DIM-3,5-Cl2
Based on 1 Customer Validation
DIM-3,5-Cl2 is an inverse NR4A1/NR4A2 agonist with KD values of 7.7 μM and 12.0 μM for NR4A1 and NR4A2, respectively. DIM-3,5-Cl2 acts as an inverse agonist to downregulate pro-oncogenic and proendometriotic gene products, and as an agonist to enhance NR4A1/2/Sp1/Sp4-mediated CD71 transactivation. DIM-3,5-Cl2 induces ferroptosis via ROS formation, lipoperoxidation, MDA production, and reduced GPX4, SLC7A11 expression. DIM-3,5-Cl2 induces apoptosis via PARP and caspase-3 cleavage, reduced BCL-2 expression, and inhibits cancer cell viability. DIM-3,5-Cl2 can be used for the research of triple negative breast cancer, endometriosis, and colorectal cancer.
For research use only. We do not sell to patients.
- Purity : 99.18%
- CAS No.: 2595179-74-9
- Formula: C23H16Cl2N2
- Molecular Weight:391.29
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Storage:Powder -20°C, 3 years ; In solvent -80°C, 6 months , -20°C, 1 month
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
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Solvent & Solubility
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
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Nur77/NR4A1 7.7 μM (Kd) |
Nurr1/NR4A2 12 μM (Kd) |
Caspase 3 |
Bcl-2 |
In Vitro
DIM-3,5-Cl2 (2.5-15 μM) potently inhibits the viability of human MDA-MB-231, MDA-MB-468, and mouse 4T1 TNBC cells[1].
DIM-3,5-Cl2 (7-15 μM; 24 h for MDA-MB-231, MDA-MB-468; 10-15 μM; 24 h for 4T1) induces apoptosis in human MDA-MB-231, MDA-MB-468, and mouse 4T1 TNBC cells via induction of cleaved PARP and cleaved caspase-3, and downregulation of pro-survival proteins BCL-2, full-length PARP, and full-length caspase-3[1].
DIM-3,5-Cl2 (7-15 μM; 24 h for MDA-MB-231, MDA-MB-468; 10-15 μM; 24 h for 4T1) modulates ferroptosis-related proteins in human MDA-MB-231, MDA-MB-468, and mouse 4T1 TNBC cells by decreasing GPX4 and SLC7A11 expression, and inducing CD71 expression at lower/mid concentrations (7, 10 μM) while decreasing CD71 at higher concentrations (12, 15 μM)[1].
DIM-3,5-Cl2 (10-12 μM; 24 h) downregulates pro-oncogenic proteins EGFR, β1-integrin, and c-Myc in human MDA-MB-231 TNBC cells[1].
DIM-3,5-Cl2 (12 μM; 16 h) potently induces ROS formation in human MDA-MB-231, MDA-MB-468, and mouse 4T1 TNBC cells[1].
DIM-3,5-Cl2 (12 μM; 16 h) potently induces lipid peroxidation in human MDA-MB-231, MDA-MB-468, and mouse 4T1 TNBC cells[1].
DIM-3,5-Cl2 (12 μM; 24 h) has its mediated downregulation of CD71, GPX4, and SLC7A11 in human MDA-MB-231 TNBC cells reversed by the ferroptosis inhibitor Ferrostatin-1 (HY-100579), confirming DIM-3,5-Cl2 acts via a ferroptotic pathway[1].
DIM-3,5-Cl2 (7-10 μM; 1, 2, 4, 6 h) time-dependently induces CD71 protein and CD71 mRNA expression in human MDA-MB-231 TNBC cells, with protein induction at 6 h and mRNA peaking at 4 h[1].
DIM-3,5-Cl2 (15 μM; 24 h) induces CD71 protein expression in NR4A1/NR4A2-expressing TNBC PDxO models (BCM-HCI-3561, BCM-4175)[1].
DIM-3,5-Cl2 (10 μM) has mediated induction of CD71 promoter activity in human MDA-MB-231 TNBC cells dependent on NR4A1 and NR4A2 expression, as knockdown of either receptor abrogates the induction[1].
DIM-3,5-Cl2 (10 μM; 4-24 h) time-dependently induces Sp1, Sp4, and CD71 protein expression in human MDA-MB-231 TNBC cells, and CD71 expression is dependent on Sp1 and Sp4 expression, as knockdown of either transcription factor decreases CD71 levels[1].
DIM-3,5-Cl2 (0.25-20 μM; 48 h) potently inhibits proliferation of IHEEC cells (IC50 = 7.34 μM) and IHESC cells (IC50 = 5.78 μM) after 48 h of treatment[2].
DIM-3,5-Cl2 (6.5 μM; 24 h) significantly inhibits migration of both IHEEC and IHESC cells[2].
DIM-3,5-Cl2 (6.5-13 μM; 24 h) modulates expression of pro-endometriotic pathway proteins in a cell-type specific manner, downregulating growth, fibrosis, and epithelial-to-mesenchymal transition (EMT) markers, upregulating apoptotic markers, and reducing NR4A1/NR4A2 levels in both IHEEC and IHESC cells[2].
DIM-3,5-Cl2 (13 μM; 12 h) reduces expression of fibrosis and EMT markers (COL1A1, N-cadherin, TWIST1) and disrupts actin filament structures in both IHEEC and IHESC cells[2].
DIM-3,5-Cl2 (5-10 μM; 24 h) decreases NR4A1, Sp1, and PD-L1 protein expression in SW480 human colon cancer cells[3].
DIM-3,5-Cl2 (2.5-7.5 μM; 24 h) decreases NR4A1, Sp1, and PD-L1 protein expression in RKO human colon cancer cells[3].
DIM-3,5-Cl2 (2.5-7.5 μM; 24 h) decreases NR4A1, Sp1, and PD-L1 protein expression in MC-38 murine colon cancer cells[3].
DIM-3,5-Cl2 (7.5 μM; 3 h) reduces the binding of NR4A1, Sp1, and PolII to the GC-rich proximal promoter of the PD-L1 gene in MC-38 murine colon cancer cells[3].
DIM-3,5-Cl2 (10 μM; 3 h) reduces the binding of NR4A1, Sp1, and PolII to the GC-rich proximal promoter of the PD-L1 gene in SW480 human colon cancer cells[3].
DIM-3,5-Cl2 (7.5 μM; 3 h) reduces the binding of NR4A1, Sp1, and PolII to the GC-rich proximal promoter of the PD-L1 gene in RKO human colon cancer cells[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:Human MDA-MB-231, MDA-MB-468, and mouse 4T1 triple negative breast cancer (TNBC) cells
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Concentration:7, 10, 12, 15 μM (MDA-MB-231, MDA-MB-468); 10, 12, 15 μM (4T1)
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Incubation Time:24 h
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Result:Induced cleaved PARP and cleaved caspase-3, and decreased BCL-2, full-length PARP, and full-length caspase-3 at 7, 10, 12 μM in MDA-MB-231 cells.
Induced cleaved PARP and cleaved caspase-3, and decreased BCL-2, full-length PARP, and full-length caspase-3 at 7, 10, 12, 15 μM in MDA-MB-468 cells.
Induced cleaved PARP and cleaved caspase-3, and decreased BCL-2, full-length PARP, and full-length caspase-3 at 10, 12, 15 μM in 4T1 cells.\nDecreased GPX4 and SLC7A11 protein levels at 7, 10, 12 μM; induced CD71 protein levels at 7, 10 μM, and decreased CD71 at 12 μM in MDA-MB-231 cells.
Decreased GPX4 and SLC7A11 protein levels at 7, 10, 12, 15 μM; induced CD71 protein levels at 7, 10 μM, and decreased CD71 at 12, 15 μM in MDA-MB-468 cells.
Decreased GPX4 and SLC7A11 protein levels at 10, 12, 15 μM; induced CD71 protein levels at 10, 12, 15 μM in 4T1 cells.
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Cell Line:Human MDA-MB-231 triple negative breast cancer (TNBC) cells
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Concentration:10, 12 μM
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Incubation Time:24 h
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Result:Decreased expression of EGFR, β1-integrin, and c-Myc in MDA-MB-231 cells.
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Cell Line:Human MDA-MB-231 triple negative breast cancer (TNBC) cells
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Concentration:12 μM
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Incubation Time:24 h
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Result:Ferrostatin-1 significantly inhibited compound-mediated downregulation of CD71, GPX4, and SLC7A11 in MDA-MB-231 cells.
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Cell Line:Human MDA-MB-231 triple negative breast cancer (TNBC) cells
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Concentration:10 μM
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Incubation Time:4, 6, 24 h
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Result:Knockdown of Sp1 or Sp4 alone decreased CD71 protein expression in MDA-MB-231 cells.
Induced Sp1, Sp4, and CD71 protein expression in MDA-MB-231 cells at 4, 6, and 24 h, with increasing induction observed over time.
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Cell Line:Immortalized human endometriotic epithelial cells (IHEEC), Immortalized human endometriotic stromal cells (IHESC)
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Concentration:6.5 μM
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Incubation Time:24 h
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Result:Significantly reduced migration of IHEEC and IHESC cells into the scratch wound area compared to vehicle controls, as measured by relative migration percentage.
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Cell Line:Immortalized human endometriotic epithelial cells (IHEEC), Immortalized human endometriotic stromal cells (IHESC)
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Concentration:6.5 μM; 13 μM
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Incubation Time:24 h
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Result:Significantly decreased protein levels of EGFR, mTOR, phospho-mTOR, β1-integrin, CTGF, FN, COL1A1, TWIST1, Slug, Snail, Vimentin, N-cadherin, ZEB1, ZO-1, β-catenin, NR4A1, and NR4A2 in IHEEC cells.
Significantly increased protein levels of cleaved poly(ADP-ribose) polymerase (C-PARP) and claudin-1 in IHEEC cells.
Had no significant effect on ERβ levels in IHEEC cells.
Significantly decreased protein levels of mTOR, phospho-mTOR, β1-integrin, ERβ, CTGF, COL1A1, TWIST1, Slug, Snail, N-cadherin, ZEB1, ZO-1, β-catenin, NR4A1, and NR4A2 in IHESC cells.
Significantly increased protein levels of C-PARP and claudin-1 in IHESC cells.
Had no significant effect on EGFR, FN, or α-SMA levels in IHESC cells.
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Cell Line:Immortalized human endometriotic epithelial cells (IHEEC), Immortalized human endometriotic stromal cells (IHESC)
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Concentration:13 μM
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Incubation Time:12 h
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Result:Significantly reduced fluorescence intensity of COL1A1, N-cadherin, and TWIST1 compared to untreated controls in both IHEEC and IHESC cells.
Caused a substantial decrease in filamentous actin structures in treated cells as shown by phalloidin staining.
In Vivo
DIM-3,5-Cl2 (2.5-7.5 mg/kg/day; i.p.; daily; 21 days) significantly inhibits MC-38 colon tumor growth in syngeneic C57BL/6 mice, downregulates tumor PD-L1 expression, and reverses T-cell exhaustion in both TILs and splenic CD8+ T-cells[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:FVB/NJ (female, 6 weeks old, surgically induced endometriosis)[2]
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Dosage:2.5 mg/kg
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Administration:i.p.; daily; 34 consecutive days
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Result:Significantly reduced ectopic lesion volume compared to vehicle control.
Significantly inhibited lesion growth as measured by luciferase imaging, while vehicle-treated mice showed continuous lesion growth.
Significantly reduced Ki-67 expression in stromal cells of ectopic lesions; Ki-67 expression in epithelial cells was not significantly affected.
Significantly increased TUNEL-positive (apoptotic) cells in ectopic lesions.
Significantly reduced Nr4a1 expression in both epithelial and stromal cells of ectopic lesions; significantly reduced Nr4a2 expression in stromal cells, with no significant effect on epithelial Nr4a2 expression.
Did not cause body weight loss, and liver panel analysis showed no evidence of liver damage compared to vehicle control.
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Animal Model:C57BL/6 (female, 4-6 weeks old, subcutaneous implantation of MC-38 colon cancer cells)[3]
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Dosage:2.5 mg/kg/day; 7.5 mg/kg/day
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Administration:i.p.; daily; 21 days
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Result:Significantly decreased tumor volumes and tumor weights relative to controls.
Showed no treatment-related toxicity, with treated mice showing a slight increase in body weight.
Decreased expression of NR4A1 and PD-L1 in tumor lysates at 2.5 mg/kg/day dose.
Significantly increased the percentage of CD8+ T-cells in tumor-infiltrating lymphocytes (TILs) at 2.5 mg/kg/day dose.
Decreased the percentage of CD8+ T-cells expressing the T-cell exhaustion markers PD-1, 2B4, and TIM3, and decreased the percentage of CD8+ T-cells co-expressing PD-1 and TIM3 in TILs at 2.5 mg/kg/day dose.
Decreased mRNA expression of NR4A1, TOX, TOX2, and NFAT, and increased mRNA expression of interferon γ, granzyme B, perforin, and T-Bet in CD8+ T-cells isolated from TILs at 2.5 mg/kg/day dose.
Significantly increased cell percentages, decreased the percentage of cells expressing PD-1, 2B4, TIM3, and PD-1/TIM3, increased the percentage of Treg cells, increased the percentage of cells expressing T-Bet and TOX/TOX2, and decreased the percentage of cells expressing NFAT1 in splenic CD8+ T-cells at 2.5 mg/kg/day dose.
Chemical Information
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CAS No. 2595179-74-9
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Appearance Solid
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Molecular Weight 391.29
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Formula C23H16Cl2N2
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Color White to off-white
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SMILES
ClC1=CC(Cl)=CC(C(C2=CNC3=C2C=CC=C3)C4=CNC5=C4C=CC=C5)=C1
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Powder -20°C 3 years In solvent -80°C 6 months -20°C 1 month
Solvent & Solubility
In Vitro:
DMSO : 100 mg/mL (255.56 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
In Vivo:
Select the appropriate dissolution method based on your experimental animal and administration route.
- For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
- To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
- The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%Saline +
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL.
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Protocols
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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Mammalian live/dead viability and cytotoxicity staining
Live/dead viability and cytotoxicity staining assays are based on the simultaneous detection of intracellular esterase activity in metabolically active (viable) cells and membrane integrity loss in non-viable cells. In commonly used dual-staining approaches, membrane-permeant fluorogenic substrates are converted by intracellular esterases into fluorescent products in live cells, while impermeant DNA-binding dyes selectively enter cells with compromised plasma membranes and label nucleic acids in dead or dying cells, enabling discrimination between viable and non-viable populations by fluorescence microscopy or flow cytometry.
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Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
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ROS/oxidative-stress fluorescent staining
ROS/oxidative-stress fluorescent staining uses cell-permeant fluorogenic probes that become fluorescent after oxidation inside cells or tissues; commonly used examples include DCFH-DA/DCFDA for broad cellular oxidant detection, DHE for superoxide-related signal detection, MitoSOX for mitochondrial superoxide-related signal detection, and CellROX probes for oxidative-stress-associated fluorescence readouts. The assay detects probe oxidation rather than a single ROS species unless the probe and analysis method have been chemically validated for that species. DCFH-DA enters cells, is deacetylated by intracellular esterases to DCFH, and produces fluorescent DCF after oxidation, so the readout is used as an operational measure of total cellular oxidative stress rather than a species-specific ROS measurement. DHE and MitoSOX can report superoxide-related oxidation, but red fluorescence alone can include non-specific ethidium-like oxidation products; HPLC or optimized spectral approaches are
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CCK-8/WST-8 Cell Proliferation Assay
The CCK-8/WST-8 assay is based on the reduction of the water-soluble tetrazolium salt WST-8 to a water-soluble formazan product by cellular dehydrogenases in metabolically active cells, where the generated formazan amount is proportional to the number of living cells and is quantified by measuring absorbance in the visible range, providing a colorimetric readout for cell viability and proliferation assessment. This class of tetrazolium-based assays improves upon earlier MTT-based systems by producing a water-soluble formazan, eliminating the need for organic solubilization steps and enabling direct spectrophotometric measurement in culture medium.
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Breast Cancer Modeling
Breast cancer is a heterogeneous cancer, and it has been distinguished into four subtypes: luminal A, luminal B, HER2-positive and basal-like. Molecular mutations, epigenetic alterations, hormone exposure and immune microenvironment are related to the progression of breast cancer.
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Cell Viability Determination by MTT Colorimetric Assay
The following protocol uses the MTT colorimetric assay as a classic literature-established method for assessing cell viability/metabolic activity in cultured mammalian cells. MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] is reduced by metabolically active cells to a colored formazan product; the amount of formazan is quantified spectrophotometrically and provides an indirect measure of metabolically active viable cells. Importantly, MTT reduction reflects cellular oxidoreductase/metabolic activity rather than an absolute direct count of living cells, so changes in cellular metabolism can alter the signal independently of cell number.
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Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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Ferroptosis Solutions
Ferroptosis is an iron-dependent, non-apoptotic form of regulated cell death characterized by lethal lipid peroxidation and sensitivity to suppression by iron chelators or lipophilic radical-trapping antioxidants. The core pathway links cystine uptake through system Xc−, glutathione availability, GPX4-dependent detoxification of phospholipid hydroperoxides, iron-dependent oxidative reactions, and polyunsaturated-phospholipid metabolism into a cell-death program that is biochemically and morphologically distinct from apoptosis, necrosis, and autophagy. The ferroptosis pathway is experimentally linked to phenotype through chemical and genetic perturbation. Erastin induces ferroptosis by inhibiting cystine uptake through system Xc− and weakening antioxidant defenses, while GPX4 inhibition or depletion causes lipid peroxide accumulation and ferroptotic cancer-cell death. ACSL4 and oxidizable arachidonoyl- or adrenoyl-containing phosphatidylethanolamines shape ferroptosis sensitivity by con
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MTT Cell Proliferation Assay
The MTT assay is a colorimetric endpoint assay for estimating viable cell number, cell growth, cytotoxicity, or cell activation in cultured mammalian cells. Living cells reduce the yellow tetrazolium salt MTT into purple/blue formazan, while dead cells do not generate the same signal; the resulting color can be quantified with a multiwell spectrophotometer. MTT reduction is commonly interpreted as a readout of metabolic activity that often correlates with viable cell number, but it should not be treated as a direct cell-counting method unless the assay is optimized for the cell type and experimental condition. Studies show that MTT reduction can involve mitochondrial and non-mitochondrial reducing systems, and formazan may accumulate in intracellular lipid droplets rather than simply marking mitochondria.
Purity & Documentation
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Data Sheet (300 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
References
[1]. Oany AR, et al. Orphan nuclear receptor 4A1 (NR4A1) and NR4A2 are endogenous regulators of CD71 and their ligands induce ferroptosis in breast cancer. Cell Death Dis. 2025 Nov 3;16(1):776. [Content Brief]
[2]. Tsui WNT, et al. Dual Targeting of Orphan Nuclear Receptors NR4A1 and NR4A2 for Nonhormonal Endometriosis Therapy. Endocrinology. 2025;166(11):bqaf144. [Content Brief]
[3]. Mohankumar K, et al. Bis-indole-derived NR4A1 antagonists inhibit colon tumor and splenic growth and T-cell exhaustion. Cancer Immunol Immunother. 2023;72(12):3985-3999. [Content Brief]
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO | 1 mM | 2.5556 mL | 12.7782 mL | 25.5565 mL | 63.8912 mL |
| 5 mM | 0.5111 mL | 2.5556 mL | 5.1113 mL | 12.7782 mL | |
| 10 mM | 0.2556 mL | 1.2778 mL | 2.5556 mL | 6.3891 mL | |
| 15 mM | 0.1704 mL | 0.8519 mL | 1.7038 mL | 4.2594 mL | |
| 20 mM | 0.1278 mL | 0.6389 mL | 1.2778 mL | 3.1946 mL | |
| 25 mM | 0.1022 mL | 0.5111 mL | 1.0223 mL | 2.5556 mL | |
| 30 mM | 0.0852 mL | 0.4259 mL | 0.8519 mL | 2.1297 mL | |
| 40 mM | 0.0639 mL | 0.3195 mL | 0.6389 mL | 1.5973 mL | |
| 50 mM | 0.0511 mL | 0.2556 mL | 0.5111 mL | 1.2778 mL | |
| 60 mM | 0.0426 mL | 0.2130 mL | 0.4259 mL | 1.0649 mL | |
| 80 mM | 0.0319 mL | 0.1597 mL | 0.3195 mL | 0.7986 mL | |
| 100 mM | 0.0256 mL | 0.1278 mL | 0.2556 mL | 0.6389 mL |
DIM-3,5-Cl2 Related Classifications
HY-179528 Related Classifications
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Keywords
- DIM-3,5-Cl2
- 2595179-74-9
- Nuclear Hormone Receptor 4A/NR4A
- Ferroptosis
- Glutathione Peroxidase
- Reactive Oxygen Species (ROS)
- Transferrin Receptor
- Apoptosis
- Bcl-2 Family
- Caspase
- IHESC cells
- ferroptosis
- IHEEC cells
- NR4A2
- MDA-MB-231
- endometriosis
- nuclear receptor 4A1
- apoptosis
- triple negative breast cancer
- colorectal cancer
- Inhibitor
- inhibitor
- inhibit