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Product name: Chelidonine
Synonym name: Stylophorine
Catalogue No.: BP0342
Cas No.: 476-32-4
Formula: C20H19NO5
Mol Weight: 353.374
Botanical Source: Chelidonium majus
Physical Description:
Type of Compound: Alkaloids
Purity: 95%~99%
Analysis Method: HPLC-DAD or/and HPLC-ELSD
Identification Method: Mass, NMR
Packing: Brown vial or HDPE plastic bottle
The product could be supplied from milligrams to grams
Inquire for bulk scale.
Description:
Chelidonine is a promising model compound for overcoming MDR and for enhancing cytotoxicity of chemotherapeutics, especially against leukaemia cells, its efficacy needs to be confirmed in animal models. Chelidonine may be a potential therapeutic agent against metastasis of invasive human cancer cells, exhibits anti‑migratory and anti‑invasive effects in MDA‑MB‑231 cells, by suppressing COL‑I‑induced integrin signaling, through inhibiting the formation of the IPP complex and subsequent down‑regulation of IPP downstream signaling molecules, such as Akt and ERK1/2.
References:
Chem Biol Interact. 2014 Sep 30;223C:141-149.
Multiple mechanisms of cell death induced by chelidonine in MCF-7 breast cancer cell line.
In a preliminary study screening anti-proliferative natural alkaloids, a very potent benzophenanthridine, Chelidonine showed strong cytotoxicity in cancer cells. While several modes of death have been identified, most of anti-cancer attempts have focused on stimulation of cells to undergo apoptosis.
METHODS AND RESULTS:
Chelidonine seems to trigger multiple mechanisms in MCF-7 breast cancer cells. It induces both apoptosis and autophagy modes of cell death in a dose dependent manner. Alteration of expression levels of bax/bcl2, and dapk1a by increasing concentration of Chelidonine approves switching the death mode from apoptosis induced by very low to autophagy by high concentrations of this compound. On the other hand, submicromolar concentrations of Chelidonine strongly suppressed telomerase at both enzyme activity and hTERT transcriptional level. Long exposure of the cells to 50 nanomolar concentration of Chelidonine considerably accelerated senescence.
CONCLUSIONS:
Altogether, Chelidonine may provide a promising chemistry from nature to treat cancer.
Phytomedicine. 2013 Feb 15;20(3-4):282-94.
Modulation of multidrug resistance in cancer cells by chelidonine and Chelidonium majus alkaloids.
Cancer cells often develop multidrug resistance (MDR) which is a multidimensional problem involving several mechanisms and targets.
METHODS AND RESULTS:
This study demonstrates that Chelidonine and an alkaloid extract from Chelidonium majus, which contains protoberberine and benzo[c]phenanthridine alkaloids, has the ability to overcome MDR of different cancer cell lines through interaction with ABC-transporters, CYP3A4 and GST, by induction of apoptosis, and cytotoxic effects. Chelidonine and the alkaloid extract inhibited P-gp/MDR1 activity in a concentration-dependent manner in Caco-2 and CEM/ADR5000 and reversed their doxorubicin resistance. In addition, Chelidonine and the alkaloid extract inhibited the activity of the drug modifying enzymes CYP3A4 and GST in a dose-dependent manner. The alkaloids induced apoptosis in MDR cells which was accompanied by an activation of caspase-3, -8,-6/9, and phosphatidyl serine (PS) exposure. cDNA arrays were applied to identify differentially expressed genes after treatment with Chelidonine and the alkaloid extract. The expression analysis identified a common set of regulated genes related to apoptosis, cell cycle, and drug metabolism. Treatment of Caco-2 cells with 50 μg/ml alkaloid extract and 50 μM Chelidonine for up to 48 h resulted in a significant decrease in mRNA levels of P-gp/MDR1, MRP1, BCRP, CYP3A4, GST, and hPXR and in a significant increase in caspase-3 and caspase-8 mRNA.
CONCLUSIONS:
Thus, Chelidonine is a promising model compound for overcoming MDR and for enhancing cytotoxicity of chemotherapeutics, especially against leukaemia cells. Its efficacy needs to be confirmed in animal models.
Toxicol Lett. 2013 Sep 12;222(1):10-22.
Cytotoxicity and apoptotic signalling cascade induced by chelidonine-loaded PLGA nanoparticles in HepG2 cells in vitro and bioavailability of nano-chelidonine in mice in vivo.
Poor oral bioavailability of Chelidonine, a bio-active ingredient of Chelidonium majus, showing anti-cancer potentials against cancer cells with multidrug resistance, makes its optimal use rather limited.
METHODS AND RESULTS:
To address this problem, we encapsulated Chelidonine in biodegradable poly(lactide-co-glycolide) (PLGA) polymers and evaluated nano-Chelidonine's (NCs) anti-cancer efficacy vis-à-vis free Chelidonine (FC) against HepG2 cells and also evaluated its bioavailability in mice. Physicochemical characteristics indicated that stable spherical NC were formed in nanometer size range (123±1.15 nm) with good yield (86.34±1.91%), better encapsulation efficiency (82.6±0.574%), negative surface charge (-19.6±2.48 mV) and ability of prolonged and sustained release of Chelidonine. Fourier transform infrared analysis revealed that NC resembled similar peaks as that of FC suggesting effective encapsulation in PLGA. NC exhibited rapid cellular uptake and stronger apoptotic effect (∼46.6% reduced IC₅₀ value) than FC, blocking HepG2 cells at G2/M phase. p53, cyclin-D1, Bax, Bcl-2, cytochrome c, Apaf-1, caspase-9 and caspase-3 expressions also corroborated well to suggest greater anticancer potentials of NC.
CONCLUSIONS:
Our in vivo studies demonstrated NC to be more bio-available than FC and showed a better tissue distribution profile without inducing any toxicity (100 mg/kg bw) in mice. Unlike FC, NC could permeate into brain tissue, indicating thereby NC's better potentials for use in therapeutic oncology.
HPLC of Chelidonine
Storage conditions：Short-term storage at 2~8℃, long-term storage at -20 ~ -80℃
73.9900
2.4000
1.7900
High
No
No
Unknown
Yes
No
Positive
Chelidonine is a typical isoquinoline alkaloid, mainly extracted from the poppy family plant Chelidonium majus L. As one of the most representative active ingredients in celandine, cestratine is widely used in traditional Chinese medicine for its effects of clearing heat, detoxifying, reducing swelling, and relieving pain. In recent years, with the development of modern pharmacology and molecular biology technologies, the biological activity and molecular mechanisms of cleogramine have gradually been revealed, especially showing significant potential in the fields of antitumor and antiviral properties. It can induce cell cycle arrest and multi-pathway apoptosis, showing inhibitory effects on various tumor cells such as Candida albicans, melanocytoma, and lung cancer, making it a hot topic in natural product pharmacology research.
This paper will systematically review the chemical structure and physicochemical properties of leukostramine, its plant origin and extraction methods, pharmacological activity, and mechanism of action. It focuses on its molecular targeting role in diseases such as lung cancer, and, combined with druggability evaluation and pharmacokinetic analysis, looks ahead to its clinical application prospects, aiming to provide theoretical basis and practical guidance for subsequent research and drug development.
Chelidonine has the chemical formula C21H21NO5 and a molecular weight of 353.37. Its structure belongs to an isoquinoline alkaloid, with a typical polycyclic structure containing multiple oxidative functional groups, exhibiting high chemical stability and biological activity. The LogP value of leukocutine is about 2.4, indicating moderate lipophilusibility, which facilitates cell membrane penetration. Its topological pole surface area (TPSA) is 73.99 Ų, and it has 6 hydrogen bond acceptors, indicating that the molecule possesses certain polarity and hydrogen bonding capabilities, which may affect its binding affinity with target proteins.
The molecular structure of leukocutine contains an isoquiline framework and multiple hydroxyl and methoxy groups. These groups not only impart excellent bioactivity but also enable the body to produce various metabolic products during metabolism. The complexity of its chemical structure provides a variety of chemical modification sites for designing derivatives and optimizing efficacy.
Celandine mainly comes from celandine (Chelidonium majus L.), a perennial herbaceous plant of the Papaveraceae family, widely distributed in parts of Europe, Asia, and North America. The whole plant of Celandsia, especially the rhizome, is rich in isoquinoline alkaloids, with Cestrasium being particularly abundant.
Traditional extraction methods usually use alcohol solvents (such as methanol and ethanol) to extract dried celandrey powder, followed by acid-base extraction and liquid-liquid distribution to enrich the alkaline components. Modern extraction technologies such as ultrasound-assisted extraction, microwave-assisted extraction, and high-performance liquid chromatography (HPLC) separation and purification have significantly improved the extraction efficiency and purity of leukostramine. In recent years, composite extraction methods combining molecular blotting and membrane separation techniques have also provided new ideas for the industrial production of brocadine.
During extraction, pH and temperature must be strictly controlled to prevent degradation and isomerization of leukostracyline, ensuring the stability and biological activity of its active components.
The pharmacological activity of leukogrammine mainly lies in its anti-tumor, antiviral, and cell cycle regulation aspects. Numerous in vitro cell experiments and some animal model studies have shown that lecetraine can significantly inhibit the proliferation of various tumor cells, induce apoptosis, and possess certain antiviral activity.
Leukocutine exhibits cytotoxic effects in various tumor cells, including melanocytoma, lung cancer, and breast cancer. It induces cell cycle G2/M phase arrest, blocks cell division, and inhibits tumor cell proliferation. In apoptosis, lecracerine can activate both caspase-dependent pathways and induce cell death through non-dependent pathways, demonstrating a multi-target, multi-pathway anti-tumor mechanism.
Cetraline exhibits inhibitory effects on various viruses, especially by blocking viral replication and infection. Although the specific targets are not yet fully understood, its potential to enhance antiviral ability by regulating host cell signaling pathways and immune responses warrants further study.
Leukoquanine can inhibit the cell cycle progression of the model organism Dugesia japonica stem cells, suggesting its potential application value in stem cell biology and regenerative medicine. Moreover, cell cycle inhibition provides important theoretical support for its anti-tumor mechanism.
The biological effects of beroctrineine depend on its regulation of various signaling pathways and molecular targets, with particularly in-depth research on its mechanisms in malignant tumors such as lung cancer.
Lecracerine induces cell cycle G2/M phase arrest, blocking mitosis and reducing cell proliferation. Its induced apoptosis depends on activation of caspase family proteins (such as CASP9) and involves non-caspase-dependent pathways, exhibiting a multiplex regulatory network.
In summary, lecratenine regulates tumor cell proliferation, apoptosis, and metabolism through multi-target and multi-pathway synergistic effects, demonstrating its complex and effective anti-tumor mechanism.
The druggability parameters of leukotraline indicate that it has certain potential for drug development, but it also carries safety risks.
Gecraceine has a molecular weight of 353.37 and a LogP of 2.4, showing moderate lipid solubility, which facilitates cell membrane penetration and oral absorption. TPSA is 73.99, which matches the polarity range of drug molecules and supports good bioavailability. Its high blood-brain barrier penetration capacity suggests it may affect the central nervous system, potentially offering therapeutic advantages but also raising concerns about neurotoxicity.
The LD50 of leukotyrine is about 100 mg/kg, which is within the moderate toxicity range. Both hepatotoxicity and cardiotoxicity have been reported, indicating that liver and heart function must be strictly monitored during drug development. A positive Ames test indicates possible genotoxicity, requiring further assessment of its mutagenic risk. The inhibitory effect of hERG channels is still unclear, and additional research is needed to assess arrhythmia risk.
Currently, there is limited systematic pharmacokinetic research on leukogeneline. Preliminary data indicate good oral absorption, but the metabolic pathway is complex, mainly via hepatic metabolism. The safety and activity of metabolites still require further study. Its high blood-brain barrier penetration suggests potential for application in central system diseases, but it also increases the risk of neurotoxicity.
As a natural isoquinoline alkaloid, lecturneline has attracted widespread attention in drug development due to its multi-target antitumor activity, especially its potential application value in malignant tumors such as lung cancer. The future clinical application prospects are mainly reflected in the following aspects:
Anti-tumor drug development
Lecchidogine coordinates tumor cell growth through multiple signaling pathways, providing a theoretical basis for the development of novel anticancer drugs. By combining modern drug design technologies, structural optimization can improve selectivity and safety, reducing toxic side effects.
Combination medication strategies
Legracerine can be used in combination with chemotherapy or targeted drugs to enhance antitumor effects and overcome drug resistance. Its regulation of signaling pathways such as STAT3 and PI3K provides molecular basis for combination therapy.
Antiviral therapeutic potential
Its antiviral activity makes it possible to develop new antiviral drugs, especially in the treatment of viral infection-related tumors, playing a dual role.
Safety and toxicity control
Due to risks of hepatotoxicity, cardiotoxicity, and genotoxicity, future research should focus on safety evaluation and explore strategies for dose optimization, administration route improvements, and toxicity mitigation strategies.
Drug formulations and delivery systems
Through modern pharmaceutical technologies such as nanocarriers and targeted delivery systems, the bioavailability and targeting of lecetraine are improved, system toxicity is reduced, and clinical value is enhanced.
Overall, as a versatile natural product, leukotramine has good potential for drug development, but its safety remains a key bottleneck in clinical translation. In the future, it is necessary to strengthen research on its pharmacological mechanisms and toxicology to promote its advancement toward clinical application.
Leukostramine, a widely sourced and structurally unique isoquinoline alkaloid, has become an important subject of natural product pharmacological research due to its remarkable antitumor and antiviral activities. It regulates the cell cycle and apoptosis through multiple targets and pathways, demonstrating complex and effective biological functions. Although its druggability parameters show certain drug development potential, safety issues such as hepatotoxicity, cardiotoxicity, and genotoxicity still require close attention.
Future research should focus on deeply elucidating its molecular mechanisms, optimizing its chemical structure to improve selectivity and safety, combining modern pharmacoceutics to improve administration methods, and conducting systematic pharmacokinetic and toxicological evaluations. Through multidisciplinary collaborative efforts, lecratenine is expected to become a new natural drug for treating lung cancer and other malignant tumors, offering new strategies and options for clinical oncology treatment.
Shenshuai
Wenjing
Hedandan
