Product name: Sanguinarine
Synonym name: Pseudochelerythrine; ψ-Chelerythrine
Catalogue No.: BP1253
Cas No.: 2447-54-3
Formula: C₂₀H₁₄NO₄+
Mol Weight: 332.334
Botanical Source:
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

Storage: Store in a well closed container, protected from air and light. Put into refrigerate or freeze for long term storage.
Whenever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20℃. Generally, these will be useable for up to two weeks.

The product could be supplied from milligrams to grams
Inquire for bulk scale.

Description:

Sanguinarine possesses anticancer, antimicrobial, anti-inflammatory, and antioxidant properties, it has therapeutic potential in preventing the neurodegenerative diseases, it may be used to develop a potential therapeutic drug for treating cardiac remodeling and heart failure and shows protective effects on teeth and alveolar bone health. Sanguinarine can inhibit osteoclast formation and bone resorption via suppressing RANKL-induced activation of NF-κB and ERK signaling pathways, and can protect against cardiac hypertrophy and fibrosis via inhibiting NF-κB activation.

References:

Clin Cancer Res. 2000 Apr;6(4):1524-8.    

Differential antiproliferative and apoptotic response of sanguinarine for cancer cells versus normal cells.    

Sanguinarine, derived from the root of Sanguinaria canadendid, has been shown to possess antimicrobial, anti-inflammatory, and antioxidant properties. Here we compared the antiproliferative and apoptotic potential of Sanguinarine against human epidermoid carcinoma (A431) cells and normal human epidermal keratinocytes (NHEKs). 

METHODS AND RESULTS:

Sanguinarine treatment was found to result in a dose-dependent decrease in the viability of A431 cells as well as NHEKs albeit at different levels because Sanguinarine-mediated loss of viability occurred at lower doses and was much more pronounced in the A431 carcinoma cells than in the normal keratinocytes. DNA ladder assay demonstrated that compared to vehicle-treated control, Sanguinarine treatment of A431 cells resulted in an induction of apoptosis at 1-, 2-, and 5-microM doses. Sanguinarine treatment did not result in the formation of a DNA ladder in NHEKs, even at the very high dose of 10 microM. The induction of apoptosis by Sanguinarine was also evident by confocal microscopy after labeling the cells with annexin V. This method also identified necrotic cells, and Sanguinarine treatment also resulted in the necrosis of A431 cells. The NHEKs showed exclusively necrotic staining at high doses (2 and 5 microM). We also explored the possibility of cell cycle perturbation by Sanguinarine in A431 cells. The DNA cell cycle analysis revealed that Sanguinarine treatment did not significantly affect the distribution of cells among the different phases of the cell cycle in A431 cells. 

CONCLUSIONS:

We suggest that Sanguinarine could be developed as an anticancer drug.    

Oncotarget. 2015 Apr 30;6(12):10335-49.    

Molecular signatures of sanguinarine in human pancreatic cancer cells: A large scale label-free comparative proteomics approach.   

Pancreatic cancer remains one of the most lethal of all human malignancies with its incidence nearly equaling its mortality rate. Therefore, it's crucial to identify newer mechanism-based agents and targets to effectively manage pancreatic cancer. Plant-derived agents/drugs have historically been useful in cancer therapeutics. Sanguinarine is a plant alkaloid with anti-proliferative effects against cancers, including pancreatic cancer. This study was designed to determine the mechanism of Sanguinarine's effects in pancreatic cancer with a hope to obtain useful information to improve the therapeutic options for the management of this neoplasm. 

METHODS AND RESULTS:

We employed a quantitative proteomics approach to define the mechanism of Sanguinarine's effects in human pancreatic cancer cells. Proteins from control and Sanguinarine-treated pancreatic cancer cells were digested with trypsin, run by nano-LC/MS/MS, and identified with the help of Swiss-Prot database. Results from replicate injections were processed with the SIEVE software to identify proteins with differential expression. We identified 37 differentially expressed proteins (from a total of 3107), which are known to be involved in variety of cellular processes. Four of these proteins (IL33, CUL5, GPS1 and DUSP4) appear to occupy regulatory nodes in key pathways. Further validation by qRT-PCR and immunoblot analyses demonstrated that the dual specificity phosphatase-4 (DUSP4) was significantly upregulated by Sanguinarine in BxPC-3 and MIA PaCa-2 cells. Sanguinarine treatment also caused down-regulation of HIF1α and PCNA, and increased cleavage of PARP and Caspase-7. 

CONCLUSIONS:

Taken together, Sanguinarine appears to have pleotropic effects, as it modulates multiple key signaling pathways, supporting the potential usefulness of Sanguinarine against pancreatic cancer.    

Environ Toxicol Pharmacol. 2014 Nov;38(3):701-10.    

Involvement of heme oxygenase-1 in neuroprotection by sanguinarine against glutamate-triggered apoptosis in HT22 neuronal cells.   

Sanguinarine is a natural compound isolated from the roots of Macleaya cordata and M. microcarpa, has been reported to possess several biological activities such as anti-inflammatory and anti-oxidant effects. 

METHODS AND RESULTS:

In the present study, we demonstrated that Sanguinarine markedly induces the expression of HO-1 which leads to a neuroprotective response in mouse hippocampus-derived neuronal HT22 cells from apoptotic cell death induced by glutamate. Sanguinarine significantly attenuated the loss of mitochondrial function and membrane integrity associated with glutamate-induced neurotoxicity. Sanguinarine protected against glutamate-induced neurotoxicity through inhibition of HT22 cell apoptosis. JC-1 staining, which is a well-established measure of mitochondrial damage, was decreased after treatment with Sanguinarine in glutamate-challenged HT22cells. In addition, Sanguinarine diminished the intracellular accumulation of ROS and Ca(2+). Sanguinarine also induced HO-1, NQO-1 expression via activation of Nrf2. Additionally, we found that si RNA mediated knock-down of Nrf2 or HO-1 significantly inhibited Sanguinarine-induced neuroprotective response. 

CONCLUSIONS:

These findings revealed the therapeutic potential of Sanguinarine in preventing the neurodegenerative diseases.    

Mol Med Rep. 2014 Jul;10(1):211-6.    

Sanguinarine protects against pressure overload‑induced cardiac remodeling via inhibition of nuclear factor-κB activation.    

Cardiac remodeling is a major determinant of heart failure characterized by cardiac hypertrophy and fibrosis. Sanguinarine exerts widespread pharmacological effects, including antitumor and anti‑inflammatory responses. In the present study, the effect of Sanguinarine on cardiac hypertrophy, fibrosis and heart function was determined using the model induced by aortic banding (AB) in mice. 

METHODS AND RESULTS:

AB surgery and sham surgery were performed on male wild‑type C57 mice, aged 8‑10 weeks, with or without administration of Sanguinarine from one week after surgery for an additional seven weeks. Sanguinarine protected against the cardiac hypertrophy, fibrosis and dysfunction induced by AB, as assessed by the heart weight/body weight, lung weight/body weight and heart weight/tibia length ratios, echocardiographic and hemodynamic parameters, histological analysis, and the gene expression levels of hypertrophic and fibrotic markers. The inhibitory effect of Sanguinarine on cardiac remodeling was mediated by inhibiting nuclear factor (NF)‑κB signaling pathway activation. 

CONCLUSIONS:

The findings indicated that Sanguinarine protected against cardiac hypertrophy and fibrosis via inhibiting NF‑κB activation. These findings may be used to develop a potential therapeutic drug for treating cardiac remodeling and heart failure.    

Biochem Biophys Res Commun. 2013 Jan 18;430(3):951-6.    

Sanguinarine inhibits osteoclast formation and bone resorption via suppressing RANKL-induced activation of NF-κB and ERK signaling pathways.   

Sanguinarine is a natural plant extract that has been supplemented in a number of gingival health products to suppress the growth of dental plaque. However, whether Sanguinarine has any effect on teeth and alveolar bone health is still unclear. 

METHODS AND RESULTS:

In this study, we demonstrated for the first time that Sanguinarine could suppress osteoclastic bone resorption and osteoclast formation in a dose-dependent manner. Sanguinarine diminished the expression of osteoclast marker genes, including TRAP, cathepsin K, calcitonin receptor, DC-STAMP, V-ATPase d2, NFATc1 and c-fos. Further investigation revealed that Sanguinarine attenuated RANKL-mediated IκBα phosphorylation and degradation, leading to the impairment of NF-κB signaling pathway during osteoclast differentiation. In addition, Sanguinarine also affected the ERK signaling pathway by inhibiting RANKL-induced ERK phosphorylation. 

CONCLUSIONS:

Collectively, this study suggested that Sanguinarine has protective effects on teeth and alveolar bone health.