Continentalic acid
Based on 1 Customer Validation
Continentalic acid is a diterpenoid organic acid. Continentalic acid exhibits multiple activities including anti-inflammatory, antioxidant, neuroprotective, antibacterial and antitumor effects. Continentalic acid alleviates oxidative stress, reduces pro-inflammatory cytokine production, inhibits MAPK phosphorylation and neutrophil infiltration, and induces growth inhibition and apoptosis of cancer cells. Continentalic acid can be used in research related to traumatic brain injury, cancer, inflammation and infections.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- Reinheit : 99.72%
- CAS. Nr.: 19889-23-7
- Formel: C20H30O2
- Molecular Weight:302.45
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Speicherung:
4°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
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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Biologische Aktivität
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Chemical Information
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Lösungsmittel & Löslichkeit
- Protokoll
- Reinheit & Dokumentation
- Verweise
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Help & FAQs
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Biologische Aktivität
Beschreibung
In Vitro
Continentalic acid (10-100 μM; 24-72 h) inhibits the growth of human hepatocellular carcinoma HepG2 cells in a time- and dose-dependent manner, with an IC50 of 50 μM[1].
Continentalic acid (25-100 μM; 72 h) induces apoptosis in human hepatocellular carcinoma HepG2 cells, including morphological changes and DNA fragmentation[1].
Continentalic acid (10-100 μM; 48 h) regulates the expression of apoptosis-related proteins in human hepatoma HepG2 cells, upregulates the levels of caspase-3, Bak and Bax, induces PARP cleavage, and downregulates the level of Bcl-2[1].
Continentalic acid (1-20 μM) dose-dependently inhibits the production of IL-6, IL-8, MMP-13, COX-2 and PGE2 stimulated by IL-1β in human osteoarthritic chondrocytes[3].
Continentalic acid (1-20 μM; 24 h) dose-dependently inhibits the phosphorylation of p38, ERK1/2 and JNK mitogen-activated protein kinases (MAP kinases) in IL-1β-stimulated human osteoarthritic chondrocytes[3].
Continentalic acid (10 μM) inhibits IL-1β-induced nuclear translocation of NF-κB/p65 in human osteoarthritic chondrocytes after 1 h of incubation[3].
Continentalic acid (8-16 µg/mL; 24 h) potently inhibits the growth of methicillin-sensitive Staphylococcus aureus ATCC 25923, methicillin-resistant Staphylococcus aureus ATCC 33591, and 12 clinical methicillin-resistant Staphylococcus aureus (MRSA) isolates, with an MIC value of 8-16 µg/mL[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:human hepatocarcinoma HepG2 cells
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Concentration:10, 25, 50, 100 μM
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Incubation Time:72 h
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Result:Induced distinct apoptotic morphological changes in HepG2 cells by 72 h, including cell shrinkage, nuclear and cytoplasmic condensation, chromatin condensation, and polylobation or fragmentation of nuclei.
Caused visible apoptotic changes in cells treated with 25, 50, and 100 μM continentalic acid.\nInduced dose-dependent DNA ladder formation in HepG2 cells after 72 h of incubation.
Caused clear laddering observed at concentrations of 25, 50, and 100 μM.
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Cell Line:IL-1β-stimulated human osteoarthritis (OA) chondrocytes
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Concentration:1, 3, 5, 10, 20 μM
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Incubation Time:24 h
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Result:Significantly inhibited IL-1β-stimulated phosphorylation of p38, ERK1/2, and JNK protein kinases in a dose-dependent manner.
In Vivo
Continentalic acid (0.97 mg/kg; i.p.; once daily; for 30 consecutive days) exerts significant anti-arthritic efficacy in MIA-induced osteoarthritis rats, restores weight-bearing balance, and prevents cartilage damage and proteoglycan loss[3].
Continentalic acid (1-50 mg/kg; i.p.; once daily for 14 consecutive days) exerts potent neuroprotective activity in a mouse traumatic brain injury (TBI) model[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c mice (6-week-old male, 27-33 g, traumatic brain injury weight-drop model)[5]
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Dosage:1 mg/kg; 10 mg/kg; 50 mg/kg
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Administration:i.p.; daily; 14 days
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Result:Reduced neurological severity score.
Restored paw withdrawal threshold.
Reduced cortical histopathological damage, increased neuronal count, and reduced cerebral microbleeds compared to the TBI group.
Downregulated mRNA and protein expression of GFAP, Iba1, TLR4, NF-κB, and cleaved caspase-3; upregulated mRNA and protein expression of IκB-α and Bcl-2 compared to the TBI group.
Reduced TBI-induced DNA damage compared to the TBI group.
Reduced levels of NO, LPO, IL-1β, and TNF-α; increased levels of GST, GSH, catalase, and SOD compared to the TBI group.
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Animal Model:BALB/c (male, 3-4 weeks old, 22-26 g, LPS-induced acute lung injury)[2]
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Dosage:10 mg/kg; 50 mg/kg; 100 mg/kg
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Administration:i.p.; single dose 30 minutes pre-LPS
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Result:Achieved an 80% 24-hour survival rate at 100 mg/kg (vs. 20% in LPS-only group); showed no protective effect on mortality at 10 mg/kg.
Significantly reduced LPS-induced pyrexia at 50 mg/kg and 100 mg/kg).
Reduced lung wet/dry ratio dose-dependently at all three doses, with marked inhibition at 100 mg/kg.
Significantly elevated lung tissue levels of GSH, GST, catalase, and SOD at all three doses, with largest increases at 100 mg/kg.
Significantly reduced lung tissue MDA levels and both plasma and lung tissue NO levels at all three doses, with effects increasing with dose.
Significantly inhibited LPS-induced increases in lung tissue IL-1β, IL-6, and TNF-α at all three doses.
Normalized total neutrophil counts (NEU) to near control levels at 50 mg/kg and 100 mg/kg; normalized WBC counts to control levels at 100 mg/kg.
Reduced lung injury scores dose-dependently; reduced neutrophilic infiltration and improved tracheal architecture at these doses.
Reduced lung tissue MPO activity at all three doses, with significant inhibition at 100 mg/kg.
Significantly reduced lung tissue iNOS expression and significantly increased Nrf2 protein expression at 100 mg/kg.
Chemical Information
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CAS. Nr. 19889-23-7
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Appearance Solid
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Molecular Weight 302.45
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Formel C20H30O2
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Color White to off-white
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SMILES
C[C@]12[C@@](CCC3=C[C@](C=C)(C)CC[C@@]23[H])([H])[C@@](C)(CCC1)C(O)=O
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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
4°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
Lösungsmittel & Löslichkeit
In Vitro:
DMSO : 100 mg/mL (330.63 mM; Need ultrasonic; 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 (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
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 (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
In Vivo:
Select the appropriate dissolution method based on your experimental animal and administration route.
- For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
- To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
- The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
Solubility: 2.5 mg/mL (8.27 mM); Suspended solution; Need ultrasonic
This protocol yields a suspended solution of 2.5 mg/mL. Suspended solution can be used for oral and intraperitoneal injection.
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: ≥ 2.5 mg/mL (8.27 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%Saline +
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL. * In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Protokoll
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Kinase activity and phosphorylation assays
Kinase activity assays measure the ability of kinases to transfer phosphate groups from ATP to specific substrates, while phosphorylation assays detect the presence and levels of phosphorylated proteins. Common methods include radiolabeled ATP incorporation (e. g. ,), ADP release detection via bioluminescence (e. g. ,[3]), enzyme-linked immunosorbent assays (ELISA) for phospho-specific epitopes (e. g. ,[6]), and microtiter-based formats for high-throughput screening (e. g. ,[8]). The ADP-Glo assay quantifies kinase activity by measuring ADP produced during phosphorylation using a luciferase-based system. Radiometric assays involve autoradiography or scintillation counting after incorporation of 32P-labeled ATP into substrate proteins. ELISA-based approaches rely on phospho-specific antibodies to detect activated kinases in cell lysates or purified samples.
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Research Protocol for Infectious Diseases
Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.
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Western Blot
Western blotting (WB) is a commonly used experimental method in molecular biology, biochemistry, and immunogenetics for identifying and quantifying target proteins. It combines gel electrophoresis with immunoassay, enabling researchers to analyze protein expression, post-translational modifications, and molecular weight.
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Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
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Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
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ROS/oxidative-stress fluorescent staining
ROS/oxidative-stress fluorescent staining uses cell-permeant fluorogenic probes that become fluorescent after oxidation inside cells or tissues; commonly used examples include DCFH-DA/DCFDA for broad cellular oxidant detection, DHE for superoxide-related signal detection, MitoSOX for mitochondrial superoxide-related signal detection, and CellROX probes for oxidative-stress-associated fluorescence readouts. The assay detects probe oxidation rather than a single ROS species unless the probe and analysis method have been chemically validated for that species. DCFH-DA enters cells, is deacetylated by intracellular esterases to DCFH, and produces fluorescent DCF after oxidation, so the readout is used as an operational measure of total cellular oxidative stress rather than a species-specific ROS measurement. DHE and MitoSOX can report superoxide-related oxidation, but red fluorescence alone can include non-specific ethidium-like oxidation products; HPLC or optimized spectral approaches are
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
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Protocol for Kinase activity and phosphorylation assays
Kinase activity assays measure transfer of phosphate from ATP to a protein or peptide substrate, generating phosphorylated substrate, ADP, or incorporated radiolabeled phosphate as the readout; phosphorylation assays measure site-specific phosphorylation in cells or tissues as a proxy for kinase-pathway activation, inhibition, or substrate regulation. Phosphorylation can be detected by phospho-specific Western blot, immunoprecipitation kinase assay, phospho-immunofluorescence, phospho-flow cytometry, luminescent ADP detection, radiolabeled ATP incorporation, or reporter-based pathway assays, and these readouts can be applied to cancer cells, primary neurons, mouse tumors, organoids, inflammatory macrophages, ferroptosis studies, and mitophagy studies when the kinase target is biologically relevant.
Reinheit & Dokumentation
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Data Sheet (285 KB)
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SDS (398 KB)
- English - EN (398 KB)
- Français - FR (398 KB)
- Deutsch - DE (398 KB)
- Norwegian - NO (398 KB)
- Español - ES (398 KB)
- Swedish - SV (398 KB)
- Italian - IT (398 KB)
- Korean - KR (398 KB)
- Portuguese - PT (398 KB)
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Handling Instructions (2659 KB)
Verweise
[1]. Kwon TO, et al. Continentalic acid from Aralia continentalis induces growth inhibition and apoptosis in HepG2 cells. Arch Pharm Res. 2008;31(9):1172-1178. [Content Brief]
[2]. Ali H, et al. Attenuation of LPS-induced acute lung injury by continentalic acid in rodents through inhibition of inflammatory mediators correlates with increased Nrf2 protein expression. BMC Pharmacol Toxicol. 2020;21(1):81. Published 2020 Nov 25. [Content Brief]
[3]. Hong R, et al. Continentalic Acid Rather Than Kaurenoic Acid Is Responsible for the Anti-Arthritic Activity of Manchurian Spikenard In Vitro and In Vivo. Int J Mol Sci. 2019;20(21):5488. Published 2019 Nov 4. [Content Brief]
[4]. Jeong SI, et al. Continentalic acid from Aralia continentalis shows activity against methicillin-resistant Staphylococcus aureus. Phytother Res. 2006;20(6):511-514. [Content Brief]
[5]. Zafar S, et al. Neuroprotective effect of Continentalic acid by targeting NF-κB/Bcl-2 and oxidative stress signaling in traumatic brain injury in male BALB/c mice. Mol Biol Rep. 2025;53(1):135. Published 2025 Nov 28. [Content Brief]
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 (protect from light). 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 | 3.3063 mL | 16.5317 mL | 33.0633 mL | 82.6583 mL |
| 5 mM | 0.6613 mL | 3.3063 mL | 6.6127 mL | 16.5317 mL | |
| 10 mM | 0.3306 mL | 1.6532 mL | 3.3063 mL | 8.2658 mL | |
| 15 mM | 0.2204 mL | 1.1021 mL | 2.2042 mL | 5.5106 mL | |
| 20 mM | 0.1653 mL | 0.8266 mL | 1.6532 mL | 4.1329 mL | |
| 25 mM | 0.1323 mL | 0.6613 mL | 1.3225 mL | 3.3063 mL | |
| 30 mM | 0.1102 mL | 0.5511 mL | 1.1021 mL | 2.7553 mL | |
| 40 mM | 0.0827 mL | 0.4133 mL | 0.8266 mL | 2.0665 mL | |
| 50 mM | 0.0661 mL | 0.3306 mL | 0.6613 mL | 1.6532 mL | |
| 60 mM | 0.0551 mL | 0.2755 mL | 0.5511 mL | 1.3776 mL | |
| 80 mM | 0.0413 mL | 0.2066 mL | 0.4133 mL | 1.0332 mL | |
| 100 mM | 0.0331 mL | 0.1653 mL | 0.3306 mL | 0.8266 mL |
Continentalic acid Related Classifications
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