Ferroptosis inducer-16
Ferroptosis inducer-16 (anti-NSCLC agent-2) is a nitric oxide (NO) donor and a ferroptosis inducer. Ferroptosis inducer-16 inhibits DNA synthesis and colony formation. Ferroptosis inducer-16 disrupts lysosomal integrity by releasing NO, triggers iron overload and oxidative stress, downregulates the SLC7A11-GPX4 axis, depletes GSH, and accumulates lipid peroxides. Ferroptosis inducer-16 inhibits tumor growth in an OVCAR8/ADR xenograft mouse model without obvious toxicity, and can be used in the study of non-small cell lung cancer and drug-resistant ovarian cancer[1,2].
For research use only. We do not sell to patients.
- CAS No.: 3063042-21-4
- Formula: C27H20Cl2N2O8S
- Molecular Weight:603.43
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Biological Activity
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GPX4 |
Cathepsin B |
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| OVCAR-8 | IC50 |
910.10 nM
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Exerts cytotoxic effects on OVCAR8 cells for 24 h.
Exerts cytotoxic effects on OVCAR8 cells for 24 h.
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42312163 |
| OVCAR8/ADR | IC50 |
4.32 nM
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Exerts dose-dependent cytotoxic effects on OVCAR8/ADR cells for 24 h.
Exerts dose-dependent cytotoxic effects on OVCAR8/ADR cells for 24 h.
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42312163 |
Ferroptosis inducer-16 (compound 6o) (10-160 nM; 48 h) effectively inhibits the proliferation of non-small cell lung cancer (NSCLC) cell lines A549, H1299, H2030, H1975, A549/T, and A549/CDDP, with IC50 values ranging from 1.54 nM to 11.72 nM, and exhibits no obvious toxicity against normal human umbilical vein endothelial cells (HUVEC) at effective inhibitory concentrations[1].
Ferroptosis inducer-16 (3A72) (24 h) exerts dose-dependent cytotoxic effects against OVCAR8/ADR cells, with an IC50 of 4.32 nM, which is significantly lower than that of the parental OVCAR8 cells (IC50 = 910.10 nM)[2].
Ferroptosis inducer-16 (5-20 nM; 24 h) inhibits colony formation and DNA synthesis (EdU assay) in OVCAR8/ADR cells[2].
Ferroptosis inducer-16 (100 μM; 2.5 h) releases 10.02 μM of nitric oxide (NO) in A549 cells[1].
The anti-proliferative activity of Ferroptosis inducer-16 (10-50 nM; 4-48 h) against A549, A549/CDDP, and OVCAR8/ADR cells is dependent on NO, as hemoglobin reverses this effect in a concentration-dependent manner; meanwhile, it increases total NO and lysosome-specific NO levels in OVCAR8/ADR cells in a dose-dependent manner, but exerts no significant effect on mitochondrial NO levels. The NO scavenger Carboxy-PTIO (HY-18734) (100 μM) and the P-gp inhibitor Tariquidar (HY-10550) partially reverse its cytotoxicity[1][2].
Ferroptosis inducer-16 (20-100 nM; 24-48 h) exerts anti-proliferative activity against A549, A549/CDDP, and OVCAR8/ADR cells in a ferroptosis-dependent manner. In OVCAR8/ADR cells, this effect is completely reversed by the iron chelator Deferoxamine (HY-B1625) (40 μM) or Ferrostatin-1 (HY-100579) (250 nM)[1][2].
Ferroptosis inducer-16 (15-60 nM; 12 h) downregulates SLC7A11 and GPX4 protein expression in A549 and A549/CDDP cells in a dose-dependent manner[1].
Ferroptosis inducer-16 (20 nM) downregulates SLC7A11 and GPX4 protein expression in OVCAR8/ADR cells, while also downregulating NCOA4, SLC40A1, and FTH expression. These effects are reversed by Carboxy-PTIO (100 μM), Deferoxamine (40 μM), Ferrostatin-1 (250 nM), and N-acetylcysteine (HY-B0215) (2 mM)[2].
Ferroptosis inducer-16 (10-20 nM) upregulates NCOA4 expression and downregulates ferritin heavy chain (FTH) and SLC40A1 protein expression in OVCAR8/ADR cells[2].
Ferroptosis inducer-16 (20 nM; 6 h) decreases calcein-AM fluorescence intensity in OVCAR8/ADR cells, indicating an elevation of the labile iron pool (LIP)[2].
Ferroptosis inducer-16 (10-80 nM) increases total ROS levels in A549, A549/CDDP, and OVCAR8/ADR cells in a dose- and time-dependent manner; additionally, in A549 and A549/CDDP cells, it is accompanied by elevated mitochondrial NO levels. The proliferative inhibition of this compound against OVCAR8/ADR cells (20 nM; 24 h) is completely reversed by the ROS scavenger Acetylcysteine (HY-B0215) (2 mM)[1][2].
Ferroptosis inducer-16 (10-80 nM; 12 h) depletes intracellular GSH and reduces the GSH/GSSG ratio in A549, A549/CDDP, and OVCAR8/ADR cells in a dose-dependent manner, disrupting redox homeostasis; meanwhile, it increases MDA levels in OVCAR8/ADR cells, indicating enhanced lipid peroxidation[1][2].
Ferroptosis inducer-16 (10-80 nM; 4-6 h) induces mitochondrial membrane potential (MMP) collapse and elevates mitochondrial ROS (superoxide) levels in A549, A549/CDDP, and OVCAR8/ADR cells in a dose-dependent manner, triggering lipid peroxidation and increasing ferrous iron accumulation[1][2].
Ferroptosis inducer-16 (10-20 nM; 6 h) disrupts lysosomal integrity in OVCAR8/ADR cells (as evidenced by decreased lysotracker red fluorescence intensity), triggers lysosomal membrane permeabilization (LMP), and concomitantly elevates cytosolic cathepsin B levels[2].
Ferroptosis inducer-16 (10-80 nM; 4-6 h) triggers lipid peroxidation in A549, A549/CDDP, and OVCAR8/ADR cells, as evidenced by enhanced BODIPY 581/591 C11 oxidation fluorescence[1][2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:OVCAR8/ADR cells
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Concentration:5, 10, 20 nM
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Incubation Time:24 h
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Result:Dose-dependently suppressed the clonogenic ability and DNA synthesis (as determined by EdU assay) of OVCAR8/ADR cells.
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Cell Line:A549, A549/CDDP
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Concentration:100 nM (compound 6o); 0, 75, 150, 300 nM (Ferrostatin-1)
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Incubation Time:48 h
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Result:Decreased in proliferation inhibition rate with increasing Ferrostatin-1 (HY-100579) concentration in a concentration-dependent manner.
Lost almost all inhibitory activity at 300 nM Ferrostatin-1, with cell viability >95%.
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Cell Line:A549, A549/CDDP
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Concentration:15, 30 nM (A549); 30, 60 nM (A549/CDDP); 300 nM (Fer-1 for reversal)
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Incubation Time:12 h (compound 6o treatment)
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Result:Dose-dependently downregulated the expression of SLC7A11 and GPX4 in both cell lines.
Fully reversed this downregulation in the presence of 300 nM Fer-1.
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Cell Line:A549, A549/CDDP
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Concentration:15, 30 nM (A549); 30, 60 nM (A549/CDDP); 300 nM (Fer-1 for reversal)
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Incubation Time:12 h (compound 6o treatment)
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Result:Dose-dependently downregulated the expression of SLC7A11 and GPX4 in both cell lines.
Fully reversed this downregulation in the presence of 300 nM Fer-1.
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Cell Line:OVCAR8/ADR cells
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Concentration:The test compound ( 20 nM) combined with Carboxy-PTIO (HY-18734) (100 μM)
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Incubation Time:24 h
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Result:Partially reversed the cytotoxic effect, restoring cell viability to 60%.
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Cell Line:OVCAR8/ADR cells
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Concentration:This compound (20 nM) combined with Ferrostatin-1 (HY-100579) (250 nM), this compound (20 nM) combined with Deferoxamine mesylate (HY-B0988) (40 μM), this compound (20 nM) combined with N-acetylcysteine (HY-B0215) (2 mM); 24 h.
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Incubation Time:24 h
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Result:The compound-induced cytotoxicity was completely reversed by Fer-1, confirming that lipid peroxidation plays a dominant role in ferroptosis; reversed by DFM, confirming that iron overload drives ferroptosis; and fully reversed by NAC, restoring cell viability to 100% and underscoring the pivotal role of ROS in cell death.
Ferroptosis inducer-16 (3A72) (5 mg/kg and 10 mg/kg; i.p.; once every 2 days) suppresses tumor growth in a subcutaneous xenograft mouse model bearing OVCAR8/ADR cells by inducing ferroptosis, exerting a potent antitumor effect comparable to that of Cisplatin, without causing significant body weight loss. Histopathological analysis of major organs shows no abnormalities, demonstrating a favorable biosafety profile[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Nude mice (female, SPF-grade, cisplatin-resistant NSCLC xenograft model)[1]
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Dosage:5 mg/kg; 10 mg/kg
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Administration:i.v. (tail vein); once every 2 days; 20 days
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Result:Significantly reduced tumor volume compared to vehicle control at 5 mg/kg.
Reduced final tumor weight compared to both vehicle control and 10 mg/kg cisplatin group at 5 mg/kg.
Achieved the greatest tumor volume reduction among all treatment groups at 10 mg/kg.
Reduced final tumor weight significantly lower than vehicle control and 10 mg/kg cisplatin group at 10 mg/kg.
Showed no significant body weight loss or behavioral abnormalities in either dose group.
Caused no treatment-related histopathological damage to heart, liver, spleen, lung, and kidney as observed via H&E staining.
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Animal Model:Female BALB/c nude mice (5-week-old) were subcutaneously injected with OVCAR8/ADR cells (1 × 107ells per mouse) suspended in a 1:1 mixture of PBS and Matrigel into the flanks. When tumor volume exceeded 250 mm3 tumors were harvested, fragmented, and serially transplanted into the flanks of BALB/c nude mice (P2 generation)[2]
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Dosage:5 mg/kg; 10 mg/kg
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Administration:Intraperitoneal injection (i.p.); once every 2 days (starting when P2 mice were randomly divided into five groups after tumor transplantation)
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Result:Dose-dependently suppressed tumor growth in the OVCAR8/ADR xenograft mouse model, as evidenced by reduced tumor volume and tumor weight, with comparable antitumor efficacy to cisplatin (CDDP) administered twice a week.
Did not significantly affect mouse body weight, whereas cisplatin caused marked weight loss.
H&E staining of major organs (heart, liver, spleen, lungs, and kidneys) from the experimental group mice showed no abnormalities, indicating favorable biosafety.
Western blotting analysis of tumor tissues revealed upregulated NCOA4 and downregulated SLC7A11, GPX4, SLC40A1, and FTH, supporting the conclusion that the comp.
Chemical Information
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CAS No. 3063042-21-4
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Molecular Weight 603.43
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Formula C27H20Cl2N2O8S
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SMILES
O=S(C1=[N+]([O-])ON=C1OCCOC2=CC(O3)=C(C=C2)C(C)=C(CC4=CC(Cl)=CC(Cl)=C4)C3=O)(C5=CC=CC=C5)=O
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Synonyms
anti-NSCLC agent-2
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
[1]. Wang W, et al. Novel Hybrids of 3-Substituted Coumarin and Phenylsulfonylfuroxan as Potent Antitumor Agents against Wild-Type and Drug-Resistant Nonsmall Cell Lung Cancer Cell Lines. J Med Chem. 2026;69(6):7238-7261. [Content Brief]
[2]. Weng J, et al. A Novel Nitric Oxide Donor Induced Ferroptosis in Drug-Resistant Ovarian Cancer Cells through Lysosomal Iron Metabolism Regulation and Lipid Peroxidation. ACS Pharmacol Transl Sci. 2026 Jun 3;9(6):1519-1530. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Ferroptosis inducer-16 Related Classifications
Cat. No.: HY-182052
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- Ferroptosis inducer-16
- 3063042-21-4
- anti-NSCLC agent-2
- Ferroptosis inducer16
- Ferroptosis inducer 16
- Glutathione Peroxidase
- Reactive Oxygen Species (ROS)
- NO Synthase
- Ferroptosis
- Apoptosis
- APC
- Ferroportin
- Cathepsin
- Ferroptosis、Apoptosis、SLC7A11、GPX4、NCOA4、FTH、SLC40A1、P-glycoprotein、Cathepsin B、hERG channel、ROS、GSH、Lipid peroxidation、MDA、NO donor、A549、H1299、H2030、H1975、HUVECs、OVCAR8、OVCAR8/ADR、Non-small cell lung cancer、Ovarian cancer、Drug-resistant ovarian cancer
- Inhibitor
- inhibitor
- inhibit