FIN56 NEW
| Price | $35 | $57 | $91 |
| Package | 2mg | 5mg | 10mg |
| Supply Ability: | 10g |
| Update Time: | 2026-07-16 |
Product Details
| Product Name: FIN56 | CAS No.: 1083162-61-1 |
| Purity: 99.72% | Supply Ability: 10g |
| Release date: 2026/07/16 |
Product Introduction
Bioactivity
| Name | FIN56 |
| Description | FIN56 is an iron death-specific inducer that binds to and activates squalene synthase, inducing ferroptosis by triggering GPX4 degradation. FIN56 can be used in studies of ferroptosis regulatory mechanisms, autophagy-ferroptosis crosstalk, and tumor therapy. |
| Cell Research | 1000 cells/36 μL are seeded in each well in 384-well plates. Lethal compounds are dissolved and a 2-fold, 12-point dilution series are prepared in DMSO. Compound solutions are further diluted with media at 1:25 and 4 μL/well of the diluted solutions are added to cell cultures immediately after cells are seeded. When ferroptosis inhibitors (100 μM α-tocopherol, 152 μM deferoxamine, or 10 μM U-0126) are co-treated with lethal inducers, they are supplemented to cell culture at the same time as lethal compounds are added, and the cells are incubated for 24 hrs. When other cell death modulating compounds (100 nM sodium selenite, 1 μM cerivastatin, 100 μg/mL mevalonic acid) are co-treated, they are first supplemented to cell culture for 24 hrs before lethal compounds are added to cell culture and further incubated for 24 hrs at 37°C under 5% CO2. On the day of the viability measurement, 10 μL/well of 50% Alamar Blue diluted in media is added and further incubated at 37°C for 6 hrs. Fluorescence intensity (ex/em: 530/590) is measured with a Victor 3 plate reader and the normalized viability is calculated by VL = (IL-I0)/(IV-I0), where VL, I0, IV, and IL are the normalized viability, raw fluorescence intensities from the wells containing media, cells treated with a vehicle (negative control), and cells with the lethal compound (L), respectively. When the effect of a chemical modulator (M) on L is calculated, we instead used the equation: VL|M = (IM, L-I0)/(IM, V-I0), where VL|M, IM, L and IM, V are the normalized viability, and fluorescence intensity from cells treated with M and V, and from cells with M and L. respectively. The viability is typically measured in biological triplicates unless otherwise specified. A representative dose-response curve, the mean and standard error of normalized viability from one replicate are plotted. |
| In vitro | Methods: Human bladder cancer cell lines J82, 253J, T24, and RT-112 were treated with FIN56 at concentration gradients (0.3, 1, 3, 10 μM) for 3, 6, 9, 24, and 72 hours, and cell viability was assessed using the CCK-8 assay. Results: FIN56 induced cell death in all four cell lines. [1] Methods: FIN56 (10 μM), α-tocopherol (ferroptosis inhibitor), and Liproxstatin-1 (ferroptosis inhibitor) were added to 253J and T24 cells and incubated for 24 hours; cell viability was assessed using the CCK-8 assay. Results: Both ferroptosis inhibitors significantly inhibited FIN56-induced cell death, confirming that FIN56 exerts its effects via ferroptosis. [1] Methods: Human glioblastoma LN229 and U118 cells. The cells were treated with 1 μM FIN56 for 24 h, or with 1 μM Ferrostatin-1 for 1 h followed by co-treatment with FIN56. Lipid peroxidation and ferroptosis levels were assessed using BODIPY 581/591 C11, CellRox Green, 4-HNE immunofluorescence, and transmission electron microscopy. Results: FIN56 significantly induced lipid peroxidation and ferrocytosis in LN229 and U118 cells, and this effect was blocked by Ferrostatin-1. [2] |
| In vivo | Methods: A subcutaneous tumor xenograft model was established in LN229-bearing nude mice. FIN56 (10 mg/kg) or a control agent was administered intraperitoneally for 30 consecutive days. Tumor volume, Ki67 (proliferation), and 4-HNE (ferroptosis) were assessed. Results: FIN56 significantly reduced tumor volume, decreased the proportion of Ki67-positive cells, and increased 4-HNE levels, thereby inhibiting glioblastoma growth and inducing ferroptosis in vivo. [2] |
| Storage | The compound is unstable in solution. Please use soon, Powder: -20°C for 3 years Shipping with blue ice/Shipping at ambient temperature. |
| Solubility Information | DMSO : 247.5 mg/mL (478.11 mM), The compound is unstable in solution, please use soon. 10% DMSO+90% Corn Oil : 3.3 mg/mL (6.37 mM), Sonication is recommended. |
| Keywords | synthase | squalene | Inhibitor | inhibit | GPX4 | FIN-56 | FIN56 | FIN 56 | Ferroptosis | degradation |
| Inhibitors Related | Rosiglitazone | Hemin | L-Glutamic acid | Sorafenib | Curcumin | Gallic Acid Monohydrate | L-Cystine | L-Glutamine | (-)-Epigallocatechin Gallate | Coenzyme Q10 | Baicalein | Sodium Molybdate |
| Related Compound Libraries | Apoptosis Compound Library | Ferroptosis Compound Library | Bioactive Compound Library | NO PAINS Compound Library | Bioactive Compounds Library Max | Anti-COVID-19 Compound Library |
Company Profile Introduction
Target Molecule Corp. (TargetMol) is a global high-tech enterprise, headquartered in Boston, MA, specializing in chemical and biological research product and service to meet the research needs of global customers.
TargetMol has evolved into one of the biggest global compound library and small molecule suppliers and a customer based on 40+ countries. TargetMol offers over 80 types of compound libraries and a wide range of high-quality research chemicals including inhibitors, activator, natural compounds, peptides, inhibitory antibodies, and novel life-science kits, for laboratory and scientific use. Besides, virtual screening service is also available for customers who would like to conduct the computer-aided drug discovery.
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