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  • Brand : BIOFRON

  • Catalogue Number : BF-R4004

  • Specification : 98%(HPLC)

  • CAS number : 465-39-4

  • Formula : C24H32O4

  • Molecular Weight : 384.51

  • PUBCHEM ID : 6917974

  • Volume : 25mg

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Catalogue Number


Analysis Method






Molecular Weight



White crystalline powder

Botanical Source

Bufo gargarizans

Structure Type



Standards;Natural Pytochemical;API




(3b,5b,15b)-14,15-Epoxy-3-hydroxy-5-bufa-20,22-dienolide/Respigon/bufogenin/Resi (VAN)/20,22,5BETA-BUFADIENOLID-14BETA,15BETA-EPOXY-3BETA-OL/Resi/3β-Hydroxy-14,15β-epoxy-5β-bufa-20,22-dienolide/Bufa-20,22-dienolide, 14,15-epoxy-3-hydroxy-, (3β,5β,15β)-/(3β,5β,15β)-3-Hydroxy-14,15-epoxybufa-20,22-dienolide/14,15β-Epoxy-3β-hydroxy-5β-bufa-20,22-dienolide/RBG/Resibufogenin/bufogenina/resibufagenin/Recibufogenin




1.3±0.1 g/cm3


Methanol; Acetontrile; DMSO

Flash Point

190.7±23.6 °C

Boiling Point

554.9±50.0 °C at 760 mmHg

Melting Point




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#:465-39-4) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Background: Necroptotic susceptibility is probably an intrinsic weakness of cancer. Here, we report that resibufogenin, a member of bufadienolide family, suppresses the growth and metastasis of colorectal cancer (CRC) through induction of necroptosis in vivo.
Methods: SW480 cells with stably expressing enhanced green fluorescence protein were xenografted to BALB/c-nu mice to observe the growth of tumors. Liver metastasis was observed by injection of MC38 cells beneath the splenic capsule of mice. Protein expression was determined by immunohistochemistry, immunofluorescence and western blot.
Results: Consolidated in vitro results indicate that resibufogenin has anti-proliferative activity on CRC cells. PI staining and transmission electron microscope imaging suggest that the cell death induced by resibufogenin are mainly through necrosis, which is further confirmed by the ineffectiveness of z-VAD, a pan-caspase general inhibitor. In particular, resibufogenin induced necrosis is substantially abrogated in receptor-interacting protein kinase 3 (RIPK3) knockout mouse embryo fibroblasts. The RIP3-dependent necrosis has been classified as necroptosis. Resibufogenin triggeres necroptosis through upregulating RIP3 and phosphorylating mixed lineage kinase domain-like protein at Ser358. Resibufogenin also activates the expression of PYGL, GLUD1 and GLUL in a RIP3-dependent manner. Resibufogenin exerts cytotoxic effect by inducing reactive oxygen species accumulation which can be neutralized by N-acetylcysteine. Remarkably, resibufogenin significantly suppresses liver-metastasis from spleen implantation. The anti-neoplastic effect of this compound can be abrogated by RIP3 knockdown.
Conclusion: Resibufogenin suppresses growth and metastasis of CRC through RIP3-mediated necroptosis.


Colorectal cancer; Metastasis; Necroptosis; Receptor-interacting protein kinase 3; Resibufogenin.


Resibufogenin Suppresses Colorectal Cancer Growth and Metastasis Through RIP3-mediated Necroptosis


Qinrui Han 1 , Ye Ma 1 , Hao Wang 1 , Yu Dai 1 , Chunhui Chen 1 , Yawei Liu 2 , Linlin Jing 3 , Xuegang Sun 4

Publish date

2018 Jul 15




Huachansu, a traditional Chinese medicine prepared from the dried toad skin, has been used in clinical studies for various cancers in China. Resibufogenin is a component of huachansu and classified as bufadienolides. Resibufogenin has been shown to exhibit the anti-proliferative effect against cancer cells. However, the molecular mechanism of resibufogenin remains unknown. Here we report that resibufogenin induces G1-phase arrest with hypophosphorylation of retinoblastoma (RB) protein and down-regulation of cyclin D1 expression in human colon cancer HT-29 cells. Since the down-regulation of cyclin D1 was completely blocked by a proteasome inhibitor MG132, the suppression of cyclin D1 expression by resibufogenin was considered to be in a proteasome-dependent manner. It is known that glycogen synthase kinase-3β (GSK-3β) induces the proteasomal degradation of cyclin D1. The addition of GSK-3β inhibitor SB216763 inhibited the reduction of cyclin D1 caused by resibufogenin. These effects on cyclin D1 by resibufogenin were also observed in human lung cancer A549 cells. These findings suggest that the anti-proliferative effect of resibufogenin may be attributed to the degradation of cyclin D1 caused by the activation of GSK-3β.


Colorectal cancer; Metastasis; Necroptosis; Receptor-interacting protein kinase 3; Resibufogenin.


Resibufogenin Induces G1-Phase Arrest Through the Proteasomal Degradation of Cyclin D1 in Human Malignant Tumor Cells


Masami Ichikawa 1 , Yoshihiro Sowa 1 , Yosuke Iizumi 1 , Yuichi Aono 1 , Toshiyuki Sakai 1

Publish date

2015 Jun 29;




Resibufogenin (RB), one of the major active compounds of the traditional Chinese medicine Chansu, has received considerable attention for its potency in cancer therapy. However, the anticancer effects and the underlying mechanisms of RB on pancreatic cancer remain elusive. Here, we found that RB inhibited the viability and induces caspase-dependent apoptosis in human pancreatic cancer cells Panc-1 and Aspc. Resibufogenin-induced apoptosis was through inhibition of constitutive nuclear factor-κB (NF-κB) activity and its target genes’ expression, which was caused by downregulation of transforming growth factor-β-activated kinase 1 (TAK1) levels and suppression of IκB kinase activity in Panc-1 and Aspc cells. This induction of TAK1-mediated NF-κB inactivation by RB was associated with increased glycogen synthase kinase-3 (GSK-3) phosphorylation and subsequent suppression of its activity. Moreover, RB-induced GSK-3 phosphorylation/inactivation acted through activation of protein kinase C but not Akt. Finally, RB suppressed human pancreatic tumor xenograft growth in athymic nude mice. Thus, our findings reveal a novel mechanism by which RB suppresses TAK1-mediated NF-κB activity through protein kinase C-dependent inhibition of GSK-3. Our findings provide a rationale for the potential application of RB in pancreatic cancer therapy.


glycogen synthase kinase-3; nuclear factor-κB; protein kinase C; resibufogenin; transforming growth factor-β-activated kinase 1.


Resibufogenin Suppresses Transforming Growth Factor-β-Activated Kinase 1-mediated Nuclear factor-κB Activity Through Protein Kinase C-dependent Inhibition of Glycogen Synthase Kinase 3


Lu Liu 1 2 , Yang Liu 1 , Xiaojia Liu 1 , Na Zhang 1 , Genxiang Mao 3 , Qingxuan Zeng 1 , Mingxiao Yin 1 , Danqing Song 1 , Hongbin Deng 1

Publish date

2018 Nov

Description :

Resibufogenin, a component of huachansu, has been shown to exhibit the anti-proliferative effect against cancer cells, and this may be attributed to the degradation of cyclin D1 caused by the activation of GSK-3β.IC50 Value:Target:In vitro: The effects of Resibufogenin on the outward delayed rectifier potassium current (IK) and outward transient potassium current (IA) in rat hippocampal neurons was investigated, and it inhibited both IK and IA, at 1 μM concentration RBG could alter some channel kinetics and gating properties of IK, such as steady-state activation and inactivation curves, open probability and time constants [1].In vivo: Resibufogenin prevented evidence of oxidative stress in "preeclamptic" rats [2].