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  • Brand : BIOFRON

  • Catalogue Number : BF-B4004

  • Specification : 98%(HPLC)

  • CAS number : 471-95-4

  • Formula : C26H36O6

  • Molecular Weight : 444.56

  • PUBCHEM ID : 12302120

  • Volume : 25mg

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Catalogue Number


Analysis Method






Molecular Weight



White needle crystal

Botanical Source

Bufo gargarizans

Structure Type



Standards;Natural Pytochemical;API




Bufotaline/Bufotalin std./16-(Acetyloxy)-3,14-dihydroxybufa-20,22-dienolide/BUFOTALIN(SH)/BUFOTALIN SULFATE/Bufa-20,22-dienolide, 16-(acetyloxy)-3,14-dihydroxy-, (3β,5β,16β)-/(3b,5b,16b)-16-(Acetyloxy)-3,14-dihydroxybufa-20,22-dienolide/(3S,5R,8R,9S,10S,13R,14S,16S,17R)-3,14-dihydroxy-10,13-dimethyl-17-(2-oxo-2H-pyran-5-yl)hexadecahydro-1H-cyclopenta[a]phenanthren-16-yl acetate/5β-Bufa-20,22-dienolide, 3β,14,16β-trihydroxy-, 16-acetate (8CI)/Bufotalin/3b,14,16b-Trihydroxy-5b-bufa-20,22-dienolide 16-Acetate/(3β,5β,16β)-16-Acetoxy-3,14-dihydroxybufa-20,22-dienolide


[(3S,5R,8R,9S,10S,13R,14S,16S,17R)-3,14-dihydroxy-10,13-dimethyl-17-(6-oxopyran-3-yl)-1,2,3,4,5,6,7,8,9,11,12,15,16,17-tetradecahydrocyclopenta[a]phenanthren-16-yl] acetate


1.3±0.1 g/cm3


Methanol; Acetontrile; DMSO

Flash Point

195.8±23.6 °C

Boiling Point

591.7±50.0 °C at 760 mmHg

Melting Point

223°C (rough estimate)



InChl Key


WGK Germany


HS Code Reference


Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:471-95-4) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Venenum bufonis has been used as an antitumor drug in China for many years. Bufotalin, as an active component of Venenum bufonis, has been proven to exhibit antitumor effects in cancer types. In the present study, the effect of bufotalin on the human melanoma skin cancer cell line A375 was analyzed using MTT and colony formation assays. Bufotalin significantly inhibited the proliferation and colony formation of A375 cells. Further studies demonstrated that bufotalin significantly upregulated the protein levels of ATM serine/threonine kinase and Chk2, downregulated CDC25C protein expression, and subsequently inhibited CDK1 expression, leading to cell cycle arrest at the G2/M phase of the A375 cells. Furthermore, bufotalin significantly increased BAX expression levels, decreased BCL‑2 expression, and then upregulated apoptosis‑related proteins, caspase‑3/-9, followed by A375 cell apoptosis. Taken together, these results show that bufotalin induces cell cycle arrest at the G2/M phase and cell apoptosis, resulting in the inhibition of A375 cell proliferation, thereby suggesting that bufotalin may be utilized in melanoma treatment


Bufotalin Induces Cell Cycle Arrest and Cell Apoptosis in Human Malignant Melanoma A375 Cells


Zhaohai Pan 1 , Chuanjun Qu 1 , Ying Chen 1 , Xiaoyu Chen 1 , Xiaona Liu 1 , Wenjin Hao 1 , Wenjuan Xu 1 , Lei Ye 1 , Peng Lu 2 , Defang Li 1 , Qiusheng Zheng 1

Publish date

2019 Apr




Chronic inflammatory autoimmune disease Sjogren’s syndrome (SS) is characterized by the reduced secretion of exocrine glands, suggesting strategies targeting inflammation to be a potential option for SS therapy. Bufotalin, an active constituent of Bufadienolides, exerts potent antitumor effects with unknown effects on autoimmune diseases including SS. This study aims to investigate whether bufotalin possesses therapeutic potentials to SS and the underlying mechanisms. The experimental Sjogren’s syndrome (ESS) murine model was constructed by SG-immunization and murine naïve CD4+ T cells were cultured under Th17 polarization conditions with or without low doses of bufotalin treatment. Saliva flow rate was measured, and flow cytometry was applied to analyze T cell subpopulations. ELISA was conducted to determine the levels of targeted inflammatory cytokines. Bufotalin-treated ESS mice showed higher saliva flow rates, lower serum levels of autoantibodies (anti-M3R and anti-SSA IgG), lower serum levels of pro-inflammatory cytokines, as well as lower Th17 cell population from spleens and cervical lymph nodes. Additionally, in vitro study showed that bufotalin inhibits Th17 polarization and secretion of cytokines IL-17 and IFN-γ. Bufotalin at a low dose significantly ameliorates ESS development, possibly via inhibiting pro-inflammatory Th17 population and secretion of inflammatory cytokines during ESS pathogenesis.


Bufotalin Ameliorates Experimental Sjogren's Syndrome Development by Inhibiting Th17 Generation


Yang Huang 1 , Guangxia Yang 1 , Jing Fei 1 , Yingyi Wu 1 , Juzhen Yan 2

Publish date

2020 Jan 16




The search for novel and more efficient chemo-agents against malignant osteoblastoma is important. In this study, we examined the potential anti-osteoblastoma function of bufotalin, and studied the underlying mechanisms. Our results showed that bufotalin induced osteoblastoma cell death and apoptosis in dose- and time-dependent manners. Further, bufotalin induced endoplasmic reticulum (ER) stress activation in osteoblastoma cells, the latter was detected by the induction of C/EBP homologous protein (CHOP), phosphorylation of inositol-requiring enzyme 1 (IRE1) and PKR-like endoplasmic reticulum kinase (PERK), as well as caspase-12 activation. Conversely, the ER stress inhibitor salubrinal, the caspase-12 inhibitor z-ATAD-fmk as well as CHOP depletion by shRNA significantly inhibited bufotalin-induced osteoblastoma cell death and apoptosis. Finally, by using a mice xenograft model, we demonstrated that bufotalin inhibited U2OS osteoblastoma cell growth in vivo. In summary, our results suggest that ER stress contributes to bufotalin-induced apoptosis in osteoblastoma cells. Bufotalin might be investigated as a novel anti-osteoblastoma agent.


Apoptosis and signaling; Bufotalin; ER stress; Osteoblastoma.


Bufotalin-induced Apoptosis in Osteoblastoma Cells Is Associated With Endoplasmic Reticulum Stress Activation


Yun-Rong Zhu 1 , Yong Xu 2 , Jian-Feng Fang 1 , Feng Zhou 1 , Xiong-Wei Deng 1 , Yun-Qing Zhang 3

Publish date

2014 Aug 15

Description :

Bufotalin is a cardiotoxic bufanolide steroid, cardiac glycoside analogue, secreted by a number of toad species; a novel anti-osteoblastoma agent.IC50 value:Target:in vitro: bufotalin induced osteoblastoma cell death and apoptosis in dose- and time-dependent manners. Further, bufotalin induced endoplasmic reticulum (ER) stress activation in osteoblastoma cells, the latter was detected by the induction of C/EBP homologous protein (CHOP), phosphorylation of inositol-requiring enzyme 1 (IRE1) and PKR-like endoplasmic reticulum kinase (PERK), as well as caspase-12 activation [1]. Bufotalin was the most potent active compound among these four bufadienolides, and it exerted stronger inhibitory effect on the viability of doxorubicin-induced multidrug resistant liver cancer cells (R-HepG2) than that of their parent cells HepG2. bufotalin treatment induced cell cycle arrest at G(2)/M phase through down-regulation of Aurora A, CDC25, CDK1, cyclin A and cyclin B1, as well as up-regulation of p53 and p21. Bufotalin treatment also induced apoptosis which was accompanied by decrease in mitochondrial membrane potential, increases in intracellular calcium level and reactive oxygen species production, activations of caspase-9 and -3, cleavage of poly ADP-ribose polymerase (PARP) as well as changes in the expressions of bcl-2 and bax [2]. Bufotalin promoted death receptor-mediated cell death, especially TRAIL-induced apoptosis, through activation of caspase-3 and PARP-1. Cotreatment of bufotalin with TRAIL resulted in the downregulation of anti-apoptotic proteins, including Bcl-XL, Mcl-1, survivin and XIAP, and the up-regulation of MAPKs and TRAIL receptor DR5. In addition, phosphorylation of STAT1 was strongly inhibited by bufotalin [3]. externalization of phosphatidylserine, accumulation of sub-G(1) cells, fragmentation of DNA, and formation of apoptotic bodies were observed in bufotalin-treated Hep 3B cells [4].