Dreiseitel, A; Schreier, P; Oehme, A; Locher, S; Rogler, G; Piberger, H; Hajak, G; Sand, P G (2009). and are poor inhibitors of CYP2D6. Methods and Findings in Experimental and Clinical Pharmacology, 31(1):3-9. Postprint available at: http://www.zora.uzh.ch

University of Zurich Posted at the Zurich Open Repository and Archive, University of Zurich. Zurich Open Repository and Archive http://www.zora.uzh.ch

Originally published at: Methods and Findings in Experimental and Clinical Pharmacology 2009, 31(1):3-9. Winterthurerstr. 190 CH-8057 Zurich http://www.zora.uzh.ch

Year: 2009

Anthocyanins and anthocyanidins are poor inhibitors of CYP2D6

Dreiseitel, A; Schreier, P; Oehme, A; Locher, S; Rogler, G; Piberger, H; Hajak, G; Sand, P G

Dreiseitel, A; Schreier, P; Oehme, A; Locher, S; Rogler, G; Piberger, H; Hajak, G; Sand, P G (2009). Anthocyanins and anthocyanidins are poor inhibitors of CYP2D6. Methods and Findings in Experimental and Clinical Pharmacology, 31(1):3-9. Postprint available at: http://www.zora.uzh.ch

Posted at the Zurich Open Repository and Archive, University of Zurich. http://www.zora.uzh.ch

Originally published at: Methods and Findings in Experimental and Clinical Pharmacology 2009, 31(1):3-9. Anthocyanins and anthocyanidins are poor inhibitors of CYP2D6

Abstract

The cytochrome P450 CYP2D6 isoform is involved in the metabolism of about 50% of all psychoactive drugs, including neuroleptic agents, selective serotonin reuptake inhibitors, selective norepinephrine reuptake inhibitors and tricyclic antidepressants. Therefore, inhibition of cytochrome P450 activity by foodstuffs has implications for drug safety. The present study addresses inhibitory effects of polyphenolic anthocyanins and their aglycons that are found in many dietary fruits and vegetables. Using a chemiluminescent assay, we obtained IC(50) values ranging from 55 microM to > 800 microM for 17 individual compounds. According to earlier data on furanocoumarins from grapefruit extract, CYP2D6 inhibition is achieved in the range of 190-900 nM. As the tested anthocyanins and anthocyanidins were shown to be about 1,000-fold less potent, they are unlikely to interfere with drug metabolism by CYP2D6. Further studies are warranted to examine the effects of the above flavonoids on other CYP isoforms for more detailed toxicity profiles. 1 Anthocyanins and anthocyanidins are poor inhibitors of

2 CYP2D6 3 4 Andrea Dreiseitel1§, Peter Schreier2, Anett Oehme2, Sanja Locher2, Gerhard Rogler3,4, Heidi 5 Piberger3, Goeran Hajak1, Philipp G Sand1 6 7 8 9 1Departments of Psychiatry and 3Internal Medicine I, University of Regensburg, Franz-Josef- 10 Strauss-Allee 11, 93053 Regensburg, Germany 11 2Chair of Food Chemistry, University of Wuerzburg, Am Hubland, 97074 Wuerzburg, 12 Germany 13 4Department of Internal Medicine, University Hospital Zurich, Raemistrasse 100, 8091 14 Zurich, Switzerland 15 16 17 §Corresponding author 18 19 20 Email addresses: 21 AD: [email protected] 22 PS: [email protected] 23 AO: [email protected] 24 SL: [email protected] 25 GR: [email protected] 26 HP: [email protected] 27 GH: [email protected] 28 PGS: [email protected] 29 Abstract

30

31 Background

32 The cytochrome P450 CYP2D6 isoform is involved in the metabolism of about 50% of all

33 psychoactive drugs, including neuroleptic agents, selective serotonin reuptake inhibitors

34 (SSRIs), selective norepinephrine reuptake inhibitors (SNRIs) and tricyclic antidepressants

35 (TCAs). Therefore, inhibition of cytochrome P450 by foodstuffs has implications for drug

36 safety. The present study addresses inhibitory effects of polyphenolic anthocyanins and their

37 aglycons that are found in many dietary fruits and vegetables.

38 Methods

39 Following incubation of membrane preparations containing recombinant human CYP2D6

40 enzyme with anthocyanins and their aglycons, inhibition of enzyme activity was determined

41 using a chemiluminescent assay.

42 Results

43 Both anthocyanins and their aglycons, the anthocyanidins, inhibited CYP2D6 activity in a

44 concentration-dependent manner with IC50 values ranging from 55 µM, for the

45 , to over 800 µM for diglycoside anthocyanins and cyanin.

46 Conclusions

47 According to earlier data on furanocoumarins from grapefruit extract, CYP2D6 inhibition is

48 achieved in the range of 190 to 900 nM. In comparison, the tested anthocyanins and

49 anthocyanidins were shown to be about 1000-fold less potent, and unlikely to interfere with

50 drug metabolism by CYP2D6. However, further studies are invited to examine effects of the

51 above flavonoids on other CYP isoforms for more detailed toxicity profiles.

2 52 Background

53

54 Cytochrome P450 enzymes represent a large family of microsomal heme-containing

55 monooxygenase isoenzymes that are expressed on smooth endoplasmic reticulum membranes

56 by liver hepatocytes, and by cells along the intestinal tract mucosal surface 1. They catalyze

57 the detoxification of a wide variety of xenobiotics such as drugs, biogenic amines derived

58 from food sources, environmental toxins and chemical carcinogens, plus the oxidation of

59 endogenous substances like steroids, fatty acids, prostaglandins and leukotrienes 2,3. In

60 addition, some isoforms have been implicated in the activation of procarcinogens 4,5.

61 Within the P450 super-family, the cytochrome P450 2D6 (CYP2D6) plays a key role in the

62 metabolism of centrally acting drugs, including many neuroleptics 6, selective serotonin

63 reuptake inhibitors (SSRIs) 7, selective norepinephrine reuptake inhibitors (SNRIs) 8 and

64 tricyclic antidepressants (TCAs) 9, by hydroxylation 10, demethylation 11 or

65 dealkylation reactions 3. The human brain’s CYP2D6 expression pattern maps to the

66 dopaminergic system 12 where CYP2D6 converts the endogenous substrate tyramine, which

67 is formed from tyrosine or phenylalanine, to dopamine. This implies that inhibitors may alter

68 tyrosine and dopamine levels via brain CYP2D6.

69 During treatment with psychoactive drugs, CYP2D6 inhibitors from food sources may

70 provoke adverse effects and limit the use of medication. Interactions with enzyme inhibitors

71 have been shown to affect both pharmacokinetic and pharmacodynamic parameters of drugs

72 13,14, and to augment drug toxicity 15. In an estimated 10% of the general population,

73 CYP2D6 substrate metabolism may be seriously compromised owing to an innate deficiency

74 in enzymatic activity 16,17.

75 The opportunity for a food-drug interaction is an everyday occurrence, of which grapefruit

76 juice provides a prominent example. Coadministration of grapefruit juice with many

3 77 therapeutic agents is known to increase the oral bioavailability of common drugs by altering

78 presystemic metabolism, particularly in the intestine 18. Compounds from grapefruit juice

79 that exhibit cytochrome P450 inhibitory activity include furanocoumarins and the flavonoids

80 naringin, quercetin and kaempferol 15. Inhibitory compounds are equally found in black

81 raspberry juice, wild grape juice, black mulberry juice 19, red wine 20 and, presumably, in

82 cranberry juice 21. Recognition of such drug-food interactions has raised concerns over

83 risks that may be posed by functional foods, and specifically, by food enriched with

84 secondary plant metabolites.

85 Among the phenolic compounds for which P450 inhibitory activity is still unknown count

86 anthocyanins. These water-soluble glycosidic derivates of flavylium salts occur in different

87 pH-dependent conformations and are most abundant in berries, grapes and red cabbage,

88 among other foodstuffs 22. When expressed per 100 g fresh weight, approximately 1480 mg

89 of anthocyanins may be obtained from chokeberries 23, 588 mg from bilberries 24, 476

90 mg from black currant, and 322 mg from red cabbage 23. The average dietary per capita and

91 day consumption of anthocyanins was originally estimated at 180 – 215 mg in Western

92 societies 25. More recent calculations from U.S. American surveys have concluded to a

93 daily intake of only 12.5 mg 23 but the actual amount has been shown to vary considerably

94 with sociodemographic and life-style factors 26, plus the seasonal availability of

95 -rich fruits and vegetables 23.

96 In recent years, numerous studies have testified to anthocyanins’ health benefits, greatly

97 promoting their popularitiy. Favourable effects have been described on free radical

98 scavenging and antioxidant systems 27,28,29, on immune defense 30, on inflammation

99 31,32, on sensory functions 33,34, and on parameters of neuroprotection 35,36,37. It has

100 been shown that anthocyanins themselves are not metabolized by cytochrome P450 enzymes

4 101 38 but their ability to interfere with the metabolism of centrally acting drugs via inhibition

102 of CYP2D6 has not been examined.

5 103 Methods

104

105 Chemicals

106 P450-GloTM screening system was purchased from Promega (Mannheim, Germany).

107 Quinidine was obtained from Sigma-Aldrich (Schnelldorf, Germany).

108 , cyanidin-3,5-diglucoside (cyanin), cyanidin-3-galactoside (ideain), cyanidin-3-

109 glucoside (kuromanin), cyanidin-3-rutinoside (keracyanin), , delphinidin-3-

110 glucoside (), , malvidin-3,5-diglucoside (), malvidin-3-galactoside,

111 malvidin-3-glucoside (), , peonidin-3-glucoside, pelargonidin, pelargonidin-3,5-

112 diglucoside (pelargonin), , and procyanidin B2 were purchased from Extrasynthese

113 (Genay, France). All test substances were dissolved and diluted in DMSO.

114

115 CYP2D6 Assay

116 Effects of test substances on CYP2D6 activity were determined using a validated and

117 isoenzyme-specific screening system (P450-GloTM) 39 according to the manufacturer’s

118 protocol. At room temperature, a membrane preparation, containing recombinant human

119 CYP2D6 and cytochrome P450 reductase, was preincubated for 10 minutes with the

120 compound under study and the ethylene glycol ester of luciferin-6’-methylether (luciferin-ME

121 EGE), a luminogenic substrate. The assay was perfomed in 96-well microtiter plates in KPO4

+ 122 buffer. NADP , glucose-6-phosphate, MgCl2, and glucose-6-phosphate dehydrogenase served

123 as a NADPH regeneration system, and were added to start the enzymatic reaction. Final

124 concentrations in the assay were 0.25 pmol CYP2D6, 100 mM KPO4, 30 µM luciferin-ME

+ 125 EGE, 1.3 mM NADP , 3.3 mM glucose-6-phosphate, 3.3 mM MgCl2, 0.4 U/ml glucose-6-

126 phosphate dehydrogenase, and 50 µM sodium citrate. Subsequent to incubation at room

127 temperature for 45 min, the reaction was stopped and a luminescent signal was initiated by

128 adding a detection reagent, containing an esterase and a firefly luciferase. After another 20

6 129 minutes, chemiluminescence values, displayed as relative light units (RLU), were recorded on

130 an Anthos Lucy 1 microplate luminometer (Anthos Labtech, Salzburg, Austria) with a

131 measuring time of 12 s for each well.

132 Anthocyanins, anthocyanidins and procyanidin B2 were diluted with DMSO to yield final

133 concentrations ranging from 20 to 800 µM in the assay. Quinidine was diluted to final

134 concentrations of 1, 10, 100 and 1000 nM.

135

136 Data analysis

137 For quantification of CYP2D6 inhibition, enzyme activity was calculated using the light

138 signal generated by oxidation of luciferin which, in turn, is produced by CYP2D6

139 demethylation of the substrate luciferin-ME EGE. As the amount of light is directly

140 proportional to the amount of luciferin released in the reaction with CYP2D6, the following

141 equation applies:

 AI  142 A 1100%    ADMSO 

143 where %A is the percentage of CYP2D6 activity remaining after the exposure to test

144 substances, AI is the activity in the presence of an inhibitor, and ADMSO is the enzyme activity

145 in the absence of inhibitors (control).

146 For each substance tested, mean values were analyzed from three separate experiments

147 performed in triplicate at up to five concentrations steps, using a non-linear regression model

148 to determine the concentration inhibiting 50% of maximum CYP2D6 activity (Prism v. 2.01,

149 GraphPad Software, CA, USA). For assessing possible effects of structural features

150 (anthocyanin sugar moiety and substitution pattern of the flavonoids’ B-ring) on CYP2D6

151 inhibition, we performed analysis of variance (ANOVA) (Stata 8, Stata Corp., College

152 Station, TX, USA). Statistical significance was set at p = 0.05. ISIS/Draw v. 2.1.4 (MDL

153 Information Systems, CA, USA) served to illustrate structures of anthocyanidins.

7 154 Results

155

156 In total, modulatory effects of sixteen anthocyanins and anthocyanidins on cytochrome P450

157 2D6 activity were investigated, plus effects of the natural anthocyanin precursor procyanidin

158 B2, an epicatechin-epicatechin dimer (figure 1). IC50 values of all flavonoids under study are

159 summarized in table 1. Test compounds inhibited CYP2D6 activity in a concentration-

160 dependent manner with IC50 values starting at 55 µM (pelargonidin), and exceeding 800 µM

161 (diglucosides of cyanidin and pelargonidin, procyanidin B2).

162 The four most potent inhibitors were the anthocyanidins pelargonidin, peonidin, delphinidin

163 and cyanidin, with IC50 values of 55, 59, 66, and 69 µM, respectively. For the remaining

164 anthocyanidins, IC50 values of 77 (malvidin) and 150 µM (petunidin) were determined.

165 Regarding the tested anthocyanins, IC50 values from 70 to 266 µM were obtained in the order

166 of decreasing potency for malvidin-3-glucoside, malvidin-3-galactoside, delphinidin-3-

167 glucoside, malvidin-3,5-diglucoside, cyanidin-3-glucoside, peonidin-3-glucoside, cyanidin-3-

168 galactoside, and cyanidin-3-rutinoside. Finally, the least potent inhibitors were identified as

169 the diglucosidic anthocyanins pelargonidin-3,5-diglucoside, plus cyanidin-3,5-diglucoside

170 and procyanidin B2, all of which featured IC50 values greater than 800 µM. Quinidine, a

171 widely used inhibitor that had been chosen for a reference, reached an IC50 value of 6 nM.

172 To investigate the modulatory effects of substances’ sugar moiety or B-ring substitution

173 pattern, analysis of variance (ANOVA) was performed, excluding cyanidin-3,5-diglucoside

174 and pelargonidin-3,5-diglucoside, for which IC50 values could not be calculated (> 800 µM).

175 When only presence vs. absence of the sugar moiety was used to predict IC50 values, the

176 model reached significance (p = 0.03, F = 5.7, R2 = 0.32). Fitting was improved when the

177 number of B-ring substituents, plus an interaction term (sugar moiety*substituents) were

178 included in the model (p = 0.006, F = 7.73, R2 = 0.78). Specifically, anthocyanins were shown

179 to be weaker CYP2D6 inhibitors than anthocyanidins (table 1), and CYP2D6 inhibition 8 180 decreased with more substituents on anthocyanidins’ B-ring, whereas it increased with more

181 substituents on anthocyanins’ B-ring.

9 182 Discussion

183

184 Dietary supplementations with anthocyanin-rich fruit extracts have been advocated in the

185 light of multiple health-promoting effects including antioxidant, anti-inflammatory, and

186 neuroprotective activities 40,41,42,43,44. However, limited data exist on possible adverse

187 effects as a consequence of food-drug interactions. Foods that contain complex mixtures of

188 phytochemicals, such as fruits, vegetables, herbs, spices and teas have great potential to

189 induce or inhibit the activity of drug-metabolizing enzymes, including cytochrome P450

190 enzymes 45,46. Such interactions are exemplified by effects of grapefruit juice, red wine,

191 black mulberry juice and black raspberry juice 13,15,18,19,20,47,48,49. Amidst growing

192 safety concerns, the present study addresses in vitro interactions with CYP2D6, an isoform

193 highly relevant to the metabolism of many psychoactive drugs 17,50,51,52,53. In

194 continuation of earlier studies with grapefruit extract 15 and the polyphenolic apple

195 constituent quercetin 54,55, CYP2D6 activity was determined in the presence of

196 anthocyanins, the corresponding aglycons, and the procyanidin dimer B2.

197 Our data show that anthocyanins and anthocyanidins are weak inhibitors of CYP2D6, with

198 IC50 values in the micromolar range, starting at 55 µM and exceeding 800 µM for several

199 compounds. When anthocyanins and anthocyanidins were compared, mean inhibitory potency

200 of anthocyanins was lower (p = 0.03, F = 5.7, R2 = 0.32). Of all molecules under study,

201 diglucosides of cyanidin and pelargonidin, plus procyanidin B2 exhibited the weakest effects.

202 Analysis of variance confirmed a modulatory role of the B-ring substitution pattern (number

203 of substituents), plus the interaction term (sugar moiety*substituents). Anthocyanidins with

204 three hydroxyl- or methoxyl-substituents on their B-ring acted as weaker inhibitors than did

205 agents with fewer substituents. In contrast, anthocyanidin-3-glycosides and anthocyanidin-

10 206 3,5-diglycosides achieved lower IC50 values when the B-ring was substituted to a greater

207 extent.

208 Only few data are available on CYP2D6 inhibitory effects of defined polyphenolic

209 compounds. Of these, quercetin exhibited an IC50 value of 24 µM 55, while flavonols and

210 flavonol glycosides from wild ginger exhibited IC50 values ranging from 5 to 51 µM 56. In

211 contrast, furanocoumarins from grapefruit juice achieved 50% inhibition in the nanomolar

212 range. Specifically, bergamottin, 6’,7’-dihydroxybergamottin (DHB) and the dimerics GF-I-1

213 (4-[[6-hydroxy-7-[[1-[(1-hydroxy-1-methyl)ethyl]-4-methyl-6-(7-oxo-7H-furo[3,2-

214 g][1]benzopyran-4-yl)-4-hexenyl]oxy]-3,7-dimethyl-2-octenyl]oxy]-7H-furo[3,2-

215 g][1]benzopyran-7-one) and GF-I-4 (4-[[6-hydroxy-7-[[4-methyl-1-(1-methylethenyl)-6-(7-

216 oxo-7H-furo[3,2-g][1]benzopyran-4-yl)-4-hexenyl]oxy]-3,7-dimethyl-2-octenyl]oxy]-7H-

217 furo[3,2-g][1]benzopyran-7-one) reached IC50 values of 190 nM, 900 nM, 200 nM and 300

218 nM, respectively 15. For comparison, psychoactive drugs have yielded CYP2D6 IC50 values

219 of 1.2 (paroxetine), 1.5 (perphenazine), 2.7 (thioridazine) and 6.5 nM (haloperidol) 57,58,59

220 (figure 2).

221 Inhibitory effects of anthocyanins on CYP2D6 are weaker by several orders of magnitude,

222 ranging from 70 µM to over 800 µM. According to in silico prediction models, structural

223 features required for effective CYP2D6 inhibition comprise a tertiary amine fragment plus a

224 positive charge on nitrogen and flat hydrophobic region 60. These ligand descriptors are not

225 met by the compounds investigated here, and relative to the cinchona alkaloid quinidine, the

226 inhibitory potential of anthocyanins and their aglycons was at least 10 000-fold lower. This

227 suggests that anthocyanins pose a limited risk of food-drug interactions mediated by CYP2D6

228 as compared to above mentioned grapefruit and apple constituents, or other phytochemicals.

229 For an extrapolation of in vitro data to in vivo effects, additional parameters must be taken

230 into account. Thus it has been proposed that CYP2D6 may be less susceptible to inhibition by

231 food constituents than other isoforms, since substances must cross the intestinal barrier before 11 232 they can act on hepatic CYP2D6, whereas high-level expression of other cytochromes in the

233 intestine allows interactions during digestion 61. Depending on anthocyanins’ in vivo portal

234 availability which has yet to be determined, the impact on metabolic processes may be even

235 smaller than anticipated.

236 Clinical relevance of CYP450 inhibition is subject to individual differences in enzyme

237 activity, i.e. the prevalence of functional genetic variants. The present data obtained with

238 recombinant human CYP2D6 count against CYP2D6 modulatory effects of anthocyanins and

239 anthocyanidins for subjects carrying the CYP2D6*1 allele 62, i.e. for the majority of the

240 Caucasian population. Whether similar effects can be expected in carriers of other CYP2D6

241 alleles remains to be determined.

242 Finally, characterization of anthocyanin effects on additional CYP450 isoforms is invited to

243 foster our understanding of polyphenolics’ biological activity. Thus inhibitors of

244 procarcinogen-activating isoforms (e.g., CYP19, CYP1A or CYP1B) may limit the generation

245 of harmful metabolites from estradiol 5, aromatic amines, heterocyclic amines 4, and

246 polycyclic aromatic hydrocarbons 5. More detailed toxicity profiles will help to unveil the

247 related benefits and novel dietary or medical applications of anthocyanins.

12 248 Conclusions

249

250 Anthocyanin-rich extracts from berry fruits have become popular food supplements

251 warranting investigations of possible interactions with drug metabolism. The present in vitro

252 study argues against such interactions with regard to metabolism by the human cytochrome

253 2D6 isoenzyme. In comparison to established enzyme inhibitors, the flavonoids examined

254 proved weaker by several orders of magnitude. However, further studies are invited to

255 examine effects of anthocyanins on other CYP isoforms for more detailed toxicity profiles.

13 256 Competing interests

257 The authors declare that they have no competing interests.

258

259 Authors’ contributions

260 AD carried out the CYP2D6 inhibition measurements, performed statistical analyses and

261 drafted the manuscript. PS, GR, HP and GH participated in study design, revised the

262 manuscript critically and finalized it for submission. AO and SL assisted with conceiving the

263 study, selecting test substances and writing the manuscript. PGS was responsible for

264 conception and design of the study, supervision of statistical analysis and helped draft the

265 manuscript. All authors read and approved the final manuscript.

266

267 Acknowledgement

268 This investigation was funded by the German Federal Ministry of Education, Science,

269 Research and Technology, BMBF – grant No. 0313848C.

270

271

272

273

274

275 Table 1. Inhibition of CYP2D6 activity by anthocyanins and anthocyanidins and mean IC50 values. 276 IC in µM IC in µM anthocyanin/anthocyanidin 50 50 (anthocyanidins) (anthocyanins) pelargonidin 55 [51 - 59]

peonidin 59 [51 - 67]

delphinidin 66 [65 - 68]

14 cyanidin 69 [64 - 74]

malvidin-3-glucoside (oenin) 70 [68 - 72]

malvidin-3-galactoside 73 [67 - 80]

malvidin 77 [69 - 85]

delphinidin-3-glucoside (myrtillin) 109 [87 - 137]

malvidin-3,5-diglucoside (malvin) 145 [133 - 157]

petunidin 150 [138 - 162]

cyanidin-3-glucoside (kuromanin) 151 [114 - 199]

peonidin-3-glucoside 217 [199 - 237]

cyanidin-3-galactoside (ideain) 245 [217 - 278]

cyanidin-3-rutinoside (keracyanin) 266 [169 - 420]

mean IC50 value +/ SD 79 +/ 32 160 +/ 71 277 278 95% confidence intervals are given in brackets. Procyanidin B2, plus the anthocyanins pelargonidin-3,5- 279 diglucoside (pelargonin) and cyanidin-3,5-diglucoside (cyanin) lacked CYP2D6 inhibitory activity (IC50 > 800 280 µM). 281 282

283

284 A R1 R2

+ B OH O R3 CA OH

285 OH 286 anthocyanidin R1 R2 R3

cyanidin OH OH H

delphinidin OH OH OH

15 malvidin O-CH3 OH O-CH3

pelargonidin H OH H

peonidin O-CH3 OH H

petunidin O-CH3 OH OH 287 B 300 OH HO R 200 R O OH OH HO 100 HO R OH R R 10.0 O OH

7.5HO

IC50 values in µM in IC50 values OH 288 5.0 289 290 2.5 291 0.0 anthocyanins anthocyanidins psychoactive drugs furanocoumarins quinidine 292

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23 463 Figures

464

465 Figure 1 – Chemical structures

466 Chemical structures of tested anthocyanidins (A) and procyanidin B2 (B),

467 an epicatechin-epicatechin dimer.

468

469 Figure 2 – IC50 values of anthocyanins, anthocyanidins, psychoactive drugs

470 (haloperidol, thioridazine, perphenazine, paroxetine), furanocoumarins (bergamottin,

471 6’,7’-DHB, GF-I-1, GF-I-4) and quinidine.

472 Only those compounds are shown for which IC50 values were available, i.e. excluding

473 cyanidin-3,5-diglucoside and pelargonidin-3,5-diglucoside.

474

475 Table

476 Table 1 - Inhibition of CYP2D6 activity by anthocyanins and anthocyanidins and mean

477 IC50 values

478 95% confidence intervals are given in brackets. Procyanidin B2, plus the anthocyanins

479 pelargonidin-3,5-diglucoside (pelargonin) and cyanidin-3,5-diglucoside (cyanin) lacked

480 CYP2D6 inhibitory activity (IC50 > 800 µM).

24