SR 11302 |
Catalog No.GC12810
One-Click Copy Product Info
|
SR 11302 is a retinoid-based, AP-1-selective transcription factor inhibitor that blocks AP-1 activity without activating retinoic acid response element (RARE)-mediated transcription.
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 160162-42-5
Sample solution is provided at 25 µL, 10mM.
SR 11302 is a retinoid-based, AP-1-selective transcription factor inhibitor that blocks AP-1 activity without activating retinoic acid response element (RARE)-mediated transcription[1]. AP-1 is a transcription factor dimer composed of proteins such as Jun/Fos, which regulates the expression of genes such as inflammation and proliferation by binding to the TRE sequence[2]. RARE serves as the cognate DNA element for the retinoic acid receptor (RAR)/retinoid X receptor (RXR) heterodimer, propagating classic retinoid signaling[3]. By silencing AP-1 while remaining inert toward RAR/RXR, SR 11302 retains anti-inflammatory and anti-proliferative efficacy yet avoids the dermal toxicity, teratogenicity, and resistance associated with conventional retinoids[4]. SR 11302 is commonly used in studies of inflammation, oncology, and AP-1–mediated signaling pathways[5-7].
In vitro, pretreating AGS gastric epithelial cells with SR 11302 (2μM; 2h) and then infecting cells with H. pylori for 24 or 48h suppressed both cell proliferation and expression of oncogene proteins β-catenin and c-Myc[7]. In hypoxia-treated human pulmonary artery endothelial cells (HPAECs), SR 11302(1μM; 1h) abolished the hypoxia-evoked rise in aldosterone by blocking c-Fos/c-Jun–driven StAR transcription[8].
In vivo, oral administration of SR 11302 (o.5 or 1mg/kg/day) for 11 days in Vldlr−/− mice reduced the total vascular lesion number by 48% and decreased the lesion size by 40%, without detectable signs of toxicity in mice, including no change in body weight[5].
References:
[1] Fanjul A, Dawson MI, Hobbs PD, et al. A new class of retinoids with selective inhibition of AP-1 inhibits proliferation. Nature. 1994;372(6501):107-111.
[2] Karin M, Liu Zg, Zandi E. AP-1 function and regulation. Curr Opin Cell Biol. 1997;9(2):240-246.
[3] Cunningham TJ, Duester G. Mechanisms of retinoic acid signalling and its roles in organ and limb development. Nat Rev Mol Cell Biol. 2015;16(2):110-123.
[4] Huang C, Ma WY, Dawson MI, Rincon M, Flavell RA, Dong Z. Blocking activator protein-1 activity, but not activating retinoic acid response element, is required for the antitumor promotion effect of retinoic acid. Proc Natl Acad Sci U S A. 1997;94(11):5826-5830.
[5] Sun Y, Lin Z, Liu CH, et al. Inflammatory signals from photoreceptor modulate pathological retinal angiogenesis via c-Fos. J Exp Med. 2017;214(6):1753-1767.
[6] Shiohara M, Dawson MI, Hobbs PD, et al. Effects of novel RAR- and RXR-selective retinoids on myeloid leukemic proliferation and differentiation in vitro. Blood. 1999;93(6):2057-2066.
[7] Byun E, Park B, Lim JW, Kim H. Activation of NF-κB and AP-1 Mediates Hyperproliferation by Inducing β-Catenin and c-Myc in Helicobacter pylori-Infected Gastric Epithelial Cells. Yonsei Med J. 2016;57(3):647-651.
[8] Maron BA, Oldham WM, Chan SY, et al. Upregulation of steroidogenic acute regulatory protein by hypoxia stimulates aldosterone synthesis in pulmonary artery endothelial cells to promote pulmonary vascular fibrosis. Circulation. 2014;130(2):168-179.
| Cell experiment [1]: | |
Cell lines | Human gastric epithelial AGS cells |
Preparation Method | Human gastric epithelial cell line AGS (adenocarcinoma gastric, ATCC CRL 1739) and H. pylori (strain NCTC 11637) were obtained from the American Type Culture Collection. H. pylori was inoculated onto chocolate agar plates at 37°C under microaerophilic conditions using GasPakTM EZ Gas Generating Pouch Systems. Prior to infection, H. pylori were harvested and then suspended in antibiotic-free cell culture medium. H. pylori was added to cultured cells at a bacterium/cell ratio 50:1. AGS cells were treated with selective AP-1 inhibitor SR 11302 (2μM) for 2h before H. pylori infection and cultured for 24h (protein levels of oncogenes) and 48h (viable cell numbers). |
Reaction Conditions | 2μM; 2h |
Applications | SR 11302 suppressed both cell proliferation and expression of oncogene proteins β-catenin and c-Myc in H. pylori-infected Gastric epithelial AGS cells. |
| Animal experiment [2]: | |
Animal models | Vldlr+/− mice |
Preparation Method | Vldlr+/− (heterozygous) mice from The Jackson Laboratory (stock no. 002529) were crossed to generate homozygous and WT littermates. SR 11302 was dissolved in corn oil. Vldlr−/− pups were orally gavaged with SR 11302 or vehicle control (corn oil) at two doses (low dose 0.5mg/kg body weight and high dose 1mg/kg body weight) daily from P5 to P15. P16 retinas were collected for PCR and neovascularization analysis. |
Dosage form | 0.5 or 1mg/kg/day for 11 days; p.o. |
Applications | SR 11302 reduced the total vascular lesion number by 48% and decreased the lesion size by 40%, without detectable signs of toxicity in mice, including no change in body weight. |
References: | |
| Cas No. | 160162-42-5 | SDF | |
| Chemical Name | 3-methyl-7-(4-methylphenyl)-9-(2,6,6-trimethylcyclohexen-1-yl)nona-2,4,6,8-tetraenoic acid | ||
| Canonical SMILES | CC1=C(C(CCC1)(C)C)C=CC(=CC=CC(=CC(=O)O)C)C2=CC=C(C=C2)C | ||
| Formula | C26H32O2 | M.Wt | 376.54 |
| Solubility | 0.5 mg/ml in ethanol; 10mg/ml in DMSO; 20mg/mL in DMF | 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. | ||
| Prepare stock solution | |||
|
1 mg | 5 mg | 10 mg |
| 1 mM | 2.6558 mL | 13.2788 mL | 26.5576 mL |
| 5 mM | 531.2 μL | 2.6558 mL | 5.3115 mL |
| 10 mM | 265.6 μL | 1.3279 mL | 2.6558 mL |
Step 1: Enter information below (Recommended: An additional animal making an allowance for loss during the experiment)
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.)
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 saline, 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.
Quality Control & SDS
- View current batch:
- Purity: >98.00% Appearance: A solid
- COA (Certificate of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Average Rating: 5 (Based on Reviews and 30 reference(s) in Google Scholar.)