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Bufotalin Sale

(Synonyms: 蟾蜍他灵) 目录号 : GC33134

A bufadienolide with cytotoxic and immunomodulatory activities

Bufotalin Chemical Structure

Cas No.:471-95-4

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10mM (in 1mL DMSO)
¥884.00
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5mg
¥803.00
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10mg
¥1,339.00
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产品描述

Bufotalin is a bufadienolide that has been found in toad (B. asiaticus) venom and has cytotoxic and immunomodulatory activities.1,2 It induces cell cycle arrest at the G1 phase and apoptosis in Hep3B cells when used at concentrations ranging from 0.13 to 1.13 ?M.1 Bufotalin (100 ?g/kg) reduces autoantibody production, serum levels of TNF-α, IL-1β, IFN-γ, IL-22, and IL-17, and the number of splenic and lymph node Th17 cells, as well as increases saliva flow rates in a mouse model of experimental Sj?rgren’s syndrome, an autoimmune disease characterized by the reduced secretion of exocrine glands.2 It also induces lethality in anesthetized dogs (LD50 = 0.36 mg/kg).3

1.Su, C.-L., Lin, T.-Y., Lin, C.-N., et al.Involvement of caspases and apoptosis-inducing factor in bufotalin-induced apoptosis of Hep 3B cellsJ. Agric. Food Chem.57(1)55-61(2009) 2.Huang, Y., Yang, G., Fei, J., et al.Bufotalin ameliorates experimental Sj?gren's syndrome development by inhibiting Th17 generationNaunyn-Schmiedeberg's Arch. Pharmacol.393(10)1977-1985(2020) 3.Hamet, R.Toxicity of bufotalin administered by oral routeCompt. Rend. Soc. Biol.152571-574(1958)

Chemical Properties

Cas No. 471-95-4 SDF
别名 蟾蜍他灵
Canonical SMILES C[C@@]1(CC[C@@]2([H])[C@@]3([H])CC[C@@]4([H])[C@@]2(CC[C@H](O)C4)C)[C@@H](C(C=C5)=COC5=O)[C@@H](OC(C)=O)C[C@@]13O
分子式 C26H36O6 分子量 444.56
溶解度 DMSO : ≥ 4.6 mg/mL (10.35 mM) 储存条件 Store at -20°C
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1 mM 2.2494 mL 11.2471 mL 22.4942 mL
5 mM 0.4499 mL 2.2494 mL 4.4988 mL
10 mM 0.2249 mL 1.1247 mL 2.2494 mL
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Research Update

Bufotalin induces ferroptosis in non-small cell lung cancer cells by facilitating the ubiquitination and degradation of GPX4

Free Radic Biol Med 2022 Feb 20;180:75-84.PMID:35038550DOI:10.1016/j.freeradbiomed.2022.01.009.

Ferroptosis is a new form of regulated cell death that is dependent on iron- and lipid reactive oxygen species. Emerging evidence indicate that induction of ferroptosis could inhibit the proliferation of diverse cancer cells, which functions as a potent tumor suppressor in cancer. Here, we firstly reported Bufotalin (BT), a natural small molecule, was a novel glutathione peroxidase 4 (GPX4) inhibitor, which could trigger the ferroptosis in non-small cell lung cancer cells. In vitro, BT significantly inhibited the proliferation of A549 cells and induced the ferroptosis, whereas ferroptosis inhibitor or iron chelator significantly reversed the cytotoxicity of BT on A549 cells. Moreover, BT also increased the intracellular Fe2+. Subsequently, immunoblotting showed that BT could inhibit the protein expression of GPX4. Notably, BT dramatically accelerated the degradation of GPX4 in A549 cells. Immunoprecipitation assay further certified the increased ubiquitination of GPX4 induced by BT. Nevertheless, BT could not further increase the lipid ROS after silencing of GPX4, suggesting the induction of ferroptosis by BT was dependent on GPX4. Furthermore, BT also observably inhibited tumor growth and promoted lipid peroxidation in vivo. In conclusion, our findings indicated that BT could induce ferroptosis and cause lipid peroxidation by accelerating the degradation of GPX4 and raising the intracellular Fe2+, and BT will hopefully serve as a lead compound in developing anti-tumor agents for targeting ferroptosis.

Bufotalin ameliorates experimental Sjögren's syndrome development by inhibiting Th17 generation

Naunyn Schmiedebergs Arch Pharmacol 2020 Oct;393(10):1977-1985.PMID:31950221DOI:10.1007/s00210-020-01817-1.

Chronic inflammatory autoimmune disease Sjögren'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 Sjögren'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 induces cell cycle arrest and cell apoptosis in human malignant melanoma A375 cells

Oncol Rep 2019 Apr;41(4):2409-2417.PMID:30816542DOI:10.3892/or.2019.7032.

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 ameliorates ovalbumin-induced allergic rhinitis by restoring the Tregs

Microb Pathog 2023 Jan;174:105918.PMID:36455750DOI:10.1016/j.micpath.2022.105918.

Background: Allergic rhinitis (AR) is one of the most common inflammatory diseases. IgE, inflammatory cytokine production and Th17/Tregs imbalance have been implicated in AR pathogenesis. Bufotalin, a component extracted from toad venom skin secretions and auricular glands, has anti-inflammatory activity and regulates Th17/Tregs balance. Here, the effects of Bufotalin on AR were explored. Methods: The AR mice model was established using ovalbumin (OVA). AR mice were treated with Bufotalin started on Day 22 with various doses (1, 10, 100 μg or 1 mg per mouse) every day to Day 30. The sneezing and rubbing frequencies were counted. Serum levels of IL-1β, IL-10 and OVA-specific IgE were measured. The superficial cervical lymph nodes were harvested and the percentage of Tregs in lymph node was determined using CD4 and Foxp3 markers. Results: OVA treatment successfully induced AR model in mice with significantly increased sneezing and rubbing frequency, elevated levels of serum histamine, IL-1β, IL-10 and OVA-specific IgE. Bufotalin treatment significantly ameliorated AR symptoms, with reduced histamine, IgE and IL-1β levels, as well as sneezing and rubbing frequency. Moreover, Bufotalin treatment decreased the serum levels of IL-1β, IL-10 and OVA-specific IgE in AR mice. Conlcusion: Bufotalin ameliorated allergic rhinitis symptoms in AR mice by restoring Tregs in lymph node.

Bufotalin-induced apoptosis in osteoblastoma cells is associated with endoplasmic reticulum stress activation

Biochem Biophys Res Commun 2014 Aug 15;451(1):112-8.PMID:25068992DOI:10.1016/j.bbrc.2014.07.077.

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.