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Catalogue Number
BN-O1724
Analysis Method
HPLC,NMR,MS
Specification
98%(HPLC)
Storage
2-8°C
Molecular Weight
166.22
Appearance
Powder
Botanical Source
Structure Type
Phenols
Category
Standards;Natural Pytochemical;API
SMILES
CC(CCC1=CC=C(C=C1)O)O
Synonyms
4-[(3S)-3-Hydroxybutyl]phenol/(+)-Rhododendrol/Benzenepropanol, 4-hydroxy-α-methyl-, (αS)-
IUPAC Name
4-[(3S)-3-hydroxybutyl]phenol
Applications
Density
1.1±0.1 g/cm3
Solubility
Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
Flash Point
153.4±15.5 °C
Boiling Point
315.4±17.0 °C at 760 mmHg
Melting Point
78-78.5℃ (chloroform )
InChl
InChI=1S/C10H14O2/c1-8(11)2-3-9-4-6-10(12)7-5-9/h4-8,11-12H,2-3H2,1H3/t8-/m0/s1
InChl Key
SFUCGABQOMYVJW-QMMMGPOBSA-N
WGK Germany
RID/ADR
HS Code Reference
2933990000
Personal Projective Equipment
Correct Usage
For Reference Standard and R&D, Not for Human Use Directly.
Meta Tag
provides coniferyl ferulate(CAS#:59092-94-3) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
No Technical Documents Available For This Product.
24890809
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.
© 2014 The Authors. Pigment Cell & Melanoma Research Published by John Wiley & Sons Ltd.
ER stress; chemical leukoderma; cytotoxicity; depigmentation; rhododendrol; tyrosinase; vitiligo
Rhododendrol, a depigmentation-inducing phenolic compound, exerts melanocyte cytotoxicity via a tyrosinase-dependent mechanism.
Sasaki M1, Kondo M, Sato K, Umeda M, Kawabata K, Takahashi Y, Suzuki T, Matsunaga K, Inoue S.
2014 Sep
