| Size | Price | Stock | Qty |
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| 10mg |
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| 100mg |
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| 250mg | |||
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| Targets |
Acetylcorynoline targets multiple cellular pathways and proteins. It significantly inhibits LPS-induced activation of IκB kinase (IKK) and mitogen-activated protein kinases (MAPKs), key components of the NF-κB and MAPK inflammatory signaling pathways. The compound suppresses inflammatory cytokines, including TNF-α, IL-1β, and IL-6. Acetylcorynoline may exert its neuroprotective and anti-apoptotic effects by decreasing egl-1 expression (a pro-apoptotic gene in C. elegans models) to suppress apoptosis pathways, and by increasing rpn5 expression to enhance proteasome activity. In the immune system, acetylcorynoline inhibits the maturation and function of bone marrow-derived dendritic cells (DCs) in mice, acting as a potent immunosuppressive agent. The compound also induces apoptosis in cancer cells and protects liver tissues from oxidative stress.
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| ln Vitro |
Tumor necrosis factor-alpha, interleukin 6, and interleukin 12p70 secreted by LPS-stimulated dendritic cells (DC) are strongly inhibited by acetylcorynoline [1]. The activation of mitogen-activated protein kinase and IκB kinase produced by LPS is greatly inhibited by acetylcorynoline [1].
In vitro studies have demonstrated that acetylcorynoline exhibits potent anti-inflammatory activity by inhibiting LPS-induced inflammatory responses. The compound significantly suppresses the activation of IKK and MAPK signaling pathways, leading to reduced production of inflammatory cytokines such as TNF-α, IL-1β, and IL-6. Acetylcorynoline inhibits the maturation of bone marrow-derived dendritic cells (DCs) in mice, preventing their differentiation and functional activation. The compound shows anti-tumor activity by inducing apoptosis in cancer cells through mechanisms involving the suppression of apoptosis pathways (via egl-1 downregulation) and enhancement of proteasome function (via rpn5 upregulation). Additionally, acetylcorynoline exhibits antimicrobial activity. Its hepatoprotective effects have been demonstrated in models of liver injury, where it protects liver tissues from oxidative stress damage. |
| ln Vivo |
In vivo studies of acetylcorynoline have confirmed its hepatoprotective and anti-inflammatory efficacy in animal models. The compound protects against acute liver injury induced by hepatotoxic agents, reducing serum transaminase levels and attenuating histopathological damage to liver tissues. In models of inflammatory disease, acetylcorynoline administration reduces inflammatory cytokine levels and suppresses immune cell activation. The compound shows potential therapeutic benefits in models of Parkinson's disease, where it may exert neuroprotective effects through modulation of apoptosis and proteasome pathways. In vivo protocols typically involve oral or intraperitoneal administration of acetylcorynoline at doses ranging from 5 to 50 mg/kg. Standard endpoints include assessment of inflammatory markers, liver enzyme levels, histopathological examination, and behavioral assessments in neurological models.
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| Enzyme Assay |
For anti-inflammatory assays, acetylcorynoline activity is assessed using LPS-stimulated macrophages or dendritic cells. Cells are cultured in RPMI-1640 or DMEM medium supplemented with 10% FBS and antibiotics. Acetylcorynoline is dissolved in DMSO and diluted in culture medium to final concentrations (typically 1-100 µM). Cells are pre-treated with acetylcorynoline for 1-2 hours, then stimulated with LPS (0.1-1 µg/ml) for 4-24 hours. Supernatants are collected for cytokine measurement by ELISA (TNF-α, IL-1β, IL-6, IL-10). Cell lysates are prepared for Western blot analysis of signaling proteins: IKK phosphorylation, IκB degradation, MAPK phosphorylation (ERK, JNK, p38), and NF-κB nuclear translocation. For NF-κB reporter assays, cells transfected with NF-κB-luciferase reporter plasmids are treated similarly and luciferase activity is measured. For apoptosis studies, cells are treated with acetylcorynoline and apoptosis is assessed by Annexin V/PI staining and flow cytometry, or by caspase-3/7 activity assays.
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| Cell Assay |
For in vitro cell-based experiments, immune cells (macrophages, dendritic cells) or cancer cell lines are cultured in appropriate medium (RPMI-1640 or DMEM) with 10% FBS and 1% penicillin-streptomycin at 37°C in 5% CO₂. Cells are seeded in 6-well or 96-well plates at densities appropriate for each assay. For dendritic cell maturation assays, bone marrow-derived dendritic cells are generated by culturing mouse bone marrow cells with GM-CSF and IL-4 for 5-7 days. Immature DCs are treated with acetylcorynoline (1-50 µM) for 1 hour, then stimulated with LPS (0.1-1 µg/ml) for 24-48 hours. DC maturation markers (CD40, CD80, CD86, MHC-II) are analyzed by flow cytometry. Cytokine production in supernatants is measured by ELISA. For cancer cell viability assays, cells are treated with acetylcorynoline (0.1-100 µM) for 48-72 hours and viability is assessed by MTT or CCK-8 assay. For hepatoprotection studies, hepatocytes are treated with hepatotoxic agents (CCl₄ or DMF) with or without acetylcorynoline, and cell viability, LDH release, and oxidative stress markers (MDA, SOD, GSH) are measured.
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| Animal Protocol |
For in vivo hepatoprotection studies, adult mice (BALB/c or C57BL/6, 6-8 weeks old) are used. Acetylcorynoline is dissolved in vehicle (e.g., saline with 0.5% DMSO or carboxymethylcellulose) and administered via oral gavage or intraperitoneal injection. For the CCl₄-induced liver injury model, mice receive acetylcorynoline (5-50 mg/kg) daily for 3-7 days, followed by a single dose of CCl₄ (0.5-1 ml/kg, diluted in olive oil, i.p.) on the final day. After 12-24 hours, blood samples are collected for serum transaminase (ALT, AST) measurement. Liver tissues are harvested for histopathological examination (H&E staining) and assessment of oxidative stress markers (MDA, SOD, GSH) and inflammatory cytokines. For the DMF-induced hepatotoxicity model, mice are treated similarly with DMF (200-400 mg/kg, i.p.). For anti-inflammatory studies, mice may be subjected to carrageenan-induced paw edema or LPS-induced endotoxemia. In the LPS model, acetylcorynoline is administered 1 hour before LPS injection (5-10 mg/kg, i.p.), and serum cytokine levels are measured 2-6 hours post-LPS.
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| ADME/Pharmacokinetics |
Pharmacokinetic data for acetylcorynoline are not extensively reported. As an isoquinoline alkaloid with moderate lipophilicity, the compound is expected to have reasonable oral bioavailability. Based on its structural features (presence of acetyl and methoxy groups), acetylcorynoline likely undergoes extensive hepatic metabolism via CYP450 enzymes, including demethylation and oxidation. Phase II conjugation reactions (glucuronidation and sulfation) are also anticipated. Plasma protein binding is predicted to be moderate to high due to the compound's aromatic structure. Tissue distribution may include the liver, brain, and other organs, consistent with its observed hepatoprotective and neuroprotective activities. The compound's half-life and elimination pathways require further investigation through dedicated pharmacokinetic studies.
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| Toxicity/Toxicokinetics |
Toxicological data for acetylcorynoline are limited as the compound is a research reagent. However, as a natural alkaloid derived from traditional medicinal plants with a history of use in traditional Chinese medicine, acetylcorynoline is generally considered to have moderate safety. In cell-based assays, the compound shows anti-inflammatory and anti-tumor activity at concentrations typically in the low micromolar range. No acute toxicity LD50 values have been reported. The compound's immunosuppressive activity suggests that it may have effects on immune function at higher doses. As with all research compounds, appropriate safety precautions should be taken when handling acetylcorynoline, including the use of personal protective equipment and work in a well-ventilated area.
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| References | |
| Additional Infomation |
Acetyl corydaline is a benzophenanthridine alkaloid. It has been reported to exist in plants of the genera Corydalis, Corydalis, and other organisms with relevant data.
Acetylcorynoline is a major alkaloid component derived from Corydalis bungeana, a traditional Chinese medicinal herb. Its IUPAC name is (5aR,12bR,13aS)-5a,13a-dimethyl-3,4,5,5a,6,7,12b,13a-octahydro-1H-[1,3]benzodioxolo[4,5-g]isochromeno[3,2-c]quinolin-12-yl acetate. The compound exhibits diverse pharmacological effects including anti-inflammatory, hepatoprotective, anti-tumor, antimicrobial, and immunosuppressive activities. Its mechanism involves inhibition of IKK and MAPK signaling, suppression of inflammatory cytokines, inhibition of dendritic cell maturation, and modulation of apoptosis and proteasome pathways. Acetylcorynoline shows potential in treating inflammatory diseases, liver injury, Parkinson's disease, and cancer. However, it has not entered clinical trials and is strictly for research use only. |
| Molecular Formula |
C23H23NO6
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|---|---|
| Molecular Weight |
409.4318
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| Exact Mass |
409.152
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| CAS # |
18797-80-3
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| PubChem CID |
177015
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| Appearance |
Off-white to light yellow solid powder
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| Density |
1.4±0.1 g/cm3
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| Boiling Point |
499.1±45.0 °C at 760 mmHg
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| Flash Point |
255.7±28.7 °C
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| Vapour Pressure |
0.0±1.3 mmHg at 25°C
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| Index of Refraction |
1.667
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| LogP |
4.05
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| Hydrogen Bond Donor Count |
0
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| Hydrogen Bond Acceptor Count |
7
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| Rotatable Bond Count |
2
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| Heavy Atom Count |
30
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| Complexity |
703
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| Defined Atom Stereocenter Count |
3
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| SMILES |
CC(=O)O[C@H]1CC2=CC3=C(C=C2[C@@H]4[C@]1(C5=C(CN4C)C6=C(C=C5)OCO6)C)OCO3
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| InChi Key |
PUHCFWFODBLSAP-WWNPGLIZSA-N
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| InChi Code |
InChI=1S/C23H23NO6/c1-12(25)30-20-7-13-6-18-19(28-10-27-18)8-14(13)22-23(20,2)16-4-5-17-21(29-11-26-17)15(16)9-24(22)3/h4-6,8,20,22H,7,9-11H2,1-3H3/t20-,22+,23-/m0/s1
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| Chemical Name |
[(1R,12S,13R)-13,24-dimethyl-5,7,18,20-tetraoxa-24-azahexacyclo[11.11.0.02,10.04,8.014,22.017,21]tetracosa-2,4(8),9,14(22),15,17(21)-hexaen-12-yl] acetate
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: This product requires protection from light (avoid light exposure) during transportation and storage. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO : ~25 mg/mL (~61.06 mM)
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| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.4424 mL | 12.2121 mL | 24.4242 mL | |
| 5 mM | 0.4885 mL | 2.4424 mL | 4.8848 mL | |
| 10 mM | 0.2442 mL | 1.2212 mL | 2.4424 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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