CAS 53003-10-4 Salinomycin - Analytical Products / Alfa Chemistry

CAT	APS53003104
CAS	53003-10-4
Synonyms	1,6,8-Trioxadispiro[4.1.5.3]pentadecane, salinomycin deriv., Stereoisomer of α-ethyl-6-[5-[2-(5-ethyltetrahydro-5-hydroxy-6-methyl-2H-pyran-2-yl)-15-hydroxy-2,10,12-trimethyl-1,6,8-trioxadispiro[4.1.5.3]pentadec-13-en-9-yl]-2-hydroxy-1,3-dimethyl-4-oxoheptyl]tetrahydro-5-methyl-2H-pyran-2-acetic acid, Salinomycin, Coxistac, Antibiotic 61477
IUPAC 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[4.1.5^{7}.3^{5}]pentadec-13-en-9-yl]-3-hydroxy-4-methyl-5-oxooctan-2-yl]-5-methyloxan-2-yl]butanoic acid
Molecular Weight	751.00
Molecular Formula	C42H70O11
EC Number	258-290-1
Canonical SMILES	CC[C@H]([C@H]1CC[C@H](C)[C@@H](O1)[C@@H](C)[C@H](O)[C@H](C)C(=O)[C@H](CC)[C@H]2O[C@@]3(O[C@@]4(CC[C@](C)(O4)[C@H]5CC[C@](O)(CC)[C@H](C)O5)[C@H](O)C=C3)[C@H](C)C[C@@H]2C)C(=O)O
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
InChI Key	KQXDHUJYNAXLNZ-XQSDOZFQSA-N

Description	from Streptomyces albus, ≥98% (HPLC)
Accurate Mass	750.4918
Assay	≥98% (HPLC)
Format	Neat
MP	112.5-113.5 °C (lit.)
Size	5MG, 25MG, 50MG
Storage Conditions	2-8°C

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Case Study

Salinomycin for the Preparation of MnFe₂O₄-Based Nanoparticles to Enhance Ferroptosis-Mediated Cancer Therapy

Liu, MengXiao, et al. Colloids and Surfaces B: Biointerfaces 245 (2025): 114352.

Salinomycin has emerged as a valuable adjuvant in nanotherapeutics for ferroptosis-based cancer treatment. In this study, Salinomycin was employed in the preparation of multifunctional MnFe₂O₄@BSA nanoparticles to enhance intracellular iron accumulation and potentiate reactive oxygen species (ROS) generation in tumor cells. These hybrid nanoparticles (MnFe₂O₄/ART/Sali NPs) co-deliver Salinomycin and Artemisinin, both of which modulate iron metabolism and promote ferroptotic cell death.
To prepare the formulation, 1.25 mL Salinomycin solution (dissolved in DMSO at concentrations ranging from 1.6 to 4.0 mg/mL) was added dropwise into 2.5 mL of MnFe₂O₄@BSA nanoparticle suspension (25 mg/mL) under ultrasonic agitation. The system was stirred at 37 °C overnight to allow efficient drug loading. The resulting Salinomycin-loaded nanocomposite was recovered by high-speed centrifugation at 21,000 g for 30 minutes. Unencapsulated Salinomycin in the supernatant was quantified using UV-Vis spectrophotometry at 288 nm to assess loading efficiency.
Functionally, Salinomycin contributed to increased intracellular iron by facilitating ferritin degradation and upregulation of transferrin receptor expression via IRP2 activation. When administered intravenously, the MnFe₂O₄/ART/Sali nanocomposite achieved a tumor inhibition rate of 67.65%, confirming its synergistic efficacy in inducing ferroptosis.
This study highlights the role of Salinomycin as a key component in the preparation of ferroptosis-amplifying nanomedicines for advanced cancer therapy.

Salinomycin for the Investigation of Autophagy-Mediated Apoptosis Regulation in Prostate Cancer Cells

Zhang, Yunsheng, et al. Life Sciences 207 (2018): 451-460.

Salinomycin has demonstrated promising anticancer properties through its ability to modulate autophagy and apoptosis in prostate cancer PC-3 cells. This study investigated the dual role of Salinomycin in inducing both apoptosis and autophagy, revealing that Salinomycin-induced autophagy may paradoxically inhibit apoptosis via the ATG3/AKT/mTOR signaling axis.
To assess the pro-apoptotic effects of Salinomycin, PC-3 cells were treated and subsequently analyzed using Annexin V-FITC/PI flow cytometry, JC-1 mitochondrial membrane potential staining, and western blotting of apoptotic markers. JC-1 fluorescence shift from orange-red to green confirmed mitochondrial dysfunction, while Salinomycin treatment led to the cleavage of caspase-3 and PARP, and an increase in cytochrome C release, confirming activation of the intrinsic apoptotic pathway.
Autophagic activity was evaluated using western blot detection of LC3-II, immunofluorescence for GFP-LC3 puncta, and electron microscopy to visualize autophagosomes. To dissect the regulatory mechanism, shRNA-mediated knockdown of ATG3, ATG5, and ATG7 was employed. Remarkably, suppression of autophagy enhanced Salinomycin-induced apoptosis, suggesting an autophagy-protective effect against cell death.
Further mechanistic studies indicated that Salinomycin downregulated ATG3 and altered the AKT/mTOR pathway, suppressing apoptotic progression. These findings suggest that Salinomycin-induced autophagy acts as a survival mechanism in PC-3 cells, offering insights into potential therapeutic strategies that combine autophagy inhibition with Salinomycin to enhance anticancer efficacy.

Salinomycin for the Inhibition of Renal Cell Carcinoma Cell Proliferation and Colony Formation

Liu, Lei, et al. Chemico-Biological Interactions 296 (2018): 145-153.

Salinomycin, a monocarboxylic polyether antibiotic, has attracted significant attention for its broad-spectrum anticancer properties. This study explored the inhibitory effects of Salinomycin on metastatic renal cell carcinoma (RCC), a malignancy known for poor prognosis and limited treatment responsiveness. Specifically, the RCC cell lines ACHN and 786-O were employed to evaluate Salinomycin's impact on cellular proliferation and viability.
Cells were treated with Salinomycin at varying concentrations for 24 and 48 hours. Cell viability assays revealed that Salinomycin suppressed proliferation in both ACHN and 786-O cell lines in a dose- and time-dependent manner. Notably, the compound demonstrated greater cytotoxicity at higher concentrations and longer exposure durations, underscoring its potential for sustained therapeutic action.
Colony formation assays further confirmed the anti-proliferative activity of Salinomycin. A significant reduction in colony-forming ability was observed across both RCC cell lines following Salinomycin treatment, indicating impaired long-term proliferative capacity.
These findings suggest that Salinomycin effectively inhibits RCC cell growth and colony formation in vitro, highlighting its promise as a chemotherapeutic candidate for metastatic renal cell carcinoma. Continued mechanistic investigations and in vivo studies are warranted to fully elucidate the pathways involved and to support the clinical translation of Salinomycin in RCC therapy.