, IRAK1, and TRAF6 (binding energies ≤ −6.53 kcal/mol) and with moderate affinity to MyD88, supporting a multi-target mechanism of action on the TLR4 signaling pathway[6].
Agrimonolide (10-50 μM; 2 h pre-incubation before LPS stimulation) dose-dependently inhibits LPS-induced P65 phosphorylation in BV2 cells with an IC50 of 20.3 μM[6].
Agrimonolide (10-50 μM; 2 h pre-incubation before LPS stimulation) dose-dependently inhibits LPS-induced phosphorylation of JNK and P38 in BV2 microglial cells[6].
Agrimonolide (10-50 μM; 2.5 h pre-incubation before LPS stimulation) dose-dependently inhibits LPS-induced nuclear translocation of the NF-κB subunit P50 in BV2 cells[6].
Agrimonolide (10-50 μM; pre-incubated before LPS stimulation) inhibits LPS-induced activation of NF-κB and MAPK signaling pathways in primary mouse astrocytes[6].
In silico molecular docking predicts that agrimonolide binds with high affinity to TLR4, IRAK1, and TRAF6 (binding energies ≤ −6.53 kcal/mol) and with moderate affinity to MyD88, supporting a multi-target mechanism of action on the TLR4 signaling pathway[6].
Innate Immunity
Cytokines & Chemokines
Agrimonolide reduces IL-1β secretion from LPS-stimulated BV2 microglial cells[6].
Agrimonolide (10-50 μM; 6 h LPS stimulation) significantly reduces mRNA expression of IL-1β, IL-6, TNF-α, and IL-18 in LPS-stimulated BV2 cells[6].
Agrimonolide (10-50 μM; 6 h LPS stimulation) reduces LPS-induced mRNA expression of TLR4, MyD88, IRAK1, and TRAF6 in BV2 microglial cells[6].
Agrimonolide (10-50 μM; pre-incubated before LPS stimulation) inhibits LPS-induced activation of primary mouse microglia, as evidenced by reduced CD68 expression and preserved ramified morphology[6].
Agrimonolide (10-50 μM; pre-incubated before LPS stimulation) significantly reduces mRNA expression of IL-1β, IL-6, TNF-α, and IL-18 in LPS-stimulated primary mouse astrocytes[6].
Agrimonolide (10-50 μM; pre-incubated before LPS stimulation) dose-dependently inhibits LPS-induced GFAP upregulation and activation of primary mouse astrocytes[6].
Agrimonolide (10-50 μM; 6 h LPS stimulation) significantly reduces mRNA expression of IL-1β, IL-6, TNF-α, and IL-18 in LPS-stimulated BV2 cells[6].
Agrimonolide (10-50 μM; 6 h LPS stimulation) reduces LPS-induced mRNA expression of TLR4, MyD88, IRAK1, and TRAF6 in BV2 microglial cells[6].
Agrimonolide (10-50 μM; pre-incubated before LPS stimulation) inhibits LPS-induced activation of primary mouse microglia, as evidenced by reduced CD68 expression and preserved ramified morphology[6].
Agrimonolide (10-50 μM; pre-incubated before LPS stimulation) significantly reduces mRNA expression of IL-1β, IL-6, TNF-α, and IL-18 in LPS-stimulated primary mouse astrocytes[6].
Agrimonolide (10-50 μM; pre-incubated before LPS stimulation) dose-dependently inhibits LPS-induced GFAP upregulation and activation of primary mouse astrocytes[6].
Innate Immunity
Cytokines & Chemokines
Lipid Inflammatory Mediators
Agrimonolide (10-50 μM; 2 h pre-incubation before LPS stimulation) dose-dependently reduces LPS-induced expression of NLRP3, iNOS, and COX-2 proteins in BV2 microglial cells[6].
Agrimonolide (10-50 μM; 2 h pre-incubation before LPS stimulation) dose-dependently reduces LPS-induced expression of TLR4, IRAK1, and TRAF6 proteins in BV2 microglial cells, while MyD88 protein levels were not notably altered under these conditions[6].
Agrimonolide (10-50 μM; 2 h pre-incubation before LPS stimulation) dose-dependently reduces LPS-induced expression of TLR4, IRAK1, and TRAF6 proteins in BV2 microglial cells, while MyD88 protein levels were not notably altered under these conditions[6].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Viability Assay[2]
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Cell Line:SKOV3, A2780 ovarian cancer cells
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Concentration:10, 20, 40 μM
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Incubation Time:0, 1, 2, 3 days
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Result:Significantly reduced the viability of both SKOV3 and A2780 ovarian cancer cells at concentrations of 20 μM and 40 μM.
Did not produce a significant effect on cell viability at 10 μM.
Cell Proliferation Assay[2]
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Cell Line:SKOV3, A2780 ovarian cancer cells
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Concentration:10, 20, 40 μM
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Incubation Time:14 days
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Result:Suppressed colony formation in both SKOV3 and A2780 cells at 20 μM and 40 μM.
Showed a lesser effect on colony formation at 10 μM compared to higher concentrations.
Western Blot Analysis[6]
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Cell Line:BV2 mouse microglial cells
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Concentration:10, 30, 50 μM
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Incubation Time:2 h pre-incubation before LPS stimulation; 45 min (LPS stimulation)
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Result:Suppressed the LPS-induced increase of p-P65 in a dose-dependent manner, yielding an IC50 of 20.3 μM based on p-P65 band densitometry quantification.\nSignificantly suppressed LPS-induced phosphorylation of both JNK and p38 kinase in a dose-dependent manner.
Eliminated the LPS-induced increase of P50 levels in the nucleus of BV2 cells in a dose-dependent manner.
Real Time qPCR[6]
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Cell Line:BV2 mouse microglial cells
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Concentration:10, 30, 50 μM
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Incubation Time:pre-incubated before LPS stimulation; 6 h (LPS stimulation)
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Result:Significantly reduced the mRNA levels of IL-1β, IL-6, TNF-α, and IL-18 in LPS-stimulated BV2 cells.\nReduced the mRNA levels of TLR4, MyD88, IRAK1, and TRAF6 in LPS-stimulated BV2 cells.
Western Blot Analysis[6]
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Cell Line:BV2 mouse microglial cells
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Concentration:10, 30, 50 μM
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Incubation Time:2 h pre-incubation before LPS stimulation; 24 h (LPS stimulation)
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Result:Markedly reduced the LPS-induced expression of NLRP3, iNOS, and COX-2 proteins in a dose-dependent manner.\nEffectively inhibited LPS-induced increases in TLR4, IRAK1, and TRAF6 protein levels in a dose-dependent manner.
Did not notably alter MyD88 protein levels.
In Vivo
Innate ImmunityAdaptive ImmunityInflammasomeLipid mediators of inflammationOxidative Stress
Innate Immunity
Adaptive Immunity
Inflammasome
Innate Immunity
Inflammasome
Agrimonolide (10-90 mg/kg; i.p.; daily; 28 days) exerts dose-dependent hepatoprotective, antifibrotic, and anti-inflammatory effects in DDC-induced chronic cholestatic liver injury in mice, reducing hepatic bile acid accumulation and normalizing bile acid homeostasis via modulation of bile acid transporters and metabolic enzymes[4].
Innate Immunity
Adaptive Immunity
Agrimonolide (90 mg/kg; i.p.; daily; 28 days) reduces hepatic hydroxyproline by 60.3%, decreases myeloid cell and macrophage infiltration, and modulates bile acid transporter expression to promote bile acid efflux and reduce hepatic bile acid accumulation in DDC-induced chronic cholestatic liver injury in mice, and these hepatoprotective, antifibrotic, and anti-inflammatory effects are diminished by the bile acid transport inhibitor BMS-986020[4].
Lipid mediators of inflammation
Inflammasome
Oxidative Stress
Agrimonolide (25-50 mg/kg; i.p.; daily; 5 days) pretreatment mitigates LPS-driven neuroinflammation in ICR mice by decreasing glial activation and expression of inflammatory mediators[6].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6J (male; 6 weeks old)[1]
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Dosage:25 mg/kg/day; 50 mg/kg/day
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Administration:i.g.; daily; starting before DSS exposure
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Result:Reduced body weight loss in a dose-dependent manner compared to the DSS-only group.
Restored colon length in a dose-dependent manner compared to the DSS-only group.
Lowered disease activity index scores in a dose-dependent manner compared to the DSS-only group.
Alleviated mucosal damage, inflammatory cell infiltration, and crypt structure destruction in the colon.
Suppressed myeloperoxidase activity in colon tissues, with the 50 mg/kg dose showing a more substantial reduction than the 25 mg/kg dose.
Decreased the production of pro-inflammatory cytokines IL-1β, TNF-α, and IL-6 in colonic tissue.
Reduced the phosphorylation levels of IKKα/β, IκBα, and p65 in the NF-κB pathway.
Increased the protein expression levels of tight junction proteins Occludin and ZO-1.
Reduced serum FITC-dextran concentration.
Decreased the absolute number of CD4+IL-17A+ Th17 cells in mesenteric lymph nodes.
Increased the percentage of CD4+CD25+Foxp3+ Treg cells in mesenteric lymph nodes.
Modulated the mRNA and protein levels of Th17-specific transcription factor RORγt and Treg-specific transcription factor Foxp3 in colon and spleen tissues.
Reduced the mRNA and protein expression of Notch-1, Jagged1, and DLL4 in colonic tissue.
Inhibited the phosphorylation of JAK2 and STAT3.
Reduced protein expression of Notch1 and STAT3 as confirmed by immunofluorescence.
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Animal Model:C57BL/6 J (male; 8 weeks old; 20-25 g; specific pathogen-free)[4]
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Dosage:10 mg/kg; 30 mg/kg; 90 mg/kg
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Administration:i.p.; daily; 28 days
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Result:Alleviated DDC-induced increase in liver-to-body weight ratio in a dose-dependent manner.
Mitigated DDC-induced elevations in serum ALT, AST, ALP, total bilirubin, and direct bilirubin in a dose-dependent manner.
Alleviated ductular proliferation, macrophage infiltration, intraductal plugs, pericholangitis, onion skin-type periductal fibrosis, and biliary fibrosis.
Reduced DDC-increased hepatic hydroxyproline accumulation in a dose-dependent manner.
Markedly decreased hepatic mRNA expression of fibrosis markers α-Sma, Col1a1, Timp1, Epcam, and Mmp2, and reduced α-SMA protein expression at 90 mg/kg.
Reduced hepatic mRNA upregulation of inflammatory cytokines Tnf-α, Il-6, Il-1β, and Tgfb1.
Alleviated excessive bile duct proliferation in all dosage groups as confirmed by CK19 staining.
Reduced hepatic bile acid levels in a dose-dependent manner.
Increased hepatic mRNA expression of bile acid synthesis enzymes Cyp7a1, Cyp8b1, and Cyp7b1 dose-dependently, and reversed DDC-induced downregulation of Cyp27a1 at 90 mg/kg.
Inhibited DDC-induced increases in TCA, T-α-MCA, β-MCA, and T-β-MCA; reversed accumulation of T-CDCA, T-DCA, and T-UDCA at 90 mg/kg.
Reversed DDC-induced downregulation of Bsep at all three doses, with 30 and 90 mg/kg increasing Bsep expression.
Decreased DDC-elevated expression of Oatp2, Mrp3, and Mrp4 in a dose-dependent manner; increased DDC-reduced Ntcp and Oatp1 expression at 30 and 90 mg/kg.
Dose-dependently alleviated DDC-induced upregulation of phase I enzymes Cyp3a11 and Cyp2b10, and reversed DDC-induced inhibition of phase II enzymes Ugt1a1 and Sult2a1.
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Animal Model:C57BL/6 J (male; 8 weeks old; 20-25 g; specific pathogen-free)[4]
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Dosage:90 mg/kg
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Administration:i.p.; daily; 28 days
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Result:Partially restored DDC-increased liver-to-body weight ratio from 10.96% to 5.31%.
Normalized serum ALT, AST, and ALP levels.
Increased hepatic expression of bile efflux genes Bsep and Mrp2.
Downregulated Oatp2, Mrp3, and Mrp4, and upregulated Ntcp and Oatp1.
Reduced DDC-increased hepatic hydroxyproline from 81.3 μg/mg liver to 32.3 μg/mg liver.
Decreased hepatic mRNA expression of fibrosis markers α-Sma, Col1a1, Timp1, and Epcam, and inhibited Tgfb1 gene expression.
Alleviated ductular proliferation, intraductal plugs, inflammatory cell infiltration, and pericholangitis as shown by immunohistochemistry.
Decreased the percentage of myeloid cells and increased the percentage of lymphoid cells, inhibited CD4+ and CD8+ lymphocyte infiltration, and decreased the numbers of both Kupffer cells and monocyte-derived macrophages as shown by flow cytometry.
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Animal Model:ICR mice (6 weeks old)[6]
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Dosage:25 mg/kg; 50 mg/kg
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Administration:i.p.; daily; 5 days
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Result:Attenuated LPS-induced activation of microglia and astrocytes in the hippocampus, as evidenced by reduced IBA-1 and GFAP immunoreactivity, decreased density of IBA-1-positive microglia and GFAP-positive astrocytes, and mitigation of morphological changes associated with activation.
Suppressed LPS-induced microglial and astrocytic activation in the cortical area.
Dose-dependently suppressed the LPS-induced upregulation of IBA-1 and GFAP protein levels in western blot analysis.
Significantly downregulated the mRNA levels of LPS-induced pro-inflammatory factors including NLRP3, iNOS, COX-2, IL-1β, IL-6, TNF-α, and IL-18 in the hippocampus in RT-qPCR analysis.
Related Protocols :
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- Naïve CD4+ T-cell subset differentiation/polarization
- BrdU Incorporation Assay
- Protocol for Cell Cycle
- CCK-8/WST-8 Cell Proliferation Assay
- Research Protocol for Inflammation-related Diseases
- Research Protocol for Neurological Diseases
- Cell Viability Determination by MTT Colorimetric Assay
- Flow cytometric DNA-content cell-cycle staining
- Cell Cytotoxicity Assay
- DSS-Induced Colitis
- TNBS-Induced Colitis
- Notch Pathway Solutions
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- Orthotopic Cell-Line Xenograft
Chemical Information
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CAS No. 21499-24-1
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Appearance Solid
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Masse moléculaire 314.33
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Formule C18H18O5
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Color White to off-white
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SMILES
O=C1C2=C(O)C=C(O)C=C2C[C@H](CCC3=CC=C(OC)C=C3)O1
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Structure Classification
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Powder -20°C 3 years In solvent -80°C 6 months -20°C 1 month
Publications (1)
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Solvant et solubilité
In Vitro:
DMSO : 25 mg/mL (79.53 mM; Need ultrasonic and warming; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
View the Complete Stock Solution Preparation Table
Preparing Stock Solutions
View the Complete Stock Solution Preparation Table
Concentration
Solvent
Mass
1 mg
5 mg
10 mg
Concentration
Solvent
Mass
1 mM
3.1814 mL
15.9069 mL
31.8137 mL
5 mM
0.6363 mL
3.1814 mL
6.3627 mL
10 mM
0.3181 mL
1.5907 mL
3.1814 mL
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
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Pureté et documentation
Select Batch:
Pureté:
99.98%
Assay:
99.98%
ee.:
99.98%
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Fiche technique (302 KB)
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SDS (393 KB)
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Instruction de manipulation (2659 KB)
Références
[1]. Jiang J, et al. Agrimonolide mitigated DSS-induced colitis by modulating the balance between Treg and Th17 cells through the suppression of the Notch and JAK2/STAT3 signaling pathways. Heliyon. 2024 Jul 15;10(13):e33803. [Content Brief]
[5]. Kim HW, et al. Acylphloroglucinolated Catechin and Phenylethyl Isocoumarin Derivatives from Agrimonia pilosa. J Nat Prod. 2016 Sep 23;79(9):2376-83. [Content Brief]
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Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO | 1 mM | 3.1814 mL | 15.9069 mL | 31.8137 mL | 79.5343 mL |
| 5 mM | 0.6363 mL | 3.1814 mL | 6.3627 mL | 15.9069 mL | |
| 10 mM | 0.3181 mL | 1.5907 mL | 3.1814 mL | 7.9534 mL | |
| 15 mM | 0.2121 mL | 1.0605 mL | 2.1209 mL | 5.3023 mL | |
| 20 mM | 0.1591 mL | 0.7953 mL | 1.5907 mL | 3.9767 mL | |
| 25 mM | 0.1273 mL | 0.6363 mL | 1.2725 mL | 3.1814 mL | |
| 30 mM | 0.1060 mL | 0.5302 mL | 1.0605 mL | 2.6511 mL | |
| 40 mM | 0.0795 mL | 0.3977 mL | 0.7953 mL | 1.9884 mL | |
| 50 mM | 0.0636 mL | 0.3181 mL | 0.6363 mL | 1.5907 mL | |
| 60 mM | 0.0530 mL | 0.2651 mL | 0.5302 mL | 1.3256 mL |
Agrimonolide Related Classifications
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