HX 531 |
| Catalog No.GC16814 |
HX 531 is a potent retinoid X receptor (RXR) antagonist.
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 188844-34-0
Sample solution is provided at 25 µL, 10mM.
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HX 531 is a potent retinoid X receptor (RXR) antagonist[1].
In vitro, Pre-treatment with HX 531 (2.5μM; 30min) attenuated the anti-apoptotic effect of all-trans retinoic acid (t-RA) in protecting mesangial cells from H₂O₂-induced apoptosis via the inhibition of the activator protein 1 (AP-1) pathway[2]. HX 531 (0.1μM; 45-60min) significantly inhibits Benzophenone-3 (BP-3)-induced neuronal apoptosis and partially reverses the effects of BP-3 on the expression of RXR receptors and epigenetic status[3].
In vivo, Wild-type mice treated with HX 531(2 weeks; p.o.) were protected from high-fat (HF) diet-induced hyperglycemia and insulin resistance[4]. The weight gain of OLETF rats treated with HX 531 (10mg/kg/day; 22 weeks; p.o.) was significantly suppressed, and the fat pad weight was significantly reduced, comparable to that of non-diabetic LETO rats[5].
References:
[1] Alique M, Lucio FJ, Herrero JF. Vitamin A active metabolite, all-trans retinoic acid, induces spinal cord sensitization. II. Effects after intrathecal administration. Br J Pharmacol. 2006 Sep;149(1):65-72.
[2] Konta T, Xu Q, Furusu A, et al. Selective roles of retinoic acid receptor and retinoid x receptor in the suppression of apoptosis by all-trans-retinoic acid. J Biol Chem. 2001 Apr 20;276(16):12697-701.
[3] Wnuk A, Rzemieniec J, Lasoń W, et al. Benzophenone-3 Impairs Autophagy, Alters Epigenetic Status, and Disrupts Retinoid X Receptor Signaling in Apoptotic Neuronal Cells. Mol Neurobiol. 2018 Jun;55(6):5059-5074.
[4] Yamauchi T, Waki H, Kamon J, et al. Inhibition of RXR and PPARgamma ameliorates diet-induced obesity and type 2 diabetes. J Clin Invest. 2001 Oct;108(7):1001-13.
[5] Nakatsuka A, Wada J, Hida K, et al. RXR antagonism induces G0 /G1 cell cycle arrest and ameliorates obesity by up-regulating the p53-p21(Cip1) pathway in adipocytes. J Pathol. 2012 Apr;226(5):784-95.
| Cell experiment [1]: | |
Cell lines | RBL-2H3 cells |
Preparation Method | Primary neuronal cell cultures were exposed to BP-3 (10-100μM) for 6 or 24h. The involvement of RXR signaling in BP-3-induced effects was verified with the high-affinity RXR antagonist HX 531 (0.1μM) and the RXR agonist DHA (1μM). Specific ligands were added to the culture media 45-60min before BP-3. Apoptotic cells were detected via Hoechst 33342 staining at 24h after treatment. Neocortical cells that were cultured on glass coverslips were washed with 10mM phosphate-buffered saline (PBS) and stained with Hoechst 33342 (0.6mg/ml) at room temperature (RT) for 5min. The cells containing bright blue fragmented nuclei, indicative of condensed chromatin, were identified as apoptotic cells. Qualitative analysis was performed using a fluorescence microscope. The level of cellular fluorescence from fluorescence microscopy images was determined using ImageJ software. |
Reaction Conditions | 0.1μM; 45-60min |
Applications | HX 531 significantly inhibits Benzophenone-3 (BP-3)-induced neuronal apoptosis and partially reverses the effects of BP-3 on the expression of RXR receptors and epigenetic status. |
| Animal experiment [2]: | |
Animal models | Eight-week-old male Otsuka Long–Evans Tokushima Fatty (OLETF) rats |
Preparation Method | Eight-week-old male Otsuka Long–Evans Tokushima Fatty (OLETF) rats, which serve as a model for obesity and type 2 diabetes, were divided into three groups: OLETF rats (OLETF group); OLETF rats treated with pioglitazone (PIO group); and OLETF rats treated with HX 531 (HX 531 group). Non-diabetic Long–Evans Tokushima Otsuka (LETO) rats were fed a chow diet and served as the control group (LETO group). Pioglitazone and HX 531 were mixed into the diet, and each group orally received 1mg pioglitazone/kg body weight/day and 10mg HX 531/kg body weight/day throughout the experimental period. After conducting the described studies, the rats were sacrificed at 30 weeks of age. |
Dosage form | 10mg/kg/day; 22 weeks; p.o. |
Applications | The weight gain of OLETF rats treated with HX 531 was significantly suppressed, and the fat pad weight was significantly reduced, comparable to that of non-diabetic LETO rats. |
References: | |
| Cas No. | 188844-34-0 | SDF | |
| Chemical Name | 4-(5,7,7,10,10-pentamethyl-2-nitro-7,8,9,10-tetrahydro-5H-benzo[b]naphtho[2,3-e][1,4]diazepin-12-yl)benzoic acid | ||
| Canonical SMILES | CC(CCC1(C)C)(C2=CC(C(C3=CC=C(C(O)=O)C=C3)=NC4=C(N5C)C=CC(N(=O)=O)=C4)=C5C=C21)C | ||
| Formula | C29H29N3O4 | M.Wt | 483.56 |
| Solubility | 0.12mg/mL in ethanol, 10mg/mL in DMSO, 15mg/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 | 2.068 mL | 10.34 mL | 20.68 mL |
| 5 mM | 413.6 μL | 2.068 mL | 4.136 mL |
| 10 mM | 206.8 μL | 1.034 mL | 2.068 mL |
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Quality Control & SDS
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- Purity: >97.00%
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Average Rating: 5 (Based on Reviews and 24 reference(s) in Google Scholar.)
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