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    Chemistry

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    Also known as: 520-36-5, 5,7-dihydroxy-2-(4-hydroxyphenyl)-4h-chromen-4-one, Chamomile, Versulin, 4',5,7-trihydroxyflavone, Apigenol
    Molecular Formula
    C15H10O5
    Molecular Weight
    270.24  g/mol
    InChI Key
    KZNIFHPLKGYRTM-UHFFFAOYSA-N
    FDA UNII
    7V515PI7F6
    Apigenin
    5,7,4'-trihydroxy-flavone, one of the FLAVONES.
    1 2D Structure

    Apigenin

    2 Identification
    2.1 Computed Descriptors
    2.1.1 IUPAC Name
    5,7-dihydroxy-2-(4-hydroxyphenyl)chromen-4-one
    2.1.2 InChI
    InChI=1S/C15H10O5/c16-9-3-1-8(2-4-9)13-7-12(19)15-11(18)5-10(17)6-14(15)20-13/h1-7,16-18H
    2.1.3 InChI Key
    KZNIFHPLKGYRTM-UHFFFAOYSA-N
    2.1.4 Canonical SMILES
    C1=CC(=CC=C1C2=CC(=O)C3=C(C=C(C=C3O2)O)O)O
    2.2 Other Identifiers
    2.2.1 UNII
    7V515PI7F6
    2.3 Synonyms
    2.3.1 Depositor-Supplied Synonyms

    1. 520-36-5

    2. 5,7-dihydroxy-2-(4-hydroxyphenyl)-4h-chromen-4-one

    3. Chamomile

    4. Versulin

    5. 4',5,7-trihydroxyflavone

    6. Apigenol

    7. Apigenine

    8. Spigenin

    9. C.i. Natural Yellow 1

    10. 5,7-dihydroxy-2-(4-hydroxyphenyl)chromen-4-one

    11. 5,7,4'-trihydroxyflavone

    12. 5,7-dihydroxy-2-(4-hydroxyphenyl)-4h-1-benzopyran-4-one

    13. Pelargidenon 1449

    14. 5,7-dihydroxy-2-(4-hydroxyphenyl)-4-benzopyrone

    15. Nsc 83244

    16. 2-(p-hydroxyphenyl)-5,7-dihydroxychromone

    17. 4h-1-benzopyran-4-one, 5,7-dihydroxy-2-(4-hydroxyphenyl)-

    18. Uccf 031

    19. Flavone, 4',5,7-trihydroxy-

    20. Chebi:18388

    21. Chembl28

    22. Mfcd00006831

    23. Nsc-83244

    24. 8002-66-2

    25. 7v515pi7f6

    26. Nsc83244

    27. Cas-520-36-5

    28. Dsstox_cid_2391

    29. Dsstox_rid_76568

    30. Dsstox_gsid_22391

    31. 4',5,7-trihydroxyflavone;apigenol;c.i. Natural Yellow 1

    32. Smr000326850

    33. Ccris 3789

    34. 4′,5,7-trihydroxyflavone

    35. Sr-01000075663

    36. Einecs 208-292-3

    37. Brn 0262620

    38. Pelargidenone

    39. Matricaria Oil

    40. Unii-7v515pi7f6

    41. Chamomile Powder

    42. Hsdb 7573

    43. 4der

    44. 4dgm

    45. 4hkk

    46. Naringenin, 18

    47. Prestwick_719

    48. Apigenin, 13

    49. Apegenin

    50. Tocris-1227

    51. 3cf9

    52. St056301

    53. Apigenin [hsdb]

    54. Apigenin [inci]

    55. 4',7-trihydroxyflavone

    56. Apigenin [mi]

    57. Biomolki_000078

    58. Prestwick0_000414

    59. Prestwick1_000414

    60. Prestwick2_000414

    61. Prestwick3_000414

    62. Spectrum2_000428

    63. Spectrum3_001882

    64. Spectrum4_001999

    65. Lopac-a-3145

    66. Apigenin [usp-rs]

    67. Apigenin [who-dd]

    68. Biomolki2_000082

    69. 4,5, 7-trihydroxyflavone

    70. Pelargidenon-1449

    71. Ci Natural Yellow 1

    72. Lopac0_000065

    73. Oprea1_622293

    74. Schembl19428

    75. 4',5,7-trihydroxy-flavone

    76. Apigenin, Analytical Standard

    77. Bspbio_000368

    78. Bspbio_003384

    79. Kbiogr_002565

    80. Spectrum200846

    81. 5-18-04-00574 (beilstein Handbook Reference)

    82. Mls000697626

    83. Mls000859991

    84. Mls001074874

    85. Mls006011839

    86. Bidd:er0135

    87. Divk1c_000798

    88. Schembl222227

    89. Spbio_000416

    90. Spbio_002307

    91. Ghl.pd_mitscher_leg0.1194

    92. Bdbm7458

    93. Bpbio1_000406

    94. Gtpl4136

    95. Megxp0_000176

    96. Uccf-031

    97. Dtxsid6022391

    98. Acon1_002450

    99. Cid_5280443

    100. Hms502h20

    101. Kbio1_000798

    102. Kbio3_002887

    103. Ninds_000798

    104. Bio1_000376

    105. Bio1_000865

    106. Bio1_001354

    107. Hms1569c10

    108. Hms1922p22

    109. Hms2096c10

    110. Hms2230d17

    111. Hms3260m11

    112. Hms3267d21

    113. Hms3373b18

    114. Hms3412a08

    115. Hms3561p09

    116. Hms3655d18

    117. Hms3676a08

    118. Hms3866d03

    119. Apigenin, >=95.0% (hplc)

    120. 4',5,7-trihydroxyflavone, 97%

    121. Bcp28288

    122. Hy-n1201

    123. Zinc3871576

    124. Tox21_201542

    125. Tox21_302884

    126. Tox21_500065

    127. Apigenin; 4',5,7-trihydroxyflavone

    128. Bbl010499

    129. Ccg-40061

    130. Hsci1_000221

    131. Lmpk12110005

    132. Nsc815095

    133. S2262

    134. Stk801630

    135. Zb1873

    136. Akos002140699

    137. Ac-8011

    138. Cs-5432

    139. Db07352

    140. Lp00065

    141. Nd-9076

    142. Nsc-815095

    143. Sdccgmls-0066379.p001

    144. Sdccgsbi-0050053.p003

    145. Idi1_000798

    146. Smp2_000338

    147. Apigenin, >=97% (tlc), From Citrus

    148. Ncgc00015049-01

    149. Ncgc00015049-02

    150. Ncgc00015049-03

    151. Ncgc00015049-04

    152. Ncgc00015049-05

    153. Ncgc00015049-06

    154. Ncgc00015049-07

    155. Ncgc00015049-08

    156. Ncgc00015049-09

    157. Ncgc00015049-10

    158. Ncgc00015049-11

    159. Ncgc00015049-12

    160. Ncgc00015049-13

    161. Ncgc00015049-14

    162. Ncgc00015049-15

    163. Ncgc00015049-16

    164. Ncgc00015049-18

    165. Ncgc00015049-28

    166. Ncgc00025057-01

    167. Ncgc00025057-02

    168. Ncgc00025057-03

    169. Ncgc00025057-04

    170. Ncgc00025057-05

    171. Ncgc00025057-06

    172. Ncgc00025057-07

    173. Ncgc00025057-08

    174. Ncgc00025057-09

    175. Ncgc00169835-01

    176. Ncgc00169835-02

    177. Ncgc00169835-03

    178. Ncgc00256419-01

    179. Ncgc00259092-01

    180. Ncgc00260750-01

    181. Ly080400

    182. Nci60_041830

    183. Sy005957

    184. Ts-00897

    185. Ly 080400

    186. Ly-080400

    187. Eu-0100065

    188. Ft-0622445

    189. Ft-0623582

    190. Ft-0662251

    191. N1828

    192. Sw196866-2

    193. 20a365

    194. A 3145

    195. C01477

    196. K00045

    197. O11338

    198. Apigenin 100 Microg/ml In Acetonitrile:methanol

    199. Apigenin, >=97% (tlc), From Parsley, Powder

    200. Biochem Biophys Res Comm 212: 767 (1997)

    201. 5,7-dihydroxy-2-(4-hydroxyphenyl)-chromen-4-one

    202. A828903

    203. Apigenin (constituent Of Chamomile) [dsc]

    204. Apigenin, Primary Pharmaceutical Reference Standard

    205. Q424567

    206. 4 Inverted Exclamation Mark ,5,7-trihydroxyflavone

    207. Q-100586

    208. Q-200822

    209. Sr-01000075663-1

    210. Sr-01000075663-3

    211. Sr-01000075663-7

    212. Sr-01000075663-8

    213. Brd-k01493881-001-10-4

    214. Brd-k01493881-001-17-9

    215. 5,7-dihydroxy-2-(4-hydroxyphenyl)-4h-chromen-4-one #

    216. 4h-1-benzopyran-4-one,7-dihydroxy-2-(4-hydroxyphenyl)-

    217. D50a2d8a-6d8b-4708-b21e-2de9580d033f

    218. Apigenin, United States Pharmacopeia (usp) Reference Standard

    2.4 Create Date
    2004-09-16
    3 Chemical and Physical Properties
    Molecular Weight 270.24 g/mol
    Molecular Formula C15H10O5
    XLogP31.7
    Hydrogen Bond Donor Count3
    Hydrogen Bond Acceptor Count5
    Rotatable Bond Count1
    Exact Mass270.05282342 g/mol
    Monoisotopic Mass270.05282342 g/mol
    Topological Polar Surface Area87 Ų
    Heavy Atom Count20
    Formal Charge0
    Complexity411
    Isotope Atom Count0
    Defined Atom Stereocenter Count0
    Undefined Atom Stereocenter Count0
    Defined Bond Stereocenter Count0
    Undefined Bond Stereocenter Count0
    Covalently Bonded Unit Count1
    4 Drug and Medication Information
    4.1 Therapeutic Uses

    /EXPL THER/ ... This report ... shows ... that apigenin markedly induces the expression of death receptor 5 (DR5) and synergistically acts with exogenous soluble recombinant human tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) to induce apoptosis in malignant tumor cells. TRAIL is a promising candidate for cancer therapeutics due to its ability to selectively induce apoptosis in cancer cells. The combined use of apigenin and TRAIL at suboptimal concentrations induces Bcl-2-interacting domain cleavage and the activation of caspases-8, -10, -9, and -3. Furthermore, human recombinant DR5/Fc chimera protein and caspase inhibitors dramatically inhibit apoptosis induced by the combination of apigenin and TRAIL. On the other hand, apigenin-mediated induction of DR5 expression is not observed in normal human peripheral blood mononuclear cells. Moreover, apigenin does not sensitize normal human peripheral blood mononuclear cells to TRAIL-induced apoptosis. These results suggest that this combined treatment with apigenin and TRAIL might be promising as a new therapy against malignant tumors.

    PMID:16648565 Horinaka M et al; Mol Cancer Ther 5(4):945-51 (2006)

    /EXPL THER/ ... The protective role of apigenin was examined against the oxidative stress caused by N-nitrosodiethylamine (NDEA) and phenobarbital (PB) in Wistar albino rats. Oxidative stress was measured in terms of lipid peroxidation (LPO) and protein carbonyl formation. Oxidative stress-induced DNA damage was measured by single cell gel electrophoresis (comet assay). Apigenin exhibited its antioxidant defense against NDEA-induced oxidative stress ... Minimal levels of LPO and DNA damage in apigenin-treated hepatoma bearing animals /were observed/.

    PMID:15924350 Jeyabal PV et al; Mol Carcinog 44(1):11-20 (2005)

    5 Pharmacology and Biochemistry
    5.1 Absorption, Distribution and Excretion

    Four hours after administration of a flavonoid glycoside extract (corresponding to 0.942 mg aglycones) by gavage, the aglycone of apigenin was observed in the lumen and the wall of the stomach, in the lumen of the small intestine and in the lumen and wall of the cecum in Wistar rats. The evidence of glycosides in the stomach wall suggested that the absorption of flavonoids did not require the presence of their aglycones. Under the study conditions, no renal excretion of apigenin was detected ...

    Pforte H et al; Nahrung 43(3): 205-208 (1999). As cited in SUMMARY OF DATA FOR CHEMICAL SELECTION: Apigenin 19p. (2000) prepared for NCI. Available from, as of March 20, 2008: https://ntp-server.niehs.nih.gov/

    Apigenin appears to be absorbable by humans after intake of parsley (Petroselinum crispum). In a randomized crossover study with two one-week intervention periods in succession, fourteen volunteers consumed a diet that included 20 g parsley. The urinary excretion of apigenin was significantly higher (P < 0.05) during the intervention with parsley (20.7 to 5727.3 g/24 hr) than during the basic diet (0 to 1571.7 g/24 hr). The half-life for apigenin was calculated to be on the order of 12 hr. Significant individual variation in the bioavailability and excretion of apigenin was observed ...

    Nielsen SE et al; Br J Nutr 81: 447-455 (1999). As cited in SUMMARY OF DATA FOR CHEMICAL SELECTION: Apigenin 19p. (2000) prepared for NCI. Available from, as of March 20, 2008: https://ntp-server.niehs.nih.gov/

    ... Eleven healthy subjects (5 women, 6 men) in the age range of 23 to 41 years and with an average body mass index of 23.9 + or - 4.1 kg/sq m took part in this study. After an apigenin- and luteolin-free diet, a single oral bolus of 2 g blanched parsley (corresponding to 65.8 + or - 15.5 umol apigenin) per kilogram body weight was consumed. Blood samples were taken at 0, 4, 6, 7, 8, 9, 10, 11 and 28 hr after parsley consumption and 24-hour urine samples were collected ... On average, a maximum apigenin plasma concentration of 127 + or - 81 nmol/L was reached after 7.2 + or - 1.3 hr with a high range of variation between subjects. For all participants, plasma apigenin concentration rose after bolus ingestion and fell within 28 hr under the detection limit (2.3 nmol/L). The average apigenin content in 24-hour urine was 144 + or - 110 nmol/24 hr corresponding to 0.22 + or - 0.16% of the ingested dose. The flavone could be detected in red blood cells without showing dose-response characteristics.

    PMID:16407641 Meyer H et al; Ann Nutr Metab 50(3):167-72 (2006)

    ... The present paper shows the study of the absorption and excretion of luteolin and apigenin in rats after a single oral dose of Chrysanthemum morifolium extract (CME) (200 mg/kg). The levels of luteolin and apigenin in plasma, urine, feces, and bile were measured by HPLC after deconjugation with hydrochloric acid or beta-glucuronidase/sulfatase. The results showed that the plasma concentrations of luteolin and apigenin reached the highest peak level at 1.1 and 3.9 hr after dosing, respectively. The area under the concentration-time curves (AUC) for luteolin and apigenin were 23.03 and 237.6 ug h/mL, respectively. The total recovery of the dose was 37.9% (6.6% in urine; 31.3% in feces) for luteolin and 45.2% (16.6% in urine; 28.6% in feces) for apigenin. The cumulative luteolin and apigenin excreted in the bile was 2.05% and 6.34% of the dose, respectively. All of the results suggest apigenin may be absorbed more efficiently than luteolin in CME in rats, and both luteolin and apigenin have a slow elimination phase, with a quick absorption, so a possible accumulation of the two flavonoids in the body can be hypothesized.

    PMID:17227053 Chen T et al; J Agric Food Chem 55(2):273-7 (2007)

    After a single oral administration of radiolabeled apigenin /to rats/, 51.0% of radioactivity was recovered in urine, 12.0% in feces, 1.2% in the blood, 0.4% in the kidneys, 9.4% in the intestine, 1.2% in the liver, and 24.8% in the rest of the body within 10 days. Sex differences appear with regard to the nature of compounds eliminated via the urinary route: immature male and female rats, like mature female rats, excreted a higher percentage of the mono-glucuronoconjugate of apigenin than the mono-sulfoconjugate of apigenin (10.0 to 31.6% versus 2.0 to 3.6%, respectively). Mature male rats excreted the same compounds in an inverse ratio (4.9% and 13.9%, respectively). Radioactivity appeared in the blood only 24 hr after oral administration. Blood kinetics showed a high elimination half-time (91.8 hr), a distribution volume of 259 mL, and a plasmatic clearance of 1.95 mL/hr. All of the parameters calculated from these experiments suggested a slow metabolism of apigenin, with a slow absorption and a slow elimination phase. Thus, a possible accumulation of this flavonoid in the body can be hypothesized.

    PMID:15466493 Gradolatto A et al; Drug Metab Dispos 33(1):49-54 (2005)

    5.2 Metabolism/Metabolites

    Ether extracts of the urine of male Wistar rats administered apigenin (200 mg) orally contained the phenolic acid metabolites phydroxyphenylpropionic acid, p-hydroxycinnamic acid, and p-hydroxybenzoic acid. Unreacted apigenin, partially characterized apigenin glucuronides, and ethereal sulfates were also identified. With the exception of p-hydroxybenzoic acid and the apigenin conjugates, all of the metabolites detected in the urine after oral administration were also formed in vitro by rat intestinal microorganisms under anaerobic conditions ... In contrast, these metabolites were not detected in SENCAR mice treated topically with apigenin. Furthermore, no evidence of metabolites were observed from the HPLC profiles of epidermal extracts from apigenin-treated mice ...

    Griffiths LA, Smith GE; Biochem J 128: 901-911 (1972). As cited in SUMMARY OF DATA FOR CHEMICAL SELECTION: Apigenin 19p. (2000) prepared for NCI. Available from, as of March 20, 2008: https://ntp-server.niehs.nih.gov/

    The main in vitro metabolite of apigenin in rat liver Aroclor 1254-induced microsomes has been identified tentatively as the corresponding 3'-hydroxylated compound, luteolin. Apigenin itself is the 3'-hydroxylated metabolite of chrysin ...

    Nielsen SE et al; Xenobiotica 28(4): 389-401 (1998). As cited in SUMMARY OF DATA FOR CHEMICAL SELECTION: Apigenin 19p. (2000) prepared for NCI. Available from, as of March 20, 2008: https://ntp-server.niehs.nih.gov/

    Apigenin has known human metabolites that include (2S,3S,4S,5R)-3,4,5-Trihydroxy-6-[5-hydroxy-2-(4-hydroxyphenyl)-4-oxochromen-7-yl]oxyoxane-2-carboxylic acid.

    S73 | METXBIODB | Metabolite Reaction Database from BioTransformer | DOI:10.5281/zenodo.4056560

    5.3 Biological Half-Life

    ... The half-life for apigenin was calculated to be on the order of 12 hr ...

    Nielsen SE et al; Br J Nutr 81: 447-455 (1999). As cited in SUMMARY OF DATA FOR CHEMICAL SELECTION: Apigenin 19p. (2000) prepared for NCI. Available from, as of March 20, 2008: https://ntp-server.niehs.nih.gov/

    5.4 Mechanism of Action

    The dietary flavonoid apigenin (Api) has been demonstrated to exert multiple beneficial effects upon the vascular endothelium. The aim of this study was to examine whether Ca(2+)-activated K(+) channels (K(Ca)) are involved in endothelial nitric oxide (NO) production and antiangiogenic effects ... Endothelial NO generation was monitored using a cyclic guanosine monophosphate radioimmunoassay. K(Ca) activity and changes of the intracellular Ca(2+) concentration [Ca(2+)](i) were analyzed using the fluorescent dyes bis-barbituric acid oxonol, potassium-binding benzofuran isophthalate, and fluo-3. The endothelial angiogenic parameters measured were cell proliferation, [(3)H]-thymidine incorporation, and cell migration (scratch assay). Akt phosphorylation was examined using immunohistochemistry ... Api caused a concentration-dependent increase in cyclic guanosine monophosphate levels, with a maximum effect at a concentration of 1 uM. Api-induced hyperpolarization was blocked by the small and large conductance K(Ca) inhibitors apamin and iberiotoxin, respectively. Furthermore, apamin and iberiotoxin blocked the late, long-lasting plateau phase of the Api-induced biphasic increase of [Ca(2+)](i). Inhibition of Ca(2+) signaling and the K(Ca) blockade both blocked NO production. Prevention of all three (NO, Ca(2+), and K(Ca) signaling) reversed the antiangiogenic effects of Api under both basal and basic fibroblast growth factor-induced culture conditions. Basic fibroblast growth factor-induced Akt phosphorylation was also reduced by Api ... Based on ... /the/ experimental results ... /the authors/ propose the following signaling cascade for the effects of Api on endothelial cell signaling. Api activates small and large conductance K(Ca), leading to a hyperpolarization that is followed by a Ca(2+) influx. The increase of [Ca(2+)](i) is responsible for an increased NO production that mediates the antiangiogenic effects of Api via Akt dephosphorylation.

    PMID:17488347 Erdogan A et al; J Thromb Haemost 5(8):1774-81 (2007)

    ... Apigenin inhibits the production of proinflammatory cytokines IL-1beta, IL-8, and TNF in LPS-stimulated human monocytes and mouse macrophages. The inhibitory effect on proinflammatory cytokine production persists even when apigenin is administered after LPS stimulation. Transient transfection experiments using NF-kappaB reporter constructs indicated that apigenin inhibits the transcriptional activity of NF-kappaB in LPS-stimulated mouse macrophages. The classical proteasome-dependent degradation of the NF-kappaB inhibitor IkappaBalpha was observed in apigenin LPS-stimulated human monocytes. Using EMSA ... apigenin does not alter NF-kappaB-DNA binding activity in human monocytes. Instead ... apigenin, as part of a non-canonical pathway, regulates NF-kappaB activity through hypophosphorylation of Ser536 in the p65 subunit and the inactivation of the IKK complex stimulated by LPS. The decreased phosphorylation on Ser536 observed in LPS-stimulated mouse macrophages treated with apigenin was overcome by the over-expression of IKKbeta. In addition ... /the/ studies indicate that apigenin inhibits in vivo LPS-induced TNF and the mortality induced by lethal doses of LPS. Collectively, these findings suggest a molecular mechanism by which apigenin suppresses inflammation and modulates the immune response in vivo.

    PMID:17982104 Nicholas C et al; J Immunol 179(10):7121-7 (2007)

    Treatment of /human prostate cancer/ LNCaP and PC-3 cells with apigenin causes G0-G1 phase arrest, decrease in total Rb protein and its phosphorylation at Ser780 and Ser807/811 in dose- and time-dependent fashion. Apigenin treatment caused increased phosphorylation of ERK1/2 and JNK1/2 and this sustained activation resulted in decreased ELK-1 phosphorylation and c-FOS expression thereby inhibiting cell survival. Use of kinase inhibitors induced ERK1/2 phosphorylation, albeit at different levels, and did not contribute to cell cycle arrest in comparison to apigenin treatment. Despite activation of MAPK pathway, apigenin caused a significant decrease in cyclin D1 expression that occurred simultaneously with the loss of Rb phosphorylation and inhibition of cell cycle progression. The reduced expression of cyclin D1 protein correlated with decrease in expression and phosphorylation of p38 and PI3K-Akt, which are regulators of cyclin D1 protein. Interestingly, apigenin caused a marked reduction in cyclin D1, D2 and E and their regulatory partners CDK 2, 4 and 6, operative in G0-G1 phase of the cell cycle. This was accompanied by a loss of RNA polymerase II phosphorylation, suggesting the effectiveness of apigenin in inhibiting transcription of these proteins. This study provides an insight into the molecular mechanism of apigenin in modulating various tyrosine kinases and perturbs cell cycle progression, suggesting its future development and use as anticancer agent in humans.

    PMID:17457054 Shukla S, Gupta S; Cell Cycle 6(9):1102-14 (2007)

    The aim of this study was to clarify the anti-inflammatory mechanism of apigenin. Apigenin inhibited the collagenase activity involved in rheumatoid arthritis (RA) and suppressed lipopolysaccharide (LPS)-induced nitric oxide (NO) production in a dose dependent manner in RAW 264.7 macrophage cells. Pretreatment with apigenin also attenuated LPS-induced cyclooxygenase-2 (COX-2) expression. In addition, apigenin profoundly reduced the tumor necrosis factor-alpha (TNF-alpha)-induced adhesion of monocytes to HUVEC monolayer. Apigenin significantly suppressed the TNF-alpha-stimulated upregulation of vascular cellular adhesion molecule-1 (VCAM-1)-, intracellular adhesion molecule-1 (ICAM-1)-, and E-selectin-mRNA to the basal levels. Taken together, these results suggest that apigenin has significant anti-inflammatory activity that involves blocking NO-mediated COX-2 expression and monocyte adherence ...

    PMID:18038911 Lee JH et al; Arch Pharm Res 30(10):1318-27 (2007)

    For more Mechanism of Action (Complete) data for APIGENIN (16 total), please visit the HSDB record page.

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