Home>>Signaling Pathways>> Metabolism>> Ferroptosis>>FIN56

FIN56 Sale

Catalog No.GC30039

FIN56, a novel ferroptosis inducer, triggers ferroptosis by increasing the degradation of GPX4 .

Products are for research use only. Not for human use. We do not sell to patients.

FIN56 Chemical Structure

Cas No.: 1083162-61-1

Size Price Stock Qty
10mM (in 1mL DMSO)
$52.00
In stock
5mg
$46.00
In stock
10mg
$77.00
In stock
25mg
$168.00
In stock
50mg
$301.00
In stock
100mg
$539.00
In stock

Tel:(909) 407-4943 Email: sales@glpbio.com

Customer Reviews

Based on customer reviews.

  • GlpBio Citations

    GlpBio Citations
  • Bioactive Compounds Premium Provider

    Bioactive Compounds Premium Provider

Sample solution is provided at 25 µL, 10mM.

Product has been cited by 1 publications

Product Documents

Quality Control & SDS

View current batch:

Protocol

Cell experiment [1]:

Cell lines

LN229 and U118 GBM cell lines

Preparation Method

Cells were plated into 96-well plates and incubated overnight. Different doses of FIN56 (0, 0.1, 0.5, 1.0, 2.0 4.0 and 8.0 µM) was added to wells. 24 h later, CCK-8 solution was added to each well. 2 h later, samples were measured at 450 nm on a microplate reader.

Reaction Conditions

FIN56 (0-8.0 µM);24 h

Applications

FIN56 decreased the cell viability of LN229 and U118 cells in a dose-dependent manner.

Animal experiment [2]:

Animal models

Nude mouse model

Preparation Method

LN229 cells were injected subcutaneously into the right shoulder of 4-week-old nude mice. 2 weeks later, nude mice (n = 10) were divided into two groups, control group and FIN56 treatment group. Subcutaneous tumors were harvested 30 days after treatment.

Dosage form

30 days

Applications

FIN56 decreased tumor volume obviously, FIN56 significantly increased protein levels of 4-HNE.

References:

[1]. Zhang X, Guo Y, et,al. FIN56, a novel ferroptosis inducer, triggers lysosomal membrane permeabilization in a TFEB-dependent manner in glioblastoma. J Cancer. 2021 Sep 13;12(22):6610-6619. doi: 10.7150/jca.58500. PMID: 34659551; PMCID: PMC8517990.

Background

FIN56, a novel ferroptosis inducer, triggers ferroptosis by increasing the degradation of GPX4 [1,4]. FIN56 also activates squalene synthase, an enzyme involved in the cholesterol synthesis [2].

FIN56 (0-8.0 µM;24 h) decreased the cell viability of LN229 and U118 cells in a dose-dependent manner. After FIN56 treatment, cell cycle of LN229 and U118 was arrested at GO/G1 phases [3]. FIN56 (1-5 µM;3-24 h) induces autophagy-associated cell death in Bladder cancer (BC) cells[4]. Inhibition of Gpx4 by FIN56 (0-20µM) abolished the protective effects of NAC on HG-induced ferroptosis[5]. the protein expression of salusin β was upregulated by ferroptosis activators, such as FIN56. Pretreatment with ferrostatin 1 (a ferroptosis inhibitor) prevented the upregulated protein expression of salusin β in HK 2 cells exposed to HG[6]. AS-IV markedly accelerated proliferation, suppressed apoptosis, and reduced ROS and LDH accumulation. The effects of AS-IV on SCI were inhibited by si-TFEB, and this inhibition was further reinforced by the addition of FIN56(5 µM)[7].

FIN56 (30days) decreased tumor volume obviously, FIN56 significantly increased protein levels of 4-HNE[3].

References:
[1]. Shimada K, Skouta R, et,al. Global survey of cell death mechanisms reveals metabolic regulation of ferroptosis. Nat Chem Biol. 2016 Jul;12(7):497-503. doi: 10.1038/nchembio.2079. Epub 2016 May 9. PMID: 27159577; PMCID: PMC4920070.
[2]. Gaschler MM, Andia AA, et,al.FINO2 initiates ferroptosis through GPX4 inactivation and iron oxidation. Nat Chem Biol. 2018 May;14(5):507-515. doi: 10.1038/s41589-018-0031-6. Epub 2018 Apr 2. PMID: 29610484; PMCID: PMC5899674.
[3]. Zhang X, Guo Y, et,al. FIN56, a novel ferroptosis inducer, triggers lysosomal membrane permeabilization in a TFEB-dependent manner in glioblastoma. J Cancer. 2021 Sep 13;12(22):6610-6619. doi: 10.7150/jca.58500. PMID: 34659551; PMCID: PMC8517990.
[4]. Lei P, Bai T, et,al.Mechanisms of Ferroptosis and Relations With Regulated Cell Death: A Review. Front Physiol. 2019 Feb 26;10:139. doi: 10.3389/fphys.2019.00139. PMID: 30863316; PMCID: PMC6399426.
[5]. Li Q, Liao J,et,al. NAC alleviative ferroptosis in diabetic nephropathy via maintaining mitochondrial redox homeostasis through activating SIRT3-SOD2/Gpx4 pathway. Free Radic Biol Med. 2022 Jul;187:158-170. doi: 10.1016/j.freeradbiomed.2022.05.024. Epub 2022 May 31. Erratum in: Free Radic Biol Med. 2022 Aug 20;189:1. PMID: 35660452.
[6].Wang WJ, Jiang X,et,al.Salusin‑β participates in high glucose‑induced HK‑2 cell ferroptosis in a Nrf‑2‑dependent manner. Mol Med Rep. 2021 Sep;24(3):674. doi: 10.3892/mmr.2021.12313. Epub 2021 Jul 23. PMID: 34296310; PMCID: PMC8335735.
[7]. Zhou Y, Li L, et,al.Astragaloside IV ameliorates spinal cord injury through controlling ferroptosis in H2O2-damaged PC12 cells in vitro. Ann Transl Med. 2022 Nov;10(21):1176. doi: 10.21037/atm-22-5196. PMID: 36467371; PMCID: PMC9708485.

Chemical Properties

Cas No. 1083162-61-1 SDF
Canonical SMILES O=S(C1=CC(/C2=N\O)=C(C3=C2C=C(S(=O)(NC4CCCCC4)=O)C=C3)C=C1)(NC5CCCCC5)=O
Formula C25H31N3O5S2 M.Wt 517.66
Solubility DMSO : ≥ 100 mg/mL (193.18 mM);Water : < 0.1 mg/mL (insoluble) Storage Store at -20°C
General tips Please select the appropriate solvent to prepare the stock solution according to the solubility of the product in different solvents; once the solution is prepared, please store it in separate packages to avoid product failure caused by repeated freezing and thawing.Storage method and period of the stock solution: When stored at -80°C, please use it within 6 months; when stored at -20°C, please use it within 1 month.
To increase solubility, heat the tube to 37°C and then oscillate in an ultrasonic bath for some time.
Shipping Condition Evaluation sample solution: shipped with blue ice. All other sizes available: with RT, or with Blue Ice upon request.

Complete Stock Solution Preparation Table

Prepare stock solution
1 mg 5 mg 10 mg
1 mM 1.9318 mL 9.6588 mL 19.3177 mL
5 mM 0.3864 mL 1.9318 mL 3.8635 mL
10 mM 0.1932 mL 0.9659 mL 1.9318 mL
  • Molarity Calculator

  • Dilution Calculator

Mass
=
Concentration
x
Volume
x
MW*
 
 
 
**When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / CoA (available online).

Calculate

In vivo Formulation Calculator (Clear solution)

Step 1: Enter information below (Recommended: An additional animal making an allowance for loss during the experiment)

mg/kg g μL

Step 2: Enter the in vivo formulation (This is only the calculator, not formulation. Please contact us first if there is no in vivo formulation at the solubility Section.)

% DMSO % % Tween 80 % ddH2O
%DMSO %

Calculation results:

Working concentration: mg/ml;

Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )

Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

Note: 1. Please make sure the liquid is clear before adding the next solvent.
2. Be sure to add the solvent(s) in order. You must ensure that the solution obtained, in the previous addition, is a clear solution before proceeding to add the next solvent. Physical methods such as vortex, ultrasound or hot water bath can be used to aid dissolving.
3. All of the above co-solvents are available for purchase on the GlpBio website.

Reviews

Review for FIN56

Average Rating: 5 ★★★★★ (Based on Reviews and 15 reference(s) in Google Scholar.)

5 Star
100%
4 Star
0%
3 Star
0%
2 Star
0%
1 Star
0%
Review for FIN56

GLPBIO products are for RESEARCH USE ONLY. Please make sure your review or question is research based.

Required fields are marked with *

You may receive emails regarding this submission. Any emails will include the ability to opt-out of future communications.