1. 497-76-7
2. Arbutoside
3. Ursin
4. Uvasol
5. P-arbutin
6. Beta-arbutin
7. 4-hydroxyphenyl Beta-d-glucopyranoside
8. P-hydroxyphenyl Beta-d-glucoside
9. 4-hydroxyphenyl-beta-d-glucopyranoside
10. Arbutinum
11. P-hydroxyphenyl Beta-d-glucopyranoside
12. Ursi
13. Hydroquinone-o-beta-d-glucopyranoside
14. Hydroquinone Beta-d-glucopyranoside
15. Ericolin
16. Hydroquinone O-beta-d-glucopyranoside
17. Hydroquinone-glucose
18. Hydroquinone
19. A-d-glucopyranoside
20. (2r,3s,4s,5r,6s)-2-(hydroxymethyl)-6-(4-hydroxyphenoxy)oxane-3,4,5-triol
21. (2r,3s,4s,5r,6s)-2-(hydroxymethyl)-6-(4-hydroxyphenoxy)tetrahydro-2h-pyran-3,4,5-triol
22. C5ina23hxf
23. 4-hydroxyphenyl-.beta.-d-glucopyranoside
24. Chembl232202
25. Chebi:18305
26. Hydroquinone Glucose
27. Nsc-4036
28. Arbutine
29. Arbutyne
30. Hydroquinone-beta-d-glucopyranoside
31. Dsstox_cid_20152
32. Dsstox_rid_79450
33. Dsstox_gsid_40152
34. Nsc 4036
35. Mfcd00016915
36. (2r,3s,4s,5r,6s)-2-(hydroxymethyl)-6-(4-hydroxyphenoxy)tetrahydropyran-3,4,5-triol
37. (2r,3s,4s,5r,6s)-2-(hydroxymethyl)-6-(4-oxidanylphenoxy)oxane-3,4,5-triol
38. Cas-497-76-7
39. Sr-05000002157
40. Unii-c5ina23hxf
41. Ccris 9273
42. B-arbutin
43. Hsdb 7661
44. Uva,p-arbutin
45. Ncgc00095599-01
46. Einecs 207-850-3
47. Beta-d-glucopyranoside, 4-hydroxyphenyl
48. Brn 0089673
49. Spectrum_000786
50. Specplus_000314
51. Arbutin [hsdb]
52. Arbutin [inci]
53. Arbutin, >=98%
54. Arbutin [mi]
55. Arbutinum [hpus]
56. Arbutin [mart.]
57. Prestwick3_001026
58. Spectrum2_000662
59. Spectrum3_001233
60. Spectrum4_001474
61. Spectrum5_000147
62. Arbutin [who-dd]
63. Bmse000365
64. Arbutin (uva, P-arbutin)
65. Arbutin, Analytical Standard
66. Schembl36351
67. Arbutin - Uva - P-arbutin
68. Bspbio_001211
69. Bspbio_002706
70. Hydroquinone-beta-d-glucoside
71. Kbiogr_002047
72. Kbioss_001266
73. Spectrum300539
74. 5-17-07-00110 (beilstein Handbook Reference)
75. Mls002207046
76. Divk1c_006410
77. Spbio_000723
78. Bpbio1_001333
79. Megxp0_001504
80. Dtxsid7040152
81. Kbio1_001354
82. Kbio2_001266
83. Kbio2_003834
84. Kbio2_006402
85. Kbio3_002206
86. Hydroquinone O--d-glucopyranoside
87. Hms2098m13
88. Hms3715m13
89. P-hydroxyphenyl Beta -d-glucoside
90. Zinc518554
91. Hy-n0192
92. 4-hydroxyphenyl-beta-glucopyranoside
93. Hydroquinone Beta -d-glucopyranoside
94. Tox21_111509
95. Tox21_302428
96. B-d-glucopyranoside, 4-hydroxyphenyl
97. Bdbm50219502
98. Ccg-38565
99. S2263
100. Akos015965305
101. Tox21_111509_1
102. Db11217
103. Ks-5252
104. Sdccgmls-0066538.p001
105. P-hydroxyphenyl Beta -d-glucopyranoside
106. Smp1_000028
107. Ncgc00166076-02
108. Ncgc00166076-03
109. Ncgc00166076-04
110. Ncgc00166076-07
111. Ncgc00166076-09
112. Ncgc00255705-01
113. Ac-20183
114. Beta -d-glucopyranoside, 4-hydroxyphenyl
115. Beta-d-glucopyranoside, 4-hydroxyphenyl-
116. I(2)-d-glucopyranoside, 4-hydroxyphenyl
117. Smr001233417
118. A0522
119. Ab00443586
120. Hydroquinone-.beta.-d-glucopyranoside
121. N1714
122. Sw199492-2
123. C06186
124. 4-hydroxyphenyl B-d-glucopyranoside, 9ci, 8ci
125. 497a767
126. A827849
127. Arbutin, Primary Pharmaceutical Reference Standard
128. Q416446
129. Sr-05000002157-2
130. Sr-05000002157-4
131. Alpha-arbutin; 4-hydroquinone-alpha-d-glucopyranoside
132. Arbutin, European Pharmacopoeia (ep) Reference Standard
133. 4e19b706-2013-4401-a1fc-a154dadf42b4
134. (2s,3r,4s,5s,6r)-2-(4-hydroxyphenoxy)-6-methylol-tetrahydropyran-3,4,5-triol
135. 7oq
| Molecular Weight | 272.25 g/mol |
|---|---|
| Molecular Formula | C12H16O7 |
| XLogP3 | -0.7 |
| Hydrogen Bond Donor Count | 5 |
| Hydrogen Bond Acceptor Count | 7 |
| Rotatable Bond Count | 3 |
| Exact Mass | 272.08960285 g/mol |
| Monoisotopic Mass | 272.08960285 g/mol |
| Topological Polar Surface Area | 120 Ų |
| Heavy Atom Count | 19 |
| Formal Charge | 0 |
| Complexity | 279 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 5 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
/EXPL THER/ Although the toxicogenomics of A375 human malignant melanoma cells treated with arbutin have been elucidated using DNA microarray, the proteomics of the cellular response to this compound are still poorly understood. ...This study ... performed proteomic analyses to investigate the anticancer effect of arbutin on the protein expression profile in A375 cells. After treatment with arbutin (8 ug/mL) for 24, 48 and 72 hr, the proteomic profiles of control and arbutin-treated A375 cells were compared, and 26 differentially expressed proteins (7 upregulated and 19 downregulated proteins) were identified by MALDI-Q-TOF MS and MS/MS. Among these proteins, 13 isoforms of six identical proteins were observed. Bioinformatic tools were used to search for protein function and to predict protein interactions. The interaction network of 14 differentially expressed proteins was found to be correlated with the downstream regulation of p53 tumor suppressor and cell apoptosis. In addition, three upregulated proteins (14-3-3G, VDAC-1 and p53) and five downregulated proteins (ENPL, ENOA, IMDH2, PRDX1 and VIME) in arbutin-treated A375 cells were validated by RT-PCR analysis. These proteins were found to play important roles in the suppression of cancer development.
PMID:18996230 Nawarak J et al; Biochim Biophys Acta Oct 18 (Epub ahead of print) (2008)
Indicated for over-the-counter use for epidermal hyperpigmentation in various skin conditions, such as melasma, freckles, and senile lentigines.
At non-toxic concentrations, arbutin inhibited the activity of tyrosinase in cultured human keratinocytes, while having minimal effect on the expression of tyrosinase mRNA or the synthesis of the enzyme. -Arbutin produced a concentration-dependent inhibition of melanin synthesis of human melanoma cells, HMV-II. No inhibitory effect on HMV-II cell growth was seen at concentrations lower than 1.0 mM. At concentrations of 0.5 mM of arbutin, tyrosinase activity was reduced to 60% of that in non-treated cells. The addition of arbutin blocked and inhibited -MSH-stimulated melanogenesis in B16 melanoma cells, brownish guinea pig, and human skin tissue. In a pilot study of healthy male adults exposed to UV B irradiation, topical administration of arbutin inhibited UV-induced nuclear factor-kappaB activation in human keratinocytes. In mouse skin, arbutin counteracted oxidative stress induced by 12-O-tetradecanoylphorbol-13-acetate.
Absorption
Arbutin was found to be extensively absorbed from the gastrointestinal tract where it is primarily converted to hydroquinone.
Route of Elimination
During the first 4 hours following ingestion of a single dose of 210 mg arbutin in healthy volunteers, 224.5 mol/L hydroquinone glucuronide and 182 mol/L of hydroquinone sulfate were recovered in the urine.
Volume of Distribution
No pharmacokinetic data available.
Clearance
No pharmacokinetic data available.
The urinary excretion of arbutin metabolites was examined in a randomized crossover design in 16 healthy volunteers after the application of a single oral dose of bearberry leaves dry extract (BLDE). There were two groups of application using either film-coated tablets (FCT) or aqueous solution (AS). The urine sample analysis was performed by a validated HPLC coolarray method (hydroquinone) and a validated capillary electrophoresis method (hydroquinone-glucuronide, hydroquinone-sulfate). The total amounts of hydroquinone equivalents excreted in the urine from BLDE were similar in both groups. With FCT, 64.8% of the arbutin dose administered was excreted; with AS, 66.7% was excreted (p = 0.61). The maximum mean urinary concentration of hydroquinone equivalents was a little higher and peaked earlier in the AS group versus the FCT group, although this did not reach statistical significance (Cur max = 1.6893 umol/mL vs. 1.1250 umol/mL, p = 0.13; tmax (t midpoint) = 3.60 h vs. 4.40 hr, p = 0.38). The relative bioavailability of FCT compared to AS was 103.3% for total hydroquinone equivalents. There was substantial intersubject variability. No significant differences between the two groups were found in the metabolite patterns detected (hydroquinone, hydroquinone-glucuronide, and hydroquinone-sulfate).
PMID:12162475 Schindler G et al; J Clin Pharmacol 42 (8): 920-7 (2002)
To study the effects of aloesin and arbutin on normal cultured human melanocytes in synergetic method. Building up the system of cultured human melanocytes. The cultured melanocytes in vitro were treated with the mixture of aloesin and arbutin. The cell viability and tyrosinase activity was measured by MTT assay, utilization of L-Dopa as the substrate respectively; melanin content was measured by image analysis system. Furthermore, the effects of the mixture on melanocytes were compared with that of aloesin and arbutin. The mixture of aloesin and arbutin showed an inhibition on tyrosinase activity of human melanocytes and reduced significantly melanin content. Between the mixture and the single use of aloesin or arbutin, there is significant difference (P<0.05). On the other hand, the mixture has little influence on melanocytes viability and there is negative significance. The mixture of aloesin and arbutin can significantly inhibit the tyrosinase activity and melanogenesis of cultured human melanocytes. It showed the effects of aloesin and arbutin in a synergistic manner.
PMID:15623110 Yang ZQ et al; Zhonghua Zheng Xing Wai Ke Za Zhi 20 (5): 369-71 (2004)
Arbutin is readily susceptible to hydrolysis in dilute acids to yield D-glucose and hydroquinone. It is expected that orally administered arbutin is easily hydrolyzed to free hydroquinone molecules by stomach acid. Hydroquinone is further metabolized into the main metabolites, hydroquinone glucuronide and hydroquinone sulfate.
No pharmacokinetic data available.
Arbutin is a hydroquinone glycoside, however the hydroquinone moiety is not solely responsible for the de-pigmentating actions of arbutin. It acts as a competitive inhibitor of tyrosinase enzyme by acting on the L-tyrosine binding site to suppress melanogenesis and mediate its de-pigmenting actions on human skin. Tyrosinase is an enzyme involved in the regulation of rate-limiting steps during the synthesis of melanin; it regulates the conversion of L-tyrosine into L-dopa, and subsequent conversion of L-dopa to L-dopaquinone. Via inhibition of tyrosinase activity in a concentration-dependent manner, arbutin attenuates the production of melanin in melanocytes. While most studies suggest that arbutin has negligible effect on the tyrosinase mRNA expression, a study assessing the effect of arbutin on melanocyte differentiation inducement system using ES cells propose that arbutin may also downregulate the expression of tyrosinase in addition to its inhibitory action on the enzyme. The contradictory findings across studies may be due to previous studies using terminally-differentiated melanocytes and melanoma cells.
...This study ... presents evidence that cotreatment of aloesin and arbutin inhibits tyrosinase activity in a synergistic manner by acting through a different action mechanism. Aloesin or arbutin similarly inhibited enzyme activity of human- and mushroom-tyrosinases with an IC50 value of 0.1 or 0.04 mM, respectively. Lineweaver-Burk plots of the enzyme kinetics data showed that aloesin inhibited tyrosinase activity noncompetitively with a Ki value of 5.3 mM, whereas arbutin did it competitively (Maeda, 1996). We then examined whether cotreatment of these agents inhibits the tyrosinase activity in a synergistic manner. The results showed that 0.01 mM aloesin in the presence of 0.03 mM arbutin inhibited activity of mushroom by 80% of the control value and the reverse was also true. The inhibitory effects were calculated to be synergistic according to the Burgi method. Taken together, we suggest that aloesin along with arbutin inhibits in synergy melanin production by combined mechanisms of noncompetitive and competitive inhibitions of tyrosinase activity.
PMID:10403123 Jin YH et al; Arch Pharm Res 22 (3): 232-6 (1999)
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