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| Targets |
J14 primarily targets sulfiredoxin, an enzyme involved in the regulation of cellular redox balance. Sulfiredoxin is responsible for reducing hyperoxidized peroxiredoxins, thereby maintaining cellular antioxidant defense mechanisms. By inhibiting sulfiredoxin activity, J14 disrupts the cellular redox signaling pathway. The compound's action leads to altered cellular responses and has been investigated for its potential therapeutic effects in conditions associated with oxidative stress. J14 has also been associated with the NF-κB target pathway.
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| ln Vitro |
J14 (0-100 μM; 0-96 hours; A549 cells) treatment inhibits A549 cell growth in a concentration- and time-dependent manner; 15.7 μM is the half-inhibitory concentration [1]. Treatment (48–72 hours; A549 cells) activates caspase-3 and caspase-9 in addition to releasing cytochrome c into the cytoplasm. J14 causes mitochondrial oxidative damage, which triggers caspase-mediated cell sanitization [1]. Intracellular ROS accumulation and sulfinate peroxidase were both markedly elevated by J14 treatment. When intracellular ROS build up excessively, oxidative damage results, ultimately leading to cell death. J14 significantly and time-pullingly promotes cell death in A549 cells, with around 40% of the cells dying in 96 hours [1]. Insulation of cells and J14 sensor short circuit damage [1]. Cells
In vitro, J14 functions as a reversible sulfiredoxin inhibitor with an IC50 of 8.1 μM. It induces oxidative stress by increasing intracellular ROS accumulation through sulfiredoxin inhibition. This mechanism leads to cytotoxicity and preferential death of cancer cells. Studies have shown that J14 causes mitochondrial damage via ROS-mediated pathways, contributing to its anticancer effects. The compound's activity has been characterized in various cancer cell lines, demonstrating its potential as a research tool for studying redox biology and oxidative stress-induced cell death. |
| ln Vivo |
J14 (50 mg/kg; i.p.; daily; for 16 days; BALB/c female nude mice) therapy significantly reduced mean tumor volume. Compared with the control experiment, the main tumor mass of the J14 treatment experiment
In vivo studies of J14 have demonstrated its ability to induce oxidative stress and promote cancer cell death through sulfiredoxin inhibition. The compound has been investigated for its role in oxidative stress-related diseases and as a tool compound for studying redox signaling pathways in living organisms. J14's mechanism involves disrupting cellular redox balance, leading to increased ROS levels and subsequent cytotoxicity in tumor tissues. While specific in vivo efficacy data is limited, the compound shows promise for therapeutic applications in cancer and other diseases associated with oxidative stress. |
| Enzyme Assay |
The cell-free enzyme assay for J14 involves measuring its inhibitory activity against purified sulfiredoxin. The assay typically uses recombinant sulfiredoxin enzyme and monitors its activity in reducing hyperoxidized peroxiredoxins in the presence of varying concentrations of J14. The IC50 value of 8.1 μM is determined by assessing the compound's ability to inhibit sulfiredoxin-mediated redox reactions. Activity is measured using spectrophotometric or fluorometric methods that detect changes in substrate conversion or product formation, allowing for quantification of enzyme inhibition and determination of the compound's potency against its primary target.
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| Cell Assay |
Cell Viability Assay [1] Cells
Cell Types: A549 Cell Tested Concentrations: 0-100 μM Incubation Duration: 0 hrs (hours), 24 hrs (hours), 48 hrs (hours), 72 hrs (hours), 96 hrs (hours) Experimental Results: Inhibited the growth of A549 cells in a concentration- and time-dependent manner. Western Blot Analysis [1] Cell Types: A549 cells Tested Concentrations: 20 μM Incubation Duration: 48 hrs (hours), 72 hrs (hours) Experimental Results: Not only caused the release of cytochrome c into the cytoplasm, but also caused the activation of caspase-3 and caspase-9. For in vitro cellular assays, J14 is typically dissolved in DMSO and diluted in cell culture medium to desired concentrations. Cancer cell lines are treated with J14 at various concentrations (ranging from sub-micromolar to millimolar) for defined periods. Cellular oxidative stress is assessed by measuring intracellular ROS levels using fluorescent probes such as DCFH-DA. Cytotoxicity is evaluated using standard assays like MTT, CCK-8, or LDH release assays. Apoptosis and mitochondrial damage can be assessed through flow cytometry using Annexin V/PI staining and JC-1 dye, respectively. Data analysis involves calculating IC50 values and comparing ROS levels between treated and control groups. |
| Animal Protocol |
Animal/Disease Models: Sixweeks old BALB/c female nude mice injected with A549 cells [1]
Doses: 50 mg/kg Route of Administration: intraperitoneal (ip) injection; and weight were Dramatically reduce[1]. Routine; 16-day Experimental Results: Significant reduction in human lung tumor growth with no acute toxicity. In vivo animal studies of J14 typically involve xenograft mouse models bearing human cancer cell lines. The compound is administered via various routes including intraperitoneal (i.p.) or oral gavage at doses determined from pharmacokinetic studies. Tumor growth inhibition is monitored by measuring tumor volume over time using calipers. Biomarkers of oxidative stress, such as ROS levels and antioxidant enzyme activities, are measured in tumor tissues and blood samples. Pharmacodynamic endpoints include assessment of sulfiredoxin inhibition, oxidative stress markers, and apoptosis in tumor tissues. Efficacy is evaluated by comparing tumor growth rates and survival between treatment and control groups. |
| ADME/Pharmacokinetics |
Pharmacokinetic properties of J14 include its molecular weight of 517.04 g/mol and molecular formula C28H25ClN4O2S. The compound has a purity of ≥95% and is typically formulated for in vivo administration using appropriate vehicles such as DMSO, PEG300, Tween 80, and saline. Specific PK parameters such as half-life, bioavailability, and tissue distribution have not been extensively reported in the available literature. As a small molecule inhibitor, J14 is expected to have moderate oral bioavailability and tissue penetration, though detailed ADME studies would be required for comprehensive characterization.
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| Toxicity/Toxicokinetics |
The toxicity profile of J14 has not been extensively characterized in published literature. As a sulfiredoxin inhibitor that induces oxidative stress, the compound may cause dose-dependent cytotoxicity in normal cells due to increased ROS levels. Preclinical safety studies would typically include acute and sub-chronic toxicity assessments in rodent models, evaluating effects on body weight, organ function, and histopathology. The compound is intended for research use only and not for therapeutic applications in humans. Standard safety precautions should be followed when handling this compound, including the use of personal protective equipment.
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| References | |
| Additional Infomation |
J14 is a research-grade chemical (purity ≥95%) primarily used as a tool compound for studying redox biology and oxidative stress. Its mechanism of action involves reversible inhibition of sulfiredoxin, leading to intracellular ROS accumulation and induction of oxidative stress-mediated cytotoxicity. The compound has been investigated for its potential in cancer research, particularly in studies exploring ROS-mediated mitochondrial damage and preferential death of cancer cells. J14 has not entered clinical trials and is not approved for therapeutic use; it is strictly for research purposes. Reference: Kim H, et al. Sulfiredoxin inhibitor induces preferential death of cancer cells through reactive oxygen species-mediated mitochondrial damage. Free Radic Biol Med. 2016 Feb;91:264-74.
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| Molecular Formula |
C28H25CLN4O2S
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| Molecular Weight |
517.0417
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| Exact Mass |
516.138
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| CAS # |
1043854-13-2
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| PubChem CID |
45987688
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| Appearance |
White to off-white solid powder
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| LogP |
6.4
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| Hydrogen Bond Donor Count |
1
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| Hydrogen Bond Acceptor Count |
7
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| Rotatable Bond Count |
7
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| Heavy Atom Count |
36
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| Complexity |
695
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| Defined Atom Stereocenter Count |
0
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| SMILES |
ClC1=C([H])C([H])=C([H])C([H])=C1N1C([H])([H])C([H])([H])N(C2C([H])=C(C3C([H])=C([H])C([H])=C([H])C=3[H])N=C(N=2)SC([H])([H])C2C([H])=C([H])C(C(=O)O[H])=C([H])C=2[H])C([H])([H])C1([H])[H]
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| InChi Key |
RSHUJZXWKLIBRE-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C28H25ClN4O2S/c29-23-8-4-5-9-25(23)32-14-16-33(17-15-32)26-18-24(21-6-2-1-3-7-21)30-28(31-26)36-19-20-10-12-22(13-11-20)27(34)35/h1-13,18H,14-17,19H2,(H,34,35)
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| Chemical Name |
4-[[4-[4-(2-chlorophenyl)piperazin-1-yl]-6-phenylpyrimidin-2-yl]sulfanylmethyl]benzoic acid
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| Synonyms |
J14; J-14
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO : ≥ 125 mg/mL (~241.76 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.17 mg/mL (4.20 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 21.7 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.17 mg/mL (4.20 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 21.7 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.9341 mL | 9.6704 mL | 19.3409 mL | |
| 5 mM | 0.3868 mL | 1.9341 mL | 3.8682 mL | |
| 10 mM | 0.1934 mL | 0.9670 mL | 1.9341 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution 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 stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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