CD 2314RARβ agonist,potent and selective CAS# 170355-37-0 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 170355-37-0 | SDF | Download SDF |
PubChem ID | 15293210 | Appearance | Powder |
Formula | C23H24O2S | M.Wt | 364.5 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | Soluble to 100 mM in DMSO | ||
Chemical Name | 5-(5,5,8,8-tetramethyl-6,7-dihydroanthracen-2-yl)thiophene-3-carboxylic acid | ||
SMILES | CC1(CCC(C2=C1C=C3C=CC(=CC3=C2)C4=CC(=CS4)C(=O)O)(C)C)C | ||
Standard InChIKey | URUSABQSUCBGGJ-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C23H24O2S/c1-22(2)7-8-23(3,4)19-11-16-9-15(6-5-14(16)10-18(19)22)20-12-17(13-26-20)21(24)25/h5-6,9-13H,7-8H2,1-4H3,(H,24,25) | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | Potent and selective RARβ receptor agonist (Kd values are 145 and >3760 nM for RARβ and RARα receptors respectively; no binding detected at RARγ). Inhibits growth of human HNSCC 22B, 183A and 22A cells (IC50 values are 3.0, 5.7 and 8.0 μM respectively). |
CD 2314 Dilution Calculator
CD 2314 Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.7435 mL | 13.7174 mL | 27.4348 mL | 54.8697 mL | 68.5871 mL |
5 mM | 0.5487 mL | 2.7435 mL | 5.487 mL | 10.9739 mL | 13.7174 mL |
10 mM | 0.2743 mL | 1.3717 mL | 2.7435 mL | 5.487 mL | 6.8587 mL |
50 mM | 0.0549 mL | 0.2743 mL | 0.5487 mL | 1.0974 mL | 1.3717 mL |
100 mM | 0.0274 mL | 0.1372 mL | 0.2743 mL | 0.5487 mL | 0.6859 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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CD 2314 is a potent and selective agonist of RARβ with Kd value of 145 and >3760 nM for RARβ and RARα receptors, respectively [1].
Retinoic acid receptor β (RARβ) is a nuclear receptor for retinoic acid and localizes to the cytoplasm and subnuclear compartments. RARβ mediates cellular signalling in cell growth, differentiation and embryonic morphogenesis.
CD 2314 is a potent and selective RARβ agonist. CD 2314 didn’t inhibit the activation-induced apoptosis of thymocytes because of the absent of RARβ in the thymus [1]. CD 2314 inhibited cells growth with IC50 values of 8.0, 3.0, 5.7 and >10 μM for human head and neck squamous cell carcinoma (HNSCC) 22A, 22B, 183A and 886 cell lines, respectively. In UMSCC22B cells, the combination of CD2314 with RXR-selective retinoids, such as SR11234, SR11203, SR11246 and SR11236 inhibited cells growth [2]. In KG-1 cells, CD 2314 didn’t induce folate receptor β (FR-β) expression, indicating that the induction of FR-β was not mediated by RARβ [3].
References:
[1]. Szondy Z, Reichert U, Bernardon JM, et al. Inhibition of activation-induced apoptosis of thymocytes by all-trans- and 9-cis-retinoic acid is mediated via retinoic acid receptor alpha. Biochem J, 1998, 331 ( Pt 3): 767-774.
[2]. Sun SY, Yue P, Mao L, et al. Identification of receptor-selective retinoids that are potent inhibitors of the growth of human head and neck squamous cell carcinoma cells. Clin Cancer Res, 2000, 6(4): 1563-1573.
[3]. Xu Y, Wang T, Tang R, et al. All-trans retinoic acid is capable of inducing folate receptor β expression in KG-1 cells. Tumour Biol, 2010, 31(6): 589-595.
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Identification of receptor-selective retinoids that are potent inhibitors of the growth of human head and neck squamous cell carcinoma cells.[Pubmed:10778990]
Clin Cancer Res. 2000 Apr;6(4):1563-73.
Retinoids modulate the growth and differentiation of cancer cells presumably by activating gene transcription via the nuclear retinoic acid receptor (RAR) alpha, beta, and gamma and retinoid X receptor (RXR) alpha, beta, and gamma. We analyzed the effects of 38 RAR-selective and RXR-selective retinoids on the proliferation of 10 human head and neck squamous cell carcinoma (HNSCC) cell lines. All of these cell lines expressed constitutively all of the receptor subtypes except RARbeta, which was detected in only two of them. Most of the RAR-selective retinoids inhibited the growth of HNSCC cells to varying degrees, whereas the RXR-selective retinoids showed very weak or no inhibitory effects. Three RAR antagonists suppressed growth inhibition by RAR-selective agonists, as well as by RAR/RXR panagonists such as 9-cis-retinoic acid. Combinations of RXR-selective and RAR-selective retinoids exhibited additive growth-inhibitory effects. Furthermore, we found that CD437, the most potent growth-inhibitory retinoid induced apoptosis and up-regulated the expression of several apoptosis-related genes in HNSCC cells. These results indicate that: (a) retinoid receptors are involved in the growth-inhibitory effects of retinoids; (b) RXR-RAR heterodimers rather than RXR-RXR homodimer are the major mediators of growth inhibition by retinoids in HNSCC cells; and (c) induction of apoptosis can account for one mechanism by which retinoids such as CD437 inhibit the growth of HNSCC cells. Finally, these studies identified several synthetic retinoids, which are much more effective than the natural RAs and can be good candidates for chemoprevention and therapy of head and neck cancers.
Inhibition of activation-induced apoptosis of thymocytes by all-trans- and 9-cis-retinoic acid is mediated via retinoic acid receptor alpha.[Pubmed:9560303]
Biochem J. 1998 May 1;331 ( Pt 3):767-74.
Thymocytes can be induced to undergo apoptotic cell death by activation through the T-cell receptor (TCR). This process requires macromolecular synthesis and has been shown to be inhibited by retinoic acids (RAs). Two groups of nuclear receptors for RAs have been identified: retinoic acid receptors (RARs) and retinoid X receptors (RXRs). All-trans-RA is the high-affinity ligand for RARs, and 9-cis-RA additionally binds to RXRs with high affinity. Because 9-cis-RA is much more potent in inhibiting TCR-mediated death than all-trans-RA, it was suggested that RXRs participate in the process. In the present study various synthetic retinoid analogues were used to address this question further. The results presented suggest that the inhibitory effect of RAs on activation-induced death of thymocytes is mediated via RARalpha, because (1) it can be reproduced by various RARalpha analogues both in vitro and in vivo, (2) the effect of RAs can be inhibited by the addition of an RARalpha antagonist, (3) CD4+CD8+thymocytes, which die on TCR stimulation, express RARalpha. Stimulation of RARgamma, in contrast, enhances the activation-induced death of thymocytes and inhibits its prevention by RARalpha stimulation. RXR co-stimulation suspends this inhibitory effect of RARgamma and permits the preventive function of RARalpha on activation-induced death. Our results suggest a complex interaction between the various isoforms of retinoid receptors and demonstrate that low (physiological) concentrations of all-trans-RA do not affect the activation-induced death of thymocytes because the RARalpha-mediated inhibitory and the RARgamma-mediated enhancing pathways are in balance, whereas if 9-cis-RA is formed, additional stimulation of RXRs permits the inhibitory action of RARalpha.