SalinomycinPolyether ionophore antibiotic;anti-cancer CAS# 53003-10-4 |
- FH535
Catalog No.:BCC1573
CAS No.:108409-83-2
- CHIR-99021 (CT99021)
Catalog No.:BCC1275
CAS No.:252917-06-9
- XAV-939
Catalog No.:BCC1120
CAS No.:284028-89-3
- Salinomycin sodium salt
Catalog No.:BCC1917
CAS No.:55721-31-8
- IWP-2
Catalog No.:BCC1665
CAS No.:686770-61-6
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 53003-10-4 | SDF | Download SDF |
| PubChem ID | 3085092 | Appearance | Powder |
| Formula | C42H70O11 | M.Wt | 751 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Synonyms | Procoxacin | ||
| Solubility | DMSO : ≥ 36.7 mg/mL (48.87 mM) *"≥" means soluble, but saturation unknown. | ||
| Chemical Name | (2R)-2-[(2R,5S,6R)-6-[(2S,3S,4S,6R)-6-[(3S,5S,7R,9S,10S,12R,15R)-3-[(2R,5R,6S)-5-ethyl-5-hydroxy-6-methyloxan-2-yl]-15-hydroxy-3,10,12-trimethyl-4,6,8-trioxadispiro[4.1.57.35]pentadec-13-en-9-yl]-3-hydroxy-4-methyl-5-oxooctan-2-yl]-5-methyloxan-2-yl]butanoic acid | ||
| SMILES | CCC(C1CCC(C(O1)C(C)C(C(C)C(=O)C(CC)C2C(CC(C3(O2)C=CC(C4(O3)CCC(O4)(C)C5CCC(C(O5)C)(CC)O)O)C)C)O)C)C(=O)O | ||
| Standard InChIKey | KQXDHUJYNAXLNZ-XQSDOZFQSA-N | ||
| Standard InChI | InChI=1S/C42H70O11/c1-11-29(38(46)47)31-15-14-23(4)36(50-31)27(8)34(44)26(7)35(45)30(12-2)37-24(5)22-25(6)41(51-37)19-16-32(43)42(53-41)21-20-39(10,52-42)33-17-18-40(48,13-3)28(9)49-33/h16,19,23-34,36-37,43-44,48H,11-15,17-18,20-22H2,1-10H3,(H,46,47)/t23-,24-,25+,26-,27-,28-,29+,30-,31+,32+,33+,34+,36+,37-,39-,40+,41-,42-/m0/s1 | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
||
| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
||
| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | Salinomycin is an inhibitor of Wnt/β-catenin signaling, which acts on the Wnt/Fzd/LRP complex. Salinomycin strongly suppresses Wnt1-stimulated reporter activity with an IC50 of 163 nM, and reduces β-catenin levels.In Vitro:Salinomycin is a potent inhibitor of the Wnt signaling cascade. Incubation of the malignant lymphocytes with Salinomycin induces apoptosis within 48 h, with a mean IC50 of 230 nM. Salinomycin is also an antibiotic potassium ionophore, has been reported recently to act as a selective breast cancer stem cell inhibitor[1]. Salinomycin is a novel and an effective anticancer drug, inhibits SW620 cells and Cisp-resistant SW620 cells with IC50 of 1.54±0.23 μM and 0.32±0.05 μM, respectively. Salinomycin is found to have the ability to kill both cancer stem cells (CSCs) and therapy-resistant cancer cells. After continuous Salinomycin treatment for 48 h, the apoptotic cells are observed under the microscope and counted randomly at least 100 cells in one field. The number of apoptotic cells which are stained by Hoechst33342 is significantly increased in Cisp-resistant SW620 cells (20.20±3.72) than that of SW620 cells (9.40±2.07) per 100 cells (p<0.05). After treatment with Salinomycin for 48 h, flow cytometric analysis is used to detect the cell apoptosis both in SW620 cells and Cisp-resistant SW620 cells. The cell apoptotic rate in Cisp-resistant SW620 cells (37.82±3.63%) is significantly higher than that of SW620 cells (16.78±2.56%) (p<0.05)[2].In Vivo:After administration of 4 mg/kg Salinomycin (Sal), 8 mg/kg Salinomycin and 10 uL/g saline water for 6 weeks, the mice are sacrificed. The size of the liver tumors in the Salinomycin treatment groups diminishes compare with the control group. The mean diameter of the tumors decreases from 12.17 mm to 3.67 mm (p<0.05) and the mean volume (V=length×width2×0.5) of the tumors decreases from 819 mm3 to 25.25 mm3 (p<0.05). Next, the tumors are harvested, followed by HE staining, immunohistochemistry, and TUNEL assays, to assess the anti-tumor activity of Salinomycin. HE staining shows that the structure of the liver cancer tissue:nuclei of different sizes, hepatic cord structure is destroyed. Immunohistochemistry shows that PCNA expression is lower after Salinomycin treatment. HE staining and TUNEL assays indicates the Salinomycin-treated groups has higher apoptosis rates than control. Furthermore, immunohistochemistry shows an increased Bax/Bcl-2 ratio after Salinomycin treatment. The protein expression of β-catenin decreases in the Salinomycin treatment groups compared with control[3]. Salinomycin is a kind of monocarboxylic acid polyether type antibiotics, produced by the fermentation of Streptomyces albus, possesses a specific cyclic structure, and can form a complex compound with the pathogenic microorganisms and the extracellular cations of coccidian, especially K+, Na+, Rb+, to alter the intracellular and extracellular ion concentrations[4]. References: | |||||
Salinomycin Dilution Calculator
Salinomycin Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 1.3316 mL | 6.6578 mL | 13.3156 mL | 26.6312 mL | 33.2889 mL |
| 5 mM | 0.2663 mL | 1.3316 mL | 2.6631 mL | 5.3262 mL | 6.6578 mL |
| 10 mM | 0.1332 mL | 0.6658 mL | 1.3316 mL | 2.6631 mL | 3.3289 mL |
| 50 mM | 0.0266 mL | 0.1332 mL | 0.2663 mL | 0.5326 mL | 0.6658 mL |
| 100 mM | 0.0133 mL | 0.0666 mL | 0.1332 mL | 0.2663 mL | 0.3329 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
Calcutta University
University of Minnesota
University of Maryland School of Medicine
University of Illinois at Chicago
The Ohio State University
University of Zurich
Harvard University
Colorado State University
Auburn University
Yale University
Worcester Polytechnic Institute
Washington State University
Stanford University
University of Leipzig
Universidade da Beira Interior
The Institute of Cancer Research
Heidelberg University
University of Amsterdam
University of Auckland
TsingHua University
The University of Michigan
Miami University
DRURY University
Jilin University
Fudan University
Wuhan University
Sun Yat-sen University
Universite de Paris
Deemed University
Auckland University
The University of Tokyo
Korea University
IC50: 7.7, 13.7 and 10.4 μM for HepG2, SMMC-7721 and BEL-7402 cell line, respectively (after 24h treatment)
Salinomycin (Sal), which is a polyether ionophore antibiotic from Streptomyces albus, has been proven to be able to kill different types of human cancer cells, most likely via interfering with ABC drug transporters, the Wnt/β-catenin signaling pathway, or other pathways.
In vitro: Several hepatocellular carcinoma (HCC) cell lines were treated with Sal. Results showed that Sal inhibited proliferation and decreased PCNA levels. Cell cycle analysis showed that Sal caused cell cycle arrest in different phases. Sal induced apoptosis as characterized by an increase in the Bax/Bcl-2 ratio. Compared to control, β-catenin expression was down-regulated by Sal treatment significantly. The Ca2+ concentration in HCC cells was examined by flow cytometry and it was found that higher Ca2+ concentrations were observed in Sal treatment groups [1].
In vivo: The in vivo anti-tumor effect of Sal was verified using the hepatoma orthotopic tumor model and results showed that the liver tumor size in Sal-treated groups decreased. Immunohistochemistry and TUNEL staining also demonstrated that Sal could in vivo inhibit proliferation and induced apoptosis [1].
Clinical trial: N/A
Reference:
[1] Wang F,He L,Dai WQ,Xu YP,Wu D,Lin CL,Wu SM,Cheng P,Zhang Y,Shen M,Wang CF,Lu J,Zhou YQ,Xu XF,Xu L,Guo CY. Salinomycin inhibits proliferation and induces apoptosis of human hepatocellular carcinoma cells in vitro and in vivo. PLoS One.2012;7(12):e50638.
- CDI (1,1′-Carbonyldiimidazole)
Catalog No.:BCC2809
CAS No.:530-62-1
- Sinapic acid
Catalog No.:BCN3539
CAS No.:530-59-6
- Syringic acid
Catalog No.:BCN5699
CAS No.:530-57-4
- 2,6-Dimethoxy-1,4-benzoquinone
Catalog No.:BCN5698
CAS No.:530-55-2
- Deoxyvasicinone
Catalog No.:BCN5697
CAS No.:530-53-0
- L-Picein
Catalog No.:BCC8336
CAS No.:530-14-3
- Indomethacin
Catalog No.:BCC3794
CAS No.:53-86-1
- Dehydroepiandrosterone
Catalog No.:BCN2202
CAS No.:53-43-0
- Oxandrolone
Catalog No.:BCC5242
CAS No.:53-39-4
- Methylprednisolone acetate
Catalog No.:BCC9043
CAS No.:53-36-1
- Cocaine hydrochloride
Catalog No.:BCC5943
CAS No.:53-21-4
- Mitotane (Lsodren)
Catalog No.:BCC3815
CAS No.:53-19-0
- Murralongin
Catalog No.:BCN5696
CAS No.:53011-72-6
- T-5224
Catalog No.:BCC5383
CAS No.:530141-72-1
- Scutebarbatine J
Catalog No.:BCN8134
CAS No.:960302-85-6
- Morellic acid
Catalog No.:BCN3073
CAS No.:5304-71-2
- 9,13-Epidioxy-8(14)-abieten-18-oic acid
Catalog No.:BCN1426
CAS No.:5309-35-3
- Dichotomin
Catalog No.:BCN2836
CAS No.:53093-47-3
- Androsin
Catalog No.:BCN3842
CAS No.:531-28-2
- Coniferin
Catalog No.:BCN5700
CAS No.:531-29-3
- Scopolin
Catalog No.:BCN5701
CAS No.:531-44-2
- 7-Methoxycoumarin
Catalog No.:BCN2707
CAS No.:531-59-9
- Esculin
Catalog No.:BCN5904
CAS No.:531-75-9
- Coumarin-3-Carboxylic Acid
Catalog No.:BCC9220
CAS No.:531-81-7
Salinomycin repressed the epithelial-mesenchymal transition of epithelial ovarian cancer cells via downregulating Wnt/beta-catenin pathway.[Pubmed:28280366]
Onco Targets Ther. 2017 Feb 28;10:1317-1325.
Epithelial ovarian cancer (EOC) is the leading cause of death among all gynecological malignancies. Most patients are diagnosed in the advanced stage and have distant metastasis ultimately. Salinomycin has been demonstrated to reduce invasive capacity of multiple tumor cells. The objective of this study was to investigate the effects of Salinomycin on EOC cells. The cell counting kit 8 (CCK-8) and Boyden chamber assays showed that Salinomycin could effectively reduce the abilities of proliferation, migration and invasion in EOC cells. The western blot assay showed that Salinomycin could increase the expression of epithelial markers (E-cadherin and Keratin) while decrease the expression of mesenchymal markers (N-cadherin and vimentin) in a dose-dependent manner. These results were ascertained by reverse transcription polymerase chain reaction (RT-PCR). Besides, Salinomycin could downregulate the expression of proteins associated with the Wnt/beta-catenin pathway and repress the nuclear translocation of beta-catenin. It was also shown that Salinomycin could reverse the aberrant activation of the canonical Wnt pathway induced by GSK-3beta inhibitor (SB216763). Our results revealed that Salinomycin could inhibit the proliferation, migration and invasion in EOC cells. In addition, the inhibitive effect of Salinomycin on the invasive ability was mediated by repressing the epithelial-mesenchymal transition (EMT) program, which may be achieved through its inhibition of the Wnt/beta-catenin pathway.
Salinomycin exhibits anti-angiogenic activity against human glioma in vitro and in vivo by suppressing the VEGF-VEGFR2-AKT/FAK signaling axis.[Pubmed:28358414]
Int J Mol Med. 2017 May;39(5):1255-1261.
Tumor angiogenesis plays a crucial role in tumor growth, progression and metastasis, and suppression of tumor angiogenesis has been considered as a promising anticancer strategy. Salinomycin (SAL), an antibiotic, displays novel anticancer potential against several human cancer cells in vitro and in vivo. However, little information concerning its anti-angiogenic properties is available. Therefore, the antiangiogenic effect of SAL and the underlying mechanism in human glioma were evaluated in the present study. The results indicated that SAL treatment significantly inhibited human umbilical vein endothelial cell (HUVEC) proliferation, migration, invasion and capillary-like tube formation. Further investigation on intracellular mechanisms showed that SAL markedly suppressed FAK and AKT phosphorylation, and downregulated vascular endothelial growth factor (VEGF) expression in HUVECs. Pretreatment of cells with a PI3K inhibitor (LY294002) and FAK inhibitor (PF562271) markedly enhanced SAL-induced inhibition of HUVEC proliferation and migration, respectively. Moreover, U251 human glioma xenograft growth was also effectively blocked by SAL treatment in vivo via inhibition of angiogenesis involving FAK and AKT depho-sphorylation. Taken together, our findings validated that SAL inhibits angiogenesis and human glioma growth through suppression of the VEGF-VEGFR2-AKT/FAK signaling axis, indicating the potential application of SAL for the treatment of human glioma.
Salinomycin: A new paradigm in cancer therapy.[Pubmed:28349817]
Tumour Biol. 2017 Mar;39(3):1010428317695035.
The primary hurdle in the treatment of cancer is acquisition of resistance by the tumor cells toward multiple drugs and selectively targeting the cancer stem cells. This problem was overcome by the chemotherapeutic property of recently discovered drug Salinomycin. Exact mechanism of action of Salinomycin is not yet known, but there are multiple pathways by which Salinomycin inhibits tumor growth. Salinomycin decreases the expression of adenosine triphosphate-binding cassette transporter in multidrug resistance cells and interferes with Akt signaling pathway, Wnt/beta-catenin, Hedgehog, and Notch pathways of cancer progression. Salinomycin selectively targets cancer stem cells. The potential of Salinomycin to eliminate both cancer stem cells and therapy-resistant cancer cells may characterize the compound as a novel and an efficient chemotherapeutic drug.
Evaluation of growth inhibitory response of Resveratrol and Salinomycin combinations against triple negative breast cancer cells.[Pubmed:28298074]
Biomed Pharmacother. 2017 May;89:1142-1151.
Resveratrol (RSVL) a dietary phytochemical showed to enhance the efficacy of chemotherapeutic drugs. Recently, Salinomycin (SAL) has gained importance as cancer therapeutic value for breast cancer (BC), however, its superfluxious toxicity delimits the utility. Taking the advantage of RSVL, the therapeutic efficacy of RSVL and SAL combination was studied in vitro and in vivo system. Firstly, the synergistic combination dose of RSVL and SAL was calculated and further, the efficacy was examined by wound healing, and Western blots analysis. Further, in vivo study was performed to confirm the effect of colony formation and apoptosis detection by flow cytometry based assays. Further, the molecular mode of action was determined at both transcript and translational level by quantitative Real Time PCR combination in Ehrlich ascitic carcinoma model.The combination of IC20 (R20) of RSVL and IC10 (S10) dose of SAL showed best synergism (CI<1) with approximately 5 fold dose advantage of SAL. Gene expression results at mRNA and protein level revealed that the unique combination of RSVL and SAL significantly inhibited epithelial mesenchymal transition (Fibronectin, Vimentin, N-Cadherin, and Slug); chronic inflammation (Cox2, NF-kB, p53), autophagy (Beclin and LC3) and apoptotic (Bax, Bcl-2) markers. Further, i n vivo study showed that low dose of SAL in combination with RSVL increased life span of Ehrlich ascitic mice. Overall, our study revealed that RSVL synergistically potentiated the anticancer potential of SAL against triple negative BC.
