|Description:||1. Bufalin can induce typical apoptosis in human leukemia U937 cells, a pathway with the persistent activation of MAP kinase in U937 cells in response to bufalin is at least one of the signal transduction pathways involved in the induction of apoptosis. |
2. Bufalin and cinobufagin may inhibit the proliferation of prostate cancer cell lines associated with sustained elevation of the [Ca 2+ ] i and that of apoptosis.
3. Bufalin is a potent small-molecule inhibitor of the steroid receptor coactivators steroid receptor coactivator (SRC)-3 and SRC-1, it as a potentially broad-spectrum small-molecule inhibitor for cancer.
4. Bufalin can partly reverse the MDR of K562/VCR cells, with a possible mechanism of down-regulating MRP1 expression and activating apoptosis pathway by altering Bcl-xL/Bax ratio.
|Targets:||PKA | cAMP | p38MAPK | Bcl-2/Bax | P-gp | Src | Akt|
|Source:||The glandular body of Bufo bufo gargarizans Cantor|
|Solvent:||Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.|
|Storage:||Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).
Wherever 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 -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
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|After receiving:||The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||2.5872 mL||12.9359 mL||25.8719 mL||51.7438 mL||64.6797 mL|
|5 mM||0.5174 mL||2.5872 mL||5.1744 mL||10.3488 mL||12.9359 mL|
|10 mM||0.2587 mL||1.2936 mL||2.5872 mL||5.1744 mL||6.468 mL|
|50 mM||0.0517 mL||0.2587 mL||0.5174 mL||1.0349 mL||1.2936 mL|
|100 mM||0.0259 mL||0.1294 mL||0.2587 mL||0.5174 mL||0.6468 mL|
Mol Med Rep. 2015 Apr 24.
|Secreted protein acidic and rich in cysteine antagonizes bufalin‑induced apoptosis in gastric cancer cells.[Pubmed: 25936899]|
|Bufalin is an active compound in the traditional Chinese medicine Chan Su, which has been shown to induce apoptosis in a range of cancer cell types. However, certain gastric cancer cells are known to be resistant to Bufalin. Intracellular secreted protein acidic and rich in cysteine (SPARC) regulates proliferation and apoptosis. This study aimed to evaluate the role of SPARC in Bufalin‑induced apoptosis in SGC7901 and MGC803 gastric cancer cells. SGC7901 cells with high SPARC expression were more resistant to Bufalin than MGC803 cells with low SPARC expression. This resistance was significantly reversed by small interfering (si)RNA‑mediated knockdown of SPARC. Furthermore, it was shown that SPARC negatively regulated Bufalin‑induced intrinsic apoptosis by protecting mitochondrial integrity, decreasing the release of cytoplasmic cytochrome c and increasing the ratio of Bcl‑2/Bax. In addition, SPARC overcame Bufalin‑induced G2/M phase arrest by increasing levels of Cyclin B1 and Cyclin A protein expression. SPARC also activated cellular survival signals, including Src and Akt, but not extracellular signal‑regulated kinase. This study demonstrated that SPARC antagonizes Bufalin‑induced apoptosis via inhibition of the intrinsic apoptosis pathway, inhibition of cell cycle arrest and activation of certain pathways involved in proliferation. This provides novel evidence for SPARC as a potential target by which to sensitize gastric cancer cells to Bufalin.|
Prostate. 2003 Feb 1;54(2):112-24.
|Effects of bufalin and cinobufagin on the proliferation of androgen dependent and independent prostate cancer cells.[Pubmed: 12497584 ]|
|Bufalin and cinobufagin inhibited proliferation of cancer cells at doses of 0.1, 1, or 10 microM after 2-4 days of culture. Cytotoxicity of Bufalin and cinobufagin on the DU145 and LNCaP cells was dose-dependent. Bufalin or cinobufagin increased [Ca(2+)](i) and apoptosis in cancer cells after a 24-hr culture as well as caspase 3 activities in DU145 and PC3 cells and caspase 9 activities in LNCaP cells. CONCLUSIONS: Bufalin and cinobufagin may inhibit the proliferation of prostate cancer cell lines associated with sustained elevation of the [Ca(2+)](i) and that of apoptosis.|
Cancer Res. 2014 Mar 1;74(5):1506-1517.
|Bufalin is a potent small-molecule inhibitor of the steroid receptor coactivators SRC-3 and SRC-1.[Pubmed: 24390736 ]|
|Virtually all transcription factors partner with coactivators that recruit chromatin remodeling factors and interact with the basal transcription machinery. Coactivators have been implicated in cancer cell proliferation, invasion, and metastasis, including the p160 steroid receptor coactivator (SRC) family composed of SRC-1 (NCOA1), SRC-2 (TIF2/GRIP1/NCOA2), and SRC-3 (AIB1/ACTR/NCOA3). Given their broad involvement in many cancers, they represent candidate molecular targets for new chemotherapeutics. Here, we report on the results of a high-throughput screening effort that identified the cardiac glycoside Bufalin as a potent small-molecule inhibitor for SRC-3 and SRC-1. Bufalin strongly promoted SRC-3 protein degradation and was able to block cancer cell growth at nanomolar concentrations. When incorporated into a nanoparticle delivery system, Bufalin was able to reduce tumor growth in a mouse xenograft model of breast cancer. Our work identifies Bufalin as a potentially broad-spectrum small-molecule inhibitor for cancer.|
J Tradit Chin Med. 2014 Dec;34(6):678-83.
|Reversal effect of bufalin on multidrug resistance in K562/VCR vincristine-resistant leukemia cell line.[Pubmed: 25618972]|
|OBJECTIVE: To probe insights into the reversal effect of Bufalin on vincristine-acquired multidrug resistance (MDR) in human leukemia cell line K562/VCR. METHODS: Proliferative inhibition rate and the reversal index (RI) of Bufalin were determined by Methyl thiazolyl tetrazolium assay. The uptake of Adriamycin (ADM) in K562/VCR cells, cell cycle and apoptosis rate were determined by flow cytometry (FCM). Cell morphologic changes were observed with Wright-Giemsa staining. The expression of P-glycoprotein (P-gp), multidrug-associated protein-1 (MRP1), Bcl-xL and Bax protein were measured by immunocytochemistry. RESULTS: The human leukemia multidrug resistant K562/VCR cells showed no cross-resistance to Bufalin. The RIs of Bufalin at concentrations of 0.0002, 0.001 and 0.005 μmol/L were 4.85, 6.94 and 14.77, respectively. Preincubation of 0.001 μmol/L Bufalin for 2 h could increase intracellular ADM fluorescence intensity to 28.07% (P < 0.05) and down-regulate MRP1 expression simultaneously, but no remarkable effect was found on P-gp protein. Cell cycle analysis indicated increased apoptosis rate and apparent decreased G2/M phase proportion after treatment with Bufalin. When exposed to 0.01 μmol/L Bufalin, typical morphological changes of apoptosis could be observed. Down-regulation of Bcl-xL and up-regulation of Bax expression in K562/VCR cells could be detected by immunocytochemistry. CONCLUSION: Bufalin could partly reverse the MDR of K562/VCR cells, with a possible mechanism of down-regulating MRP1 expression and activating apoptosis pathway by altering Bcl-xL/Bax ratio.|
J Biol Chem. 1996 Jun 14;271(24):14067-72.
|The cooperative interaction of two different signaling pathways in response to bufalin induces apoptosis in human leukemia U937 cells.[Pubmed: 8662906]|
|Bufalin, an active principle of Chinese medicine, chan'su, induced typical apoptosis in human leukemia U937 cells. When U937 cells were treated with 10(-8) M Bufalin in the absence of serum, mitogen-activated protein (MAP) kinase activity was markedly increased 6 h after the start of treatment and elevated so for 12 h. Prior to the activation of MAP kinase, increased activities of Ras, Raf-1, and MAP kinase kinase were found, but these enzymes were transiently activated by the treatment with Bufalin. These results suggest that the signal was transmitted sequentially from Ras, Raf-1, and MAP kinase kinase to MAP kinase. In association with this signal transduction, the concentration of cAMP in the cells decreased markedly, suggesting that Raf-1 was also activated by a decrease in the extent of phosphorylation by protein kinase A. In fact, pretreatment of U937 cells with forskolin and 3-isobutyl-1-methylxanthine, which are known to increase the concentration of cAMP in the cells, and subsequent treatment with Bufalin resulted in a decrease in both Raf-1 activity and DNA fragmentation. To confirm the participation of MAP kinase in the apoptotic process, antisense cDNA for MAP kinase kinase 1 was expressed in U937 cells. The transformants were significantly resistant to both DNA fragmentation and cell death in response to Bufalin. Our findings suggest that a pathway with the persistent activation of MAP kinase in U937 cells in response to Bufalin is at least one of the signal transduction pathways involved in the induction of apoptosis.|