RhododendrolCAS# 501-96-2 |
- (+)-Rhododendrol
Catalog No.:BCN7091
CAS No.:59092-94-3
- Rhododenol
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 501-96-2 | SDF | Download SDF |
PubChem ID | 919205 | Appearance | Powder |
Formula | C10H14O2 | M.Wt | 166.2 |
Type of Compound | Phenols | Storage | Desiccate at -20°C |
Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
Chemical Name | 4-[(3R)-3-hydroxybutyl]phenol | ||
SMILES | CC(CCC1=CC=C(C=C1)O)O | ||
Standard InChIKey | SFUCGABQOMYVJW-MRVPVSSYSA-N | ||
Standard InChI | InChI=1S/C10H14O2/c1-8(11)2-3-9-4-6-10(12)7-5-9/h4-8,11-12H,2-3H2,1H3/t8-/m1/s1 | ||
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 | 1. (+)-Rhododendrol and epi-rhododendrin have anti-inflammatory effect, they can suppress the NO production by activated macrophages in vivo. 2. Rhododendrol is an inhibitor of melanin synthesis developed for lightening/whitening cosmetics, it can competitively inhibit mushroom tyrosinase and serve as a good substrate, while it also shows cytotoxicity against cultured human melanocytes at high concentrations sufficient for inhibiting tyrosinase. |
Targets | NO |
Rhododendrol Dilution Calculator
Rhododendrol Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 6.0168 mL | 30.0842 mL | 60.1685 mL | 120.3369 mL | 150.4212 mL |
5 mM | 1.2034 mL | 6.0168 mL | 12.0337 mL | 24.0674 mL | 30.0842 mL |
10 mM | 0.6017 mL | 3.0084 mL | 6.0168 mL | 12.0337 mL | 15.0421 mL |
50 mM | 0.1203 mL | 0.6017 mL | 1.2034 mL | 2.4067 mL | 3.0084 mL |
100 mM | 0.0602 mL | 0.3008 mL | 0.6017 mL | 1.2034 mL | 1.5042 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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Depigmentation caused by application of the active brightening material, rhododendrol, is related to tyrosinase activity at a certain threshold.[Pubmed:25082450]
J Dermatol Sci. 2014 Oct;76(1):16-24.
BACKGROUND: Tyrosinase, the rate-limiting enzyme required for melanin production, has been targeted to develop active brightening/lightening materials for skin products. Unexpected depigmentation of the skin characterized with the diverse symptoms was reported in some subjects who used a tyrosinase-competitive inhibiting quasi-drug, Rhododendrol. OBJECTIVE: To investigate the mechanism underlying the depigmentation caused by Rhododendrol-containing cosmetics, this study was performed. METHODS: The mechanism above was examined using more than dozen of melanocytes derived from donors of different ethnic backgrounds. The RNAi technology was utilized to confirm the effect of tyrosinase to induce the cytotoxicity of Rhododendrol and liquid chromatography-tandem mass spectrometry was introduced to detect Rhododendrol and its metabolites in the presence of tyrosinase. RESULTS: Melanocyte damage was related to tyrosinase activity at a certain threshold. Treatment with a tyrosinase-specific siRNA was shown to dramatically rescue the Rhododendrol-induced melanocyte impairment. Hydroxyl-Rhododendrol was detected only in melanocytes with higher tyrosinase activity. When an equivalent amount of hydroxyl-Rhododendrol was administered, cell viability was almost equally suppressed even in melanocytes with lower tyrosinase activity. CONCLUSION: The generation of a tyrosinase-catalyzed hydroxyl-metabolite is one of the causes for the diminishment of the melanocyte viability by Rhododendrol.
Chemical synthesis and tyrosinase inhibitory activity of rhododendrol glycosides.[Pubmed:24332496]
Bioorg Med Chem Lett. 2014 Jan 1;24(1):122-5.
The concise synthesis of Rhododendrol glycosides 3-8, which are novel derivatives of (+)-epirhododendrin (1) and (-)-rhododendrin (2), has been achieved in six steps from benzaldehyde 9. The key reactions include aldol condensation and trichloroacetimidate glycosylation. From biological studies, it has been determined that synthetic derivatives of 1 and 2 possess potent tyrosinase inhibitory activity. Particularly, the inhibitory activity of cellobioside 8 (IC50=1.51muM) is six times higher than that of kojic acid. The R-epimers (4, 6, and 8) possessed more potent activity than the corresponding S-epimers (3, 5, and 7), indicating that tyrosinase inhibitory activity is significantly governed by stereochemistry of Rhododendrol glycosides.
Rhododendrol, a depigmentation-inducing phenolic compound, exerts melanocyte cytotoxicity via a tyrosinase-dependent mechanism.[Pubmed:24890809]
Pigment Cell Melanoma Res. 2014 Sep;27(5):754-63.
Rhododendrol, an inhibitor of melanin synthesis developed for lightening/whitening cosmetics, was recently reported to induce a depigmentary disorder principally at the sites of repeated chemical contact. Rhododendrol competitively inhibited mushroom tyrosinase and served as a good substrate, while it also showed cytotoxicity against cultured human melanocytes at high concentrations sufficient for inhibiting tyrosinase. The cytotoxicity was abolished by phenylthiourea, a chelator of the copper ions at the active site, and by specific knockdown of tyrosinase with siRNA. Hence, the cytotoxicity appeared to be triggered by the enzymatic conversion of Rhododendrol to active product(s). No reactive oxygen species were detected in the treated melanocytes, but up-regulation of the CCAAT-enhancer-binding protein homologous protein gene responsible for apoptosis and/or autophagy and caspase-3 activation were found to be tyrosinase dependent. These results suggest that a tyrosinase-dependent accumulation of ER stress and/or activation of the apoptotic pathway may contribute to the melanocyte cytotoxicity.
(+)-rhododendrol and epi-rhododendrin suppress the NO production by activated macrophages in vivo.[Pubmed:9810263]
Planta Med. 1998 Oct;64(7):598-602.
In this study, we investigated the effect of (+)-Rhododendrol (1) and epi-rhododendrin (2) isolated from Acer nikoense Maxim. (Aceraceae) on nitric oxide (NO) production in mouse peritoneal macrophages elicited by bacillus Calmette-Guerin and in vitro stimulated by lipopolysaccharide. The NO production was not affected by an oral administration of methanol extract at a dose of 100 mg/kg/day. However, the AcOEt soluble fraction significantly reduced the NO production. (+)-Rhododendrol (1) isolated as an active substance from the AcOEt fraction suppressed the NO production. epi-Rhododendrin (2), the glucoside of (+)-Rhododendrol (1) isolated from the n-BuOH fraction, also suppressed the NO production. As NO is one of the critical mediators in inflammation, these results suggest that (+)-Rhododendrol (1) and epi-rhododendrin (2) contribute in part to the anti-inflammatory effect of A. nikoense.