Cat. No.: HY-N0885

Telocinobufagin

(Synonyms: Telobufotoxin; Telocinobufogenin)

1 Cited Publications

Customer Review

Based on 1 publication(s) in Google Scholar

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 typhimurium infection. 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.

Purity: 99.50%
CAS No.: 472-26-4
Formula: C₂₄H₃₄O₅
Molecular Weight:402.52

Storage:

Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 2 years , -20°C, 1 year

Telocinobufagin Chemical Structure

CAS No.: 472-26-4

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Fluorescent Dye

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biological Activity
- Description
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- In Vivo
Chemical Information
Publications (1)
Solvent & Solubility
- In Vitro
- In Vivo
Purity & Documentation
References
Help & FAQs
Classifications
Bioz

Biological Activity

Description

IC₅₀ & Target^[1]^[2]^[6]^[7]^[8]^[9]

STAT3

JAK2

PLK1

Akt

PI3K

mTOR

All JAK Isoforms :

All STAT Isoforms :

All mTOR Isoforms :

All PI3K Isoforms :

All Akt Isoforms :

All Polo-like Kinase (PLK) Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
A549	IC₅₀	0.1244 μM Compound: Tel	Cytotoxicity in human A549 cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay Cytotoxicity in human A549 cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay	[PMID: 35200033]
A549	IC₅₀	3 μM Compound: 10	Cytotoxicity against human A549 cells after 24 hrs by MTT assay Cytotoxicity against human A549 cells after 24 hrs by MTT assay	[PMID: 24050254]
HepG2	IC₅₀	2.4 μM Compound: 10	Cytotoxicity against human HepG2 cells after 24 hrs by MTT assay Cytotoxicity against human HepG2 cells after 24 hrs by MTT assay	[PMID: 24050254]
HL-60	IC₅₀	<0.01 μg/mL Compound: 19	Cytotoxicity against human HL60 cells after 72 hrs by MTT assay Cytotoxicity against human HL60 cells after 72 hrs by MTT assay	[PMID: 11575946]
KB	IC₅₀	1.3 μg/mL Compound: 19	Cytotoxicity against human KB cells after 72 hrs by MTT assay Cytotoxicity against human KB cells after 72 hrs by MTT assay	[PMID: 11575946]
MH60	IC₅₀	>25 μg/mL Compound: 19	Cytotoxicity against mouse MH60 cells after 72 hrs by MTT assay Cytotoxicity against mouse MH60 cells after 72 hrs by MTT assay	[PMID: 11575946]
NCI-H1299	IC₅₀	0.1066 μM Compound: Tel	Cytotoxicity in human NCI-H1299 cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay Cytotoxicity in human NCI-H1299 cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay	[PMID: 35200033]
PC-9	IC₅₀	0.6185 μM Compound: Tel	Cytotoxicity in human PC-9 cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay Cytotoxicity in human PC-9 cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay	[PMID: 35200033]
SK-MEL	IC₅₀	0.05 μM Compound: 8	Cytotoxicity against human SK-MEL cells assessed as reduction in cell viability measured after 48 hrs by MTT assay Cytotoxicity against human SK-MEL cells assessed as reduction in cell viability measured after 48 hrs by MTT assay	[PMID: 33882233]

In Vitro

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.

Cell Viability Assay^[1]

Cell Line:

A549, PC9, and H1299 cells
Concentration:

0.01, 0.1, 1, 10, 100 μM
Incubation Time:

48 h
Result:

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.

Cell Migration Assay ^[1]

Cell Line:

A549, PC9, and H1299 cells
Concentration:

0.125, 0.25 and 0.5 μM
Incubation Time:

PC9 and H1299 cells for 8 h, and A549 cells for 24 h
Result:

Remarkably suppressed cell migration in the Transwell migration assay.

Apoptosis Analysis^[1]

Cell Line:

PC9, and H1299 cells
Concentration:

0.125, 0.25 and 0.5 μM
Incubation Time:

24 h (H1299) or 48 h (PC9)
Result:

Increased the apoptotic rates in both cell lines in a concentration-dependent manner.

Western Blot Analysis^[1]

Cell Line:

A549, PC9, and H1299 cells
Concentration:

0.25, 0.5 and 1 μM
Incubation Time:

4, 6, 8, 12 h
Result:

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.

Cell Proliferation Assay^[2]

Cell Line:

143B, HOS, MG63, U2OS, SJSA and Saos-2 cells
Concentration:

0, 0.05, 0.1, 0.2, 0.5 and 1 μM
Incubation Time:

48 h
Result:

Inhibited cell proliferation in six osteosarcoma cell lines in a concentration-dependent manner.

Cell Migration Assay ^[2]

Cell Line:

143B and HOS cells
Concentration:

0.1, 0.2 and 0.5 μM
Incubation Time:

12 h
Result:

Displayed strong inhibitory activity against tumor cell migration.

Cell Migration Assay ^[2]

Cell Line:

143B and HOS cells
Concentration:

0.1, 0.2 and 0.5 μM
Incubation Time:

12 h
Result:

Displayed strong inhibitory activity against tumor cell invasion.

Apoptosis Analysis^[2]

Cell Line:

143B and HOS cells
Concentration:

0.2 and 0.5 μM
Incubation Time:

48 h
Result:

Significantly induced tumor cell apoptosis.

Western Blot Analysis^[2]

Cell Line:

143B, HOS and MG63 cells
Concentration:

0.1, 0.2 and 0.5 μM
Incubation Time:

2, 4, 8, 12, 24, 48 h
Result:

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.

RT-PCR^[5]

Cell Line:

HK2 cells, NHMCs, SYF, SYF + cSrc cells
Concentration:

10 and 100 nM
Incubation Time:

24 h
Result:

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.

Cell Migration Assay ^[7]^[8]

Cell Line:

4T1 cells
Concentration:

0.05 and 0.5 μg/mL
Incubation Time:

24 h
Result:

Concentration-dependently inhibited 4T1 cell migration and significantly reduced the number of cells passed through.

Cell Invasion Assay^[7]^[8]

Cell Line:

4T1 cells
Concentration:

0.05 and 0.5 μg/mL
Incubation Time:

24 h
Result:

Effectively inhibited the movement of cells through the matrix gel.

Western Blot Analysis^[7]^[8]

Cell Line:

4T1 cells
Concentration:

0.05 and 0.5 μg/mL
Incubation Time:

24 h
Result:

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.

Cell Viability Assay^[9]

Cell Line:

Cal-27 and SCC-25 cells
Concentration:

1, 2, 4, 6, 8, 16, 32, 64, 128, 256, 512, 1024 μM
Incubation Time:

24 h
Result:

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 PSTAT3^Y705, 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.

Chemical Information

CAS No. 472-26-4
Appearance Solid
Molecular Weight 402.52
Formula C₂₄H₃₄O₅
Color White to off-white
SMILES

O[C@@]([C@@]1(CC2)C)(CC[C@@H]1C(C=C3)=COC3=O)[C@@](CC[C@@]45O)([H])[C@@]2([H])[C@]4(CC[C@H](O)C5)C
Synonyms

Telobufotoxin; Telocinobufogenin
Structure Classification
- Steroids
Initial Source
- Animals
toad
Shipping

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

Publications (1)

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Phytomedicine

Telocinobufagin, a PLK1 suppressor that inhibits tumor growth and metastasis by modulating CDC25c and CTCF in HNSCC cells. [Abstract]

2024 May:127:155440. PMID: 38452691

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)

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

View the Complete Stock Solution Preparation Table

Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

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

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.

Molarity Calculator

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

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Molecular Weight Molecular Weight

Dilution Calculator

Concentration _(start) × Volume _(start) = Concentration _(final) × Volume _(final)

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In Vivo:

Select the appropriate dissolution method based on your experimental animal and administration route.

Stock Solution Working Solution

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.

Protocol 1

Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline

Solubility: ≥ 2.5 mg/mL (6.21 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO 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.

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 μL DMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.

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 μL DMSO stock solution (25.0 mg/mL) to 900 μL Corn oil, and mix evenly.

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Please enter your animal formula composition:

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Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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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).

Working solution concentration: 0.22 mg/mL

Purity & Documentation

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (307 KB)
SDS (396 KB)
- English - EN (396 KB)
- Français - FR (396 KB)
- Deutsch - DE (396 KB)
- Norwegian - NO (396 KB)
- Español - ES (396 KB)
- Swedish - SV (396 KB)
- Italian - IT (396 KB)
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- Portuguese - PT (396 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

References

[1]. Shen Y, et al. Telocinobufagin Has Antitumor Effects in Non-Small-Cell Lung Cancer by Inhibiting STAT3 Signaling. J Nat Prod. 2022 Apr 22;85(4):765-775. [Content Brief]

[2]. Ma X, et al. Telocinobufagin inhibits osteosarcoma growth and metastasis by inhibiting the JAK2/STAT3 signaling pathway. Eur J Pharmacol. 2023 Mar 5;942:175529. [Content Brief]

[3]. Wu SC, et al. Telocinobufagin enhances the Th1 immune response and protects against Salmonella typhimurium infection. Int Immunopharmacol. 2015 Apr;25(2):353-62. [Content Brief]

[4]. Feitosa GIMC,et al. Potent nonopioid antinociceptive activity of telocinobufagin in models of acute pain in mice. Pain Rep. 2019 Oct 8;4(6):e791. [Content Brief]

[5]. Kennedy DJ, et al. Telocinobufagin, a Novel Cardiotonic Steroid, Promotes Renal Fibrosis via Na⁺/K⁺-ATPase Profibrotic Signaling Pathways. Int J Mol Sci. 2018 Aug 29;19(9):2566. [Content Brief]

[6]. Qiang LZ, Fang SZ. Telocinobufagin suppresses malignant metastasis of undifferentiated thyroid carcinoma via modulation of the LARP1-mTOR pathway. Kaohsiung J Med Sci. 2025 Mar;41(3):e12934. [Content Brief]

[7]. Gao Y, et al. Telocinobufagin inhibits the epithelial-mesenchymal transition of breast cancer cells through the phosphoinositide 3-kinase/protein kinase B/extracellular signal-regulated kinase/Snail signaling pathway. Oncol Lett. 2018 May;15(5):7837-7845. [Content Brief]

[8]. Gao Y, et al. Erratum: Telocinobufagin inhibits the epithelial-to-mesenchymal transition of breast cancer cells through the PI3K/Akt/Snail signaling pathway. Oncol Lett. 2021 Apr;21(4):242. doi: 10.3892/ol.2021.12503. Epub 2021 Jan 31. Erratum for: Oncol Lett. 2018 May;15(5):7837-7845. [Content Brief]

[9]. Li J, et al. Telocinobufagin, a PLK1 suppressor that inhibits tumor growth and metastasis by modulating CDC25c and CTCF in HNSCC cells. Phytomedicine. 2024 May;127:155440. [Content Brief]

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Complete Stock Solution Preparation Table

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.

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	2.4843 mL	12.4217 mL	24.8435 mL	62.1087 mL
	5 mM	0.4969 mL	2.4843 mL	4.9687 mL	12.4217 mL
	10 mM	0.2484 mL	1.2422 mL	2.4843 mL	6.2109 mL
	15 mM	0.1656 mL	0.8281 mL	1.6562 mL	4.1406 mL
	20 mM	0.1242 mL	0.6211 mL	1.2422 mL	3.1054 mL
	25 mM	0.0994 mL	0.4969 mL	0.9937 mL	2.4843 mL
	30 mM	0.0828 mL	0.4141 mL	0.8281 mL	2.0703 mL
	40 mM	0.0621 mL	0.3105 mL	0.6211 mL	1.5527 mL
	50 mM	0.0497 mL	0.2484 mL	0.4969 mL	1.2422 mL
	60 mM	0.0414 mL	0.2070 mL	0.4141 mL	1.0351 mL
	80 mM	0.0311 mL	0.1553 mL	0.3105 mL	0.7764 mL
	100 mM	0.0248 mL	0.1242 mL	0.2484 mL	0.6211 mL

Telocinobufagin

1 Cited Publications

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Telocinobufagin

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Natural Product Diversity Scaffold Library

Tonifying Traditional Chinese Medicine Monomer Compound Library

Lactylation Compound Library

Mass Spectrometry Natural Product Library

Natural Product and Natural Product-Like Compound Library

Anti-Infection Compound Library

Apoptosis Compound Library

Cell Cycle/DNA Damage Compound Library

Epigenetics Compound Library

Immunology/Inflammation Compound Library

JAK/STAT Compound Library

Kinase Inhibitor Library

Membrane Transporter/Ion Channel Compound Library

PI3K/Akt/mTOR Compound Library

Protein Tyrosine Kinase Compound Library

Stem Cell Signaling Compound Library

Natural Product Library

Anti-Cancer Compound Library

Autophagy Compound Library

Small Molecule Immuno-Oncology Compound Library

Anti-Aging Compound Library

Publications Citing Use of MedChemExpress (MCE) Telocinobufagin

All JAK Isoforms