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Telocinobufagin (Telobufotoxin; Telocinobufogenin) is an orally active bufadienolide with potential anti-tumor effects. Telocinobufagin exerts its anti-cancer effects on non-small cell carcinoma, osteosarcoma, thyroid cancer, breast cancer and head and neck squamous cell carcinoma by inhibiting the STAT3, JAK2/STAT3, LARP1-mTOR, PI3K/Akt/Snail and PLK1 pathways, and can also induce tumor cell apoptosis. Telocinobufagin enhances the Th1 immune response and protects against Salmonella typhimuriuminfection. Telocinobufagin has a strong cardiac-stimulating effect by inhibiting the activity of Na+/K+-ATPase, and it can promote renal fibrosis. Telocinobufagin demonstrates non-opioid analgesic effects in various acute pain models.
For research use only. We do not sell to patients.
Telocinobufagin (Telobufotoxin; Telocinobufogenin) is an orally active bufadienolide with potential anti-tumor effects. Telocinobufagin exerts its anti-cancer effects on non-small cell carcinoma, osteosarcoma, thyroid cancer, breast cancer and head and neck squamous cell carcinoma by inhibiting the STAT3, JAK2/STAT3, LARP1-mTOR, PI3K/Akt/Snail and PLK1 pathways, and can also induce tumor cell apoptosis. Telocinobufagin enhances the Th1 immune response and protects against Salmonella typhimuriuminfection. Telocinobufagin has a strong cardiac-stimulating effect by inhibiting the activity of Na+/K+-ATPase, and it can promote renal fibrosis. Telocinobufagin demonstrates non-opioid analgesic effects in various acute pain models[1][2][3][4][5][6][7][8][9].
Telocinobufagin (0.01-100 μM, 0-96 h) suppresses proliferation and metastasis in human NSCLC cells, osteosarcoma cells, anaplastic thyroid cancer (ATC) cells, 4T1 breast cancer cells and neck squamous cell carcinoma (HNSCC)[1][2][6][7][8][9].
Telocinobufagin (0.125-5 μM, 24-48 h) induces apoptosis in human NSCLC cells and osteosarcoma cells and HNSCC cells[1][2][9].
Telocinobufagin (1-5 μM) induces G2/M phase arrest in Cal-27 cells and SCC-25 cells[9].
Telocinobufagin (0.5 μg/mL) suppresses malignant metastasis of undifferentiated thyroid carcinoma via modulation of the LARP1-mTOR pathway in CAL-62 cells[6].
Telocinobufagin (0.1-1 μM, 2-48 h) blocks STAT3 and JAK2/STAT3 signaling and inhibits PLK1[1][2][9].
Telocinobufagin (0.05-0.5 μg/mL, 24 h) reverses the epithelial-mesenchymal transition (EMT) process in breast cancer cells, downregulates the Snail transcription factor, and inhibits the PI3K/Akt/ERK signaling pathway.
Telocinobufagin (10-100 nM, 24 h) activates the pro-fibrotic phenotype of renal tubular epithelial cells (HK2 cells) and primary normal human renal mesangial cells (NHMCs), but is ineffective against SYF fibroblasts[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Inhibited cell viability in a concentration-dependent manner, and the corresponding half-maximal inhibitory concentrations (IC50) were 124.4, 618.5, and 106.6 nM, respectively.
Strongly upregulated cleaved PARP1 protein, but down-regulated anti-apoptotic BCL2 protein.
Inhibited STAT3 phosphorylation at tyrosine 705 (Y705) and its downstream targets.
Inhibited STAT3 nuclear translocation in a concentration-dependent manner.
Exhibited a dose-dependent significant inhibition of STAT3 phosphorylation and STAT3 phosphorylation induced by IL-6.
Down-regulated Cyclin D1, Bcl-2, Mcl-1 and Survivin.
Selectively inhibited the phosphorylation of JAK2, and had no significant effect on JAK1 and JAK3.
Down-regulated Snail and vimentin, and up-regulated E-cadherin.
Caused a dose-dependent increase in the expression of collagen 1 and collagen 3 mRNA in HK2 cells.
Significantly increased the expression of collagen 1 in NHMCs.
Increased collagen 1, collagen 3, TGFβ, CTGF mRNA.
Did not cause significant changes in the above indicators in the SYF cells.
Increased the expression of the epithelial marker E-cadherin and reduced the expression of interstitial markers vimentin and fibronectin.
Significantly reduced the level of Snail protein and had no significant effect on other EMT transcription factors (Slug, Twist1, Zeb1, Zeb2).
Reduced the protein levels of p-Akt, p-mTOR and p-ERK and did not affect the expression of total Akt, mTOR and ERK proteins.
Exhibited IC50s against Cal-27 and SCC-25 cells of 7.97 and 5.39 μM.
In Vivo
Telocinobufagin (1-2 mg/kg, i.p., every 2 days for 18 days) inhibits tumor growth in a human NSCLC xenograft model in mice[1].
Telocinobufagin (5-10 mg/kg, i.p., every 2 days for 20 days) significantly suppresses tumor growth and metastasis by inhibiting the JAK2/STAT3 signaling pathway in an osteosarcoma xenograft model in mice[2].
Telocinobufagin (10-40 μg, s.c., two doses, 14-day interval) enhances a Th1 immune response to control intracellular S. typhimurium infections in mice[3].
Telocinobufagin (0.062-10 mg/kg, i.p. and p.o, single dose) exhibits potent analgesic effects in various acute pain models in mice, and it does not rely on the opioid system or affect motor function. Its analgesic potency is four times that of morphine[4].
Telocinobufagin (0.1 mg/kg, i.p., once daily for 4 weeks) promotes renal fibrosis via Na+/K+-ATPase profibrotic signaling pathways[5].
Telocinobufagin (10-20 µg/mouse, i.p., 3 times a day for 2 weeks) inhibits breast cancer tumor growth and the epithelial mesenchymal transition in 4T1 cells xenograft model in mice[7][8].
Telocinobufagin (4-16 mg/kg, i.p., once daily for 30 days) inhibits tumor growth and lung metastasis in HNSCC cells-bearing mice[9].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
A549 xenograft tumor model established in female nude mice (BALB/c nude, 4-5-week-old)[1]
Dosage:
1 and 2 mg/kg
Administration:
Intraperitoneal injection (i.p.), every 2 days for a total of 18 days
Result:
Significantly reduced tumor size.
Showed no weight loss and had no noticeable toxicity on the heart, liver, lungs, or kidneys at this concentration.
Reduced the expression of PSTAT3Y705, MCL1, and BCL2 and increased the levels of cleaved PARP1.
Animal Model:
143B cells xenograft tumor model established in male nude mice (BALB/c nude, 6-8-week-old)[2]
Dosage:
5 mg/kg and 10 mg/kg
Administration:
Intraperitoneal injection (i.p.), every 2 days for a total of 20 days
Result:
Significantly reduced tumor weights.
Reduced the numbers of metastatic nodules.
Reduced the levels of phospho-STAT3 and phospho-JAK2.
Increased the proportion of cleaved caspase-3-positive tumor cells.
Animal Model:
S. typhimurium infection model established in female ICR mice (five weeks old, Grade II)[3]
Dosage:
10, 20, and 40 μg dissolved in saline
Administration:
Subcutaneous injection (s.c.), two doses on day 1 and day 15
Result:
Increased the survival rate of mice and reduced bacterial load.
Increased the levels of specific IgG2a (Th1-related antibodies) in OVA and FIST, while the level of IgG1 (Th2-related antibody) did not change significantly.
Promoted the secretion of IFN-γ (a key cytokine for Th1 cells) by spleen cells, but inhibited IL-4 (a marker for Th2 cells) and IL-17A (a marker for Th17 cells).
Upregulated the mRNA expression of the transcription factor T-bet (a key regulatory factor for Th1 cells), while having no significant effect on GATA-3 (Th2) and RORγt (Th17).
Animal Model:
Acetic acid-induced writhing test, formalin test, tail-flick test, hot-plate test, open-field test, rotarod test established in male Swiss Webster mice (25-30 g)[4]
Dosage:
0.062, 0.125, 0.25, 0.5, and 1 mg/kg (i.p.) and 0.625, 1.125, 2.5, 5, and 10mg/kg (p.o.)
Administration:
Intraperitoneal injection (i.p.) and oral administration (p.o.), single dose
Result:
Significantly inhibited the number of contortions in mice in a dose-dependent manner.
Significantly inhibited the licking time during the first 5 minutes after intraplantar injection of formalin.
Significantly increased the reaction time (the withdrawal by a brief vigorous movement) in a dose-dependent manner.
Significantly increased the reaction time (the withdrawal by a brief vigorous movement) in a dose-dependent manner.
Presented significant reaction latencies for 3 hours after administration (1 mg/kg, i.p; 10 mg/kg, p.o).
Did not affect locomotion in mice in open-field test and rotarod test.
Exhibited the potency about 4 times higher than that of morphine.
Animal Model:
Measurement of renal fibrosis model established in wild-type male SvJ/Black Swiss mice (25-30 g) (WT), as well as SvJ/Black Swiss mice heterozygous for the Na+/K+-ATPase-α-1 (referred to as NKA α-1+/−)[5]
Dosage:
0.1 mg/kg
Administration:
Intraperitoneal injection (i.p.), once daily for 4 weeks
Result:
Caused a significant increase in systolic blood pressure in both wild-type mice and NKAα-1+/− mice, but at 4 weeks, the amount of urinary protein excreted by NKAα-1+/− mice was significantly less than that of the wild-type control group.
Resulted in mild to moderate periglomerular and peritubular fibrosis of the renal cortex and the degree of renal fibrosis in NKAα-1+/− mice was lower than that in the wild-type control group at 4 weeks.
Animal Model:
4T1 cells xenograft tumor model established in six week old female BALB/c nude mice (18 22 g)[7][8]
Dosage:
10 or 20 µg/mouse
Administration:
Intraperitoneal injection (i.p.), three times a week for two consecutive weeks.
Result:
Significantly reduced the tumor volume and weight.
Reduced the number of lung metastatic lesions
Observed EMT markers and signaling pathway proteins in tumor tissues consistent with those in the in vitro experiments.
Animal Model:
Cal-27 cells xenograft tumor model and normal or PLK1 over-expressed HNSCC cells induced lung metastasis model established in BALB/c nude mice[9]
Dosage:
4, 8, and 16 mg/kg (xenograft tumor model) and 8 mg/kg (lung metastasis model)
Administration:
Intraperitoneal injection (i.p.), once daily for 30 days
Result:
Significantly inhibited the growth of transplanted tumors and lung metastasis.
Downregulated the expressions of PLK1, CDC25c and Ki67 in tumor tissues and overexpression of PLK1 can completely reverse the anti-tumor effect of TBG.
Room temperature in continental US; may vary elsewhere.
Storage
Powder
-20°C
3 years
4°C
2 years
In solvent
-80°C
2 years
-20°C
1 year
Solvent & Solubility
In Vitro:
DMSO : 50 mg/mL (124.22 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Preparing Stock Solutions
ConcentrationSolventMass
1 mg
5 mg
10 mg
1 mM
2.4843 mL
12.4217 mL
24.8435 mL
5 mM
0.4969 mL
2.4843 mL
4.9687 mL
10 mM
0.2484 mL
1.2422 mL
2.4843 mL
View the Complete Stock Solution Preparation Table
*Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles. Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for in vivo experiments, it is recommended to prepare freshly and use it on the same day. The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Protocol 2
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: 2.5 mg/mL (6.21 mM); Suspended solution; Need ultrasonic
This protocol yields a suspended solution of 2.5 mg/mL. Suspended solution can be used for oral and intraperitoneal injection.
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
Protocol 3
Add each solvent one by one: 10% DMSO 90% Corn Oil
Solubility: ≥ 2.5 mg/mL (6.21 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (25.0 mg/mL) to 900 μLCorn oil, and mix evenly.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
Dosage
mg/kg
Animal weight (per animal)
g
Dosing volume (per animal)
μL
Number of animals
Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
%
DMSO+
%
+
%
Tween-80
+
%
Saline
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
The co-solvents required include: DMSO,
. All of co-solvents are available by MedChemExpress (MCE).
, Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Calculation results:
Working solution concentration:
mg/mL
Method for preparing stock solution:
mg
drug dissolved in
μL
DMSO (Stock solution concentration: mg/mL).
The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only. If necessary, please contact MedChemExpress (MCE).
Method for preparing in vivo working solution for animal experiments: Take
μL DMSO stock solution, add
μL .
μL , mix evenly, next add
μL Tween 80, mix evenly, then add
μL Saline.
Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution
If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
*Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles. Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.
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