1. Coxistac
2. K 364
3. Salinomycin Monosodium Salt
1. Procoxacin
2. 53003-10-4
3. Coxistac
4. Bio-cox
5. Chebi:80025
6. 62uxs86t64
7. Salinomycin (inn)
8. Salinomycin [inn]
9. Salinomicina
10. Salinomycine
11. Salinomycinum
12. Salinomycin [inn:ban]
13. Salinomycine [inn-french]
14. Salinomycinum [inn-latin]
15. Salinomycin (procoxacin)
16. Salinomicina [inn-spanish]
17. Unii-62uxs86t64
18. K 364
19. Hsdb 7032
20. Procoxacin (tn)
21. Ahr 3096
22. Einecs 258-290-1
23. Salinomycin [mi]
24. Salinomycin [jan]
25. Salinomycin [hsdb]
26. Schembl36890
27. Chembl1208572
28. Dtxsid4048486
29. Gtpl11088
30. Nsc757437
31. S2352
32. S8129
33. Zinc85540254
34. Salinomycin (from Streptomyces Albus)
35. Ccg-208535
36. Cs-1299
37. Db11544
38. Nsc-757437
39. (2r)-2-[(2r,5s,6r)-6-[(2s,3s,4s,6r)-6-[(2s,5s,7r,9s,10s,12r,15r)-2-[(2r,5r,6s)-5-ethyl-5-hydroxy-6-methyloxan-2-yl]-15-hydroxy-2,10,12-trimethyl-1,6,8-trioxadispiro[4.1.5?.3?]pentadec-13-en-9-yl]-3-hydroxy-4-methyl-5-oxooctan-2-yl]-5-methyloxan-2-yl]butanoic Acid
40. Bs-17023
41. E716
42. Hy-15597
43. D08502
44. A829344
45. Q411909
46. J-524236
47. Sr-05000002207-3
48. Salinomycin, From Streptomyces Albus, >=98% (hplc)
49. Salinomycin, Ready Made Solution, From Streptomyces Albus, >=98% (hplc)
50. (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
51. (r)-2-((2r,5s,6r)-6-((2s,3s,4s,6r)-6-((2s,5s,7r,9s,10s,12r,15r)-2-((2r,5r,6s)-5-ethyl-5-hydroxy-6-methyltetrahydro-2h-pyran-2-yl)-15-hydroxy-2,10,12-trimethyl-1,6,8-trioxadispiro[4.1.57.35]pentadec-13-en-9-yl)-3-hydroxy-4-methyl-5-oxooctan-2-yl)-5-methyltetrahydro-2h-pyran-2-yl)butanoic Acid
52. (r)-2-((2r,5s,6r)-6-((2s,3s,4s,6r)-6-((2s,5s,7r,9s,10s,12r,15r)-2-((2r,5r,6s)-5-ethyl-5-hydroxy-6-methyltetrahydro-2h-pyran-2-yl)-15-hydroxy-2,10,12-trimethyl-1,6,8-trioxadispiro[4.1.57.35]pentadec-13-en-9-yl)-3-hydroxy-4-methyl-5-oxooctan-2-yl)-5-methyltetrahydro-2h-pyran-2-yl)butanoicacid
53. Sodium 2-[6-[5-[3-(5-ethyl-5-hydroxy-6-methyl-tetrahydropyran-2-yl)-15-hydroxy-3,10,12-trimethyl-4,6,8-trioxadispiro[4.1.5^{7}.3^{5}]pentadec-13-en-9-yl]-2-hydroxy-1,3-dimethyl-4-oxo-heptyl]-5-methyl-tetrahydropyran-2-yl]butanoate
| Molecular Weight | 751.0 g/mol |
|---|---|
| Molecular Formula | C42H70O11 |
| XLogP3 | 5.7 |
| Hydrogen Bond Donor Count | 4 |
| Hydrogen Bond Acceptor Count | 11 |
| Rotatable Bond Count | 12 |
| Exact Mass | 750.49181304 g/mol |
| Monoisotopic Mass | 750.49181304 g/mol |
| Topological Polar Surface Area | 161 Ų |
| Heavy Atom Count | 53 |
| Formal Charge | 0 |
| Complexity | 1320 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 18 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
Anti-Bacterial Agents; Coccidiostats
National Library of Medicine's Medical Subject Headings. Salinomycin. Online file (MeSH, 2015). Available from, as of August 20, 2015: https://www.nlm.nih.gov/mesh/2014/mesh_browser/MBrowser.html
EXPL: The drug target profile proposed by the Medicines for Malaria Venture for a malaria elimination/eradication policy focuses on molecules active on both asexual and sexual stages of Plasmodium, thus with both curative and transmission-blocking activities. The aim of the present work was to investigate whether the class of monovalent ionophores, which includes drugs used in veterinary medicine and that were recently proposed as human anticancer agents, meets these requirements. The activity of salinomycin, monensin, and nigericin on Plasmodium falciparum asexual and sexual erythrocytic stages and on the development of the Plasmodium berghei and P. falciparum mosquito stages is reported here. Gametocytogenesis of the P. falciparum strain 3D7 was induced in vitro, and gametocytes at stage II and III or stage IV and V of development were treated for different lengths of time with the ionophores and their viability measured with the parasite lactate dehydrogenase (pLDH) assay. The monovalent ionophores efficiently killed both asexual parasites and gametocytes with a nanomolar 50% inhibitory concentration (IC50). Salinomycin showed a fast speed of kill compared to that of standard drugs, and the potency was higher on stage IV and V than on stage II and III gametocytes. The ionophores inhibited ookinete development and subsequent oocyst formation in the mosquito midgut, confirming their transmission-blocking activity. Potential toxicity due to hemolysis was excluded, since only infected and not normal erythrocytes were damaged by ionophores. Our data strongly support the downstream exploration of monovalent ionophores for repositioning as new antimalarial and transmission-blocking leads.
PMID:26055362 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4538477 D'Alessandro S et al; Antimicrob Agents Chemother 59 (9): 5135-44 (2015)
EXPL: Salinomycin has been introduced as a novel alternative to traditional anti-cancer drugs. The aim of this study was to test a strategy designed to deliver salinomycin to glioblastoma cells in vitro. Salinomycin-encapsulated polysorbate 80-coated poly(lactic-co-glycolic acid) nanoparticles (P80-SAL-PLGA) were prepared and characterized with respect to particle size, morphology, thermal properties, drug encapsulation efficiency and controlled salinomycin-release behaviour. The in vitro cellular uptake of P80-SAL-PLGA (5 and 10 uM) or uncoated nanoparticles was assessed in T98G human glioblastoma cells, and the cell viability was investigated with respect to anti-growth activities. SAL, which was successfully transported to T98G glioblastoma cells via P80 coated nanoparticles (~14% within 60 min), greatly decreased (p < 0.01) the cellular viability of T98G cells. Substantial morphological changes were observed in the T98G cells with damaged actin cytoskeleton. Thus, P80-SAL-PLGA nanoparticles induced cell death, suggesting a potential therapeutic role for this salinomycin delivery system in the treatment of human glioblastoma.
PMID:26476239 Tigli Aydin RS et al; J Biomed Mater Res A. 2015 Oct 17. doi: 10.1002/jbm.a.35591. (Epub ahead of print)
MEDICATION (VET): Use Sacox 60 ... for the prevention of coccidiosis in quail caused by Eimeria dispersa and E. lettyae.
NIH; DailyMed. Current Medication Information for Cacox 60 (Salinomycin) Powder (Updated: June 2012). Available from, as of October 29, 2015: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=124e6803-6f35-42dd-98b3-75e956f5be2a
MEDICATION (VET): Use Sacox 60 ... for the prevention of coccidiosis in broiler, roaster and replacement chickens caused by Eimeria tenella, E. necatrix, E. acervulina, E. maxima, E. brunetti and E. mivati.
NIH; DailyMed. Current Medication Information for Cacox 60 (Salinomycin) Powder (Updated: June 2012). Available from, as of October 29, 2015: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=124e6803-6f35-42dd-98b3-75e956f5be2a
Do not feed to laying hens producing eggs for human consumption.
NIH; DailyMed. Current Medication Information for Cacox 60 (Salinomycin) Powder (Updated: June 2012). Available from, as of October 29, 2015: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=124e6803-6f35-42dd-98b3-75e956f5be2a
May be fatal if accidentally fed to adult turkeys or to horses.
NIH; DailyMed. Current Medication Information for Cacox 60 (Salinomycin) Powder (Updated: June 2012). Available from, as of October 29, 2015: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=124e6803-6f35-42dd-98b3-75e956f5be2a
Anti-Bacterial Agents
Substances that inhibit the growth or reproduction of BACTERIA. (See all compounds classified as Anti-Bacterial Agents.)
Coccidiostats
Agents useful in the treatment or prevention of COCCIDIOSIS in man or animals. (See all compounds classified as Coccidiostats.)
Salinomycin was administered to chickens orally and intravenously to determine blood concentration, kinetic behavior, bioavailability and tissue residues. The drug was given by intracrop and intravenous routes in a single dose of 20 mg kg-1 body-weight. The highest serum concentrations of salinomycin were reached half an hour after oral dosage with an absorption half-life (t0.5(ab)) of 3.64 hours and elimination half-life (t0.5(beta)) of 1.96 hours. The systemic bioavailability percentage was 73.02 per cent after intracrop administration, indicating the high extent of salinomycin absorption from this route in chickens. Following intravenous injection the kinetics of salinomycin can be described by a two-compartment open model with a t1/2(alpha) of 0.48 hours, Vd ss (volume of distribution) of 3.28 litre kg-1 and Cl(beta) (total body clearance) of 27.39 ml kg-1 min-1. The serum protein-binding tendency of salinomycin as calculated in vitro was 19.78 per cent. Salinomycin concentrations in the serum and tissues of birds administered salinomycin premix (60 ppm) for two weeks were lower than those after administration of a single intracrop dose of pure salinomycin (20 mg kg-1 bodyweight). The highest concentration of salinomycin residues were present in the liver followed by the kidneys, muscles, fat, heart and skin. No salinomycin residues were detected in tissues after 48 hours except in the liver and these had disappeared completely by 72 hours.
PMID:8460256 Atef M et al; Res Vet Sci 54 (2): 179-83 (1993)
... Salinomycin (SAL), a broad spectrum antibiotic and a coccidiostat has been found to counter tumour resistance and kill cancer stem cells with better efficacy than the existing chemotherapeutic agents; paclitaxel and doxorubicin. This refocused its importance for treatment of human cancers. In this study, we studied the in vitro drug metabolism and pharmacokinetic parameters of SAL. SAL undergoes rapid metabolism in liver microsomes and has a high intrinsic clearance. SAL metabolism is mainly mediated by CYP enzymes; CYP3A4 the major enzyme metabolising SAL. The percent plasma protein binding of SAL in human was significantly lower as compared to mouse and rat plasma. CYP inhibition was carried out by chemical inhibition and recombinant enzyme studies. SAL was found to be a moderate inhibitor of CYP2D6 as well as CYP3A4. As CYP3A4 was the major enzyme responsible for metabolism of SAL, in vivo pharmacokinetic study in rats was done to check the effect of concomitant administration of Ketoconazole (KTC) on SAL pharmacokinetics. KTC, being a selective CYP3A4 inhibitor increased the systemic exposure of SAL significantly to 7-fold in AUC0-a and 3-fold increase in Cmax of SAL in rats with concomitant KTC administration.
PMID:26282489 Resham K et al; Chem Biol Interact 240: 146-152 (2015)
... The drug was given by intracrop and intravenous routes in a single dose of 20 mg kg-1 body-weight. The highest serum concentrations of salinomycin were reached half an hour after oral dosage with an absorption half-life (t0.5(ab)) of 3.64 hours and elimination half-life (t0.5(beta)) of 1.96 hours. ...
PMID:8460256 Atef M et al; Res Vet Sci 54 (2): 179-83 (1993)
Cancer stem cells (CSCs) play important roles in the formation, growth and recurrence of tumors, particularly following therapeutic intervention. Salinomycin has received recent attention for its ability to target breast cancer stem cells (BCSCs), but the mechanisms of action involved are not fully understood. In the present study, we sought to investigate the mechanisms responsible for salinomycin's selective targeting of BCSCs and its anti-tumor activity. Salinomycin suppressed cell viability, concomitant with the downregulation of cyclin D1 and increased p27(kip1) nuclear accumulation. Mammosphere formation assays revealed that salinomycin suppresses self-renewal of ALDH1-positive BCSCs and downregulates the transcription factors Nanog, Oct4 and Sox2. TUNEL analysis of MDA-MB-231-derived xenografts revealed that salinomycin administration elicited a significant reduction in tumor growth with a marked downregulation of ALDH1 and CD44 levels, but seemingly without the induction of apoptosis. Our findings shed further light on the mechanisms responsible for salinomycin's effects on BCSCs.
PMID:26407842 An H et al; Biochem Biophys Res Commun 466 (4): 696-703 (2015)
Salinomycin, an antibiotic potassium ionophore, has been reported recently to act as a selective breast cancer stem cell inhibitor, but the biochemical basis for its anticancer effects is not clear. The Wnt/beta-catenin signal transduction pathway plays a central role in stem cell development, and its aberrant activation can cause cancer. In this study, we identified salinomycin as a potent inhibitor of the Wnt signaling cascade. In Wnt-transfected HEK293 cells, salinomycin blocked the phosphorylation of the Wnt coreceptor lipoprotein receptor related protein 6 (LRP6) and induced its degradation. Nigericin, another potassium ionophore with activity against cancer stem cells, exerted similar effects. In otherwise unmanipulated chronic lymphocytic leukemia cells with constitutive Wnt activation nanomolar concentrations of salinomycin down-regulated the expression of Wnt target genes such as LEF1, cyclin D1, and fibronectin, depressed LRP6 levels, and limited cell survival. Normal human peripheral blood lymphocytes resisted salinomycin toxicity. These results indicate that ionic changes induced by salinomycin and related drugs inhibit proximal Wnt signaling by interfering with LPR6 phosphorylation, and thus impair the survival of cells that depend on Wnt signaling at the plasma membrane.
PMID:21788521 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3156152 Lu D et al; Proc Natl Acad Sci U S A 108 (32): 13253-7 (2011)
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