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Fig. 1 · Structure
Cat. No.
A10146
CAS No.
491-80-5
Formula
C16H12O5
Mol. Weight
284.3

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Biochanin A (4-Methylgenistein)

Cat. No. A10146 CAS 491-80-5

Biochanin A is an antiproliferative and anti-inflammatory agent that inhibits iNOS expression and lipopolysacharide (LPS)-induced nitric oxide production in macrophages. Additionally, Biochanin A displays the ability to block phosphorylation of IκBα and p38 MAPK, which prevents NF-κB activation. Furthermore, Biochanin A has been observed to suppress IL-6, IL-1β, and TNF-α production.

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Biological Activity

Bioactivity / Mechanism

Biochanin A inhibits FAAH in enzyme assays. A recombinant human FAAH membrane assay reported an IC50 of 2.4 µM with 0.5 µM anandamide substrate; an independent screening assay reported 2.1 ± 0.24 µM under different assay conditions. These values describe assay-dependent potency and do not establish selectivity across other targets. [1,2]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Target & Activity

Target Activity Value
FAAH (rat) 1.4 μM
FAAH (mouse) 1.8 μM
FAAH (human) 2.4 μM
EGFR 91.5 μM

Cellular Effect

Cell Line Activity Value Description Reference
A549 IC50 > 100 μM Cytotoxicity against human A549 cells after 72 hrs by MTT assay [PMID: 18440233]
A549 ED50 19.77 μg/mL Cytotoxicity against human A549 cells after 7 days [PMID: 8201311]
B16-BL6 IC50 > 100 μM Cytotoxicity against mouse B16-BL6 cells after 72 hrs by MTT assay [PMID: 18440233]
BALB/3T3 IC50 219.5 μM Growth inhibition of BALB/c mouse cloned 3T3/A31 cells after 72 hrs by nigrosin assay [PMID: 10096863]
GES1 IC50 > 32 μM Cytotoxicity against human GES1 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay [PMID: 33619958]
GES1 IC50 > 32 μM Cytotoxicity against human GES1 cells assessed as cell viability measured after 72 hrs by MTT assay [PMID: 33581557]
HeLa IC50 > 100 μM Cytotoxicity against human HeLa cells after 72 hrs by MTT assay [PMID: 18440233]
HT-1080 IC50 > 100 μM Cytotoxicity against human HT1080 cells after 72 hrs by MTT assay [PMID: 18440233]
HT-29 ED50 28.38 μg/mL Cytotoxicity against human HT-29 cells after 7 days [PMID: 8201311]
Ishikawa EC50 0.42 μM Estrogenic activity at estrogen receptor in human Ishikawa cells assessed as induction of alkaline phosphatase expression after 72 hrs by microplate reader [PMID: 22464681]
Lewis lung carcinoma cell line IC50 > 100 μM Cytotoxicity against mouse LLC cells after 72 hrs by MTT assay [PMID: 18440233]
Macrophage cell line CC50 50.4 μM Cytotoxicity in human monocyte-derived macrophages assessed as reduction in cell viability incubated for 3 days by alamar blue dye based assay [PMID: 28964936]
MCF7 EC50 0.21 μM Antiproliferative activity against estrogen-deficient human MCF7 cells after 72 hrs by MTT assay [PMID: 22464681]
MCF7 IC50 10 μM Antiproliferative activity against human MCF7 cells assessed as inhibition of cell growth incubated for 6 days by SRB assay [PMID: 33257172]
MCF7 IC50 40 μg/mL Antiproliferative activity against human MCF7 cells assessed as inhibition of cell growth incubated for 2 days by WST-1 assay [PMID: 33257172]
MCF7 IC50 40 μg/mL Inhibition of DNA synthesis in human MCF7 cells incubated for 4 days by BrdU incorporation assay [PMID: 33257172]
MCF7 ED50 5.49 μg/mL Cytotoxicity against human MCF7 cells after 7 days [PMID: 8201311]
MGC-803 IC50 2.95 μM Antiproliferative activity against human MGC-803 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay [PMID: 33619958]
MGC-803 IC50 6.77 μM Antiproliferative activity against human MGC-803 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay [PMID: 33619958]
MGC-803 IC50 6.77 μM Antiproliferative activity against human MGC-803 cells assessed as reduction in cell viability after 72 hrs by MTT assay [PMID: 33581557]

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In Vitro Studies

Inhibition of recombinant human FAAH

Biochemical assay · Membranes from COS7 cells expressing human FAAH [1]

Biochanin A inhibited radiolabeled anandamide hydrolysis in a membrane assay. The human-enzyme IC50 is an assay endpoint, not a cellular treatment dose.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Hydrolysis of 0.5 µM [3H]AEAIC50 2.4 µM[1]
Inhibition of recombinant human FAAHpI50 5.62 ± 0.07[1]

Literature-Reported Treatment Conditions

Treatment concentration
Biochanin A concentration–response; substrate: 0.5 µM [3H]AEA
Method
Radiometric FAAH activity assay
Vehicle
Ethanol
Reported limits
Assay incubation duration and final ethanol fraction are not specified in the retained human-FAAH description.
Methods and source locations

Compound reported in the paper: Biochanin A; Compound label in the paper: Biochanin A

Evidence concerns the reported Biochanin A material; it does not validate an Adooq lot or formulation.

Table 2 (human FAAH column); Figure 1A and caption; Methods: FAAH expression/activity and Compounds

Hydrolysis of 0.5 µM [3H]AEA: Concentration–response fitting; human substrate utilization <5%; buffer blanks. Figure 1 gives n=4–5 for human curves, means and SEM. — Table 2 (human FAAH column); Figure 1A and caption; Methods: FAAH expression/activity and Compounds

Inhibition of recombinant human FAAH: Reported fitted potency in Table 2; no independent uncertainty assigned to the IC50. — Table 2: Biochanin A, human FAAH column

Independent FAAH inhibitor screening assay

Biochemical assay · FAAH Inhibitor Screening Assay Kit (Cayman #10005196); enzyme species not specified in the article [2]

An independent enzyme-screening experiment reported concentration-dependent inhibition by Biochanin A.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
FAAH activity inhibitionIC50 2.1 ± 0.24 µM[2]

Literature-Reported Treatment Conditions

Treatment concentration
0.1–200 µM Biochanin A
Method
Commercial fluorescence-based FAAH inhibition assay
Co-treatment
JZL-195 at 10 and 20 µM served as the reference inhibitor.
Reported limits
Article does not specify enzyme species, incubation duration, final solvent fraction, or IC50 fitting method.
Methods and source locations

Compound reported in the paper: Biochanin A; Compound label in the paper: biochanin-A

Evidence concerns the reported Biochanin A material; it does not validate an Adooq lot or formulation.

Methods 2.2 and 2.4; Results 3.2; Figure 2B and caption

FAAH activity inhibition: Methods 2.2 describes testing in triplicate with average fluorescence. Results 3.2 reports the fitted value; general statistics describe mean ± SEM, without a separate definition for IC50 uncertainty. — Methods 2.2 and 2.4; Results 3.2; Figure 2B and caption

In Vivo Studies

Anandamide responses differed across mouse experiments. Acute Biochanin A (15 mg/kg intravenously) did not significantly increase whole-brain anandamide at 60 min. After 30 mg/kg intraperitoneally daily for 14 days in a separate study, prefrontal anandamide increased following forced-swim testing, with reduced immobility and lower blood corticosterone. The repeated-dose study found no significant treatment effect on locomotion. Differences in regimen, sampled region and testing context prevent a direct reconciliation; the cause of the different anandamide responses remains unknown. [1,2]

Whole-brain anandamide after acute intravenous treatment

Animal study · ICR mice, whole-brain lipid analysis after behavioral testing [1]

A single intravenous Biochanin A dose did not significantly increase whole-brain AEA under the tested conditions.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Whole-brain AEA concentrationBetween-group difference No significant differences; P > 0.05[1]

Conditions shared by the study groups

Route
Intravenous, tail vein
Frequency
Single Biochanin A administration
Treatment course
Brains sampled 60 min after Biochanin A; behavioral testing and a second vehicle injection preceded collection
Vehicle
Ethanol:Emulphor-620:physiological saline, 1:1:18 v/v
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Biochanin A
15 mg·kg−1		Vehicle-treated mice; Figure 8 also includes a separate daidzein groupNo significant difference in brain AEA among groups (one-way ANOVA, P > 0.05).[1]
Biochanin A
Model: ICR mice
Reported limits: Sex and exact interval between injections are not stated in the retained description; no exposure concentration was measured.
Methods and source locations

Compound reported in the paper: Biochanin A; Compound label in the paper: Biochanin A

Evidence concerns the reported Biochanin A material; it does not validate an Adooq lot or formulation.

Figure 8 and caption; Methods: Behavioural effects and Quantification of AEA levels in the brain; Results: Behavioural effects

Whole-brain AEA concentration: LC/MS; one-way ANOVA. Means ± SEM; n=6 for Biochanin A and n=12 for vehicle; the analysis also included n=6 daidzein-treated mice. — Figure 8 and caption; Methods: Quantification of AEA levels in the brain

Biochanin A · Figure 8 and caption; Methods: Behavioural effects and Quantification of AEA levels in the brain; Results: Behavioural effects

Repeated treatment, mouse behavior and prefrontal anandamide

Animal study · Male and female CD1 mice; open field, forced swim, prefrontal cortex AEA and blood corticosterone [2]

Repeated Biochanin A treatment reduced forced-swim immobility without a significant locomotor treatment effect. Biochemical measures from the same treatment design showed increased prefrontal AEA and decreased blood corticosterone; these associations do not establish FAAH-dependent behavioral causality.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Forced-swim immobility timeComparison with vehicle Reduced in males and females; p < .001 versus vehicle in Results 3.3[2]
Open-field distance traveledTreatment effect No significant treatment effect; F[11, 84] = 1.605, p = .1122[2]
Prefrontal cortex AEA after forced swimComparison with vehicle Increased; p < .003 for Biochanin A in Results 3.4[2]
Blood corticosterone after forced swimComparison with vehicle Decreased; p < .001 for Biochanin A in Results 3.4[2]

Conditions shared by the study groups

Route
Intraperitoneal
Frequency
Daily for 14 consecutive days
Treatment course
14 days; testing on the final day, followed immediately by tissue/blood collection
Vehicle
Vehicle control: 10% DMSO in sterile water
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Biochanin A
30 mg/kg		Vehicle; fluoxetine 10 mg/kg and arachidonyl serotonin 5 mg/kg were reference comparatorsReduced forced-swim immobility and increased prefrontal AEA with lower blood corticosterone; no significant treatment effect on open-field locomotion.[2]
Biochanin A
Model: Male and female CD1 mice; mice arrived at 7 weeks old and treatment assignment followed one week later
Reported limits: Methods says n=8 per group; figure captions clarify n=8 per group per sex for behavior and n=4–8 per group per sex for biochemical measures. Specific Biochanin A biochemical n is not given.
Methods and source locations

Compound reported in the paper: Biochanin A; Compound label in the paper: biochanin-A

Evidence concerns the reported Biochanin A material; it does not validate an Adooq lot or formulation.

Methods 2.3–2.10; Results 3.3–3.4; Figures 3B, 4B and 5 with captions

Forced-swim immobility time: Blinded scoring of the last 4 min of a 6-min test. Figure 4: means ± SEM, n=8 per group per sex. Numerical bar heights were not digitized. — Methods 2.7; Results 3.3; Figure 4B and caption

Open-field distance traveled: Overall treatment test across groups, not a Biochanin A-specific equivalence test. Figure 3B: means ± SEM, n=8 per group per sex. — Methods 2.6; Results 3.3; Figure 3B and caption

Prefrontal cortex AEA after forced swim: LC–MS/MS, normalized to tissue weight. Figure 5: means ± SEM, n=4–8 per group per sex; exact Biochanin A n not specified. — Methods 2.9; Results 3.4; Figure 5A and caption

Blood corticosterone after forced swim: Enzyme immunoassay. Figure 5: means ± SEM, n=4–8 per group per sex. Methods calls the separated fraction plasma, whereas Results refers to serum; no matrix-specific concentration is adopted. — Methods 2.8; Results 3.4; Figure 5B and caption

Biochanin A · Methods 2.3–2.10; Results 3.3–3.4; Figures 3B, 4B and 5 with captions

Specifications

Manufacturer Adooq Bioscience
CAS Number 491-80-5
Formula C16H12O5
Molecular Weight 284.3
Synonyms 4-Methylgenistein
SMILES
COC1=CC=C(C=C1)C2=COC3=CC(=CC(=C3C2=O)O)O

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 51 mg/mL (179.41 mM)
Water Insoluble
Ethanol 8 mg/mL (28.14 mM)

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Thors L, Burston JJ, Alter BJ, et al. Biochanin A, a naturally occurring inhibitor of fatty acid amide hydrolase. British Journal of Pharmacology (2010). PMID: 20590565 DOI: 10.1111/j.1476-5381.2010.00716.x Source material
  2. [2] Zada W, VanRyzin JW, Perez-Pouchoulen M, et al. Fatty acid amide hydrolase inhibition and N-arachidonoylethanolamine modulation by isoflavonoids: A novel target for upcoming antidepressants. Pharmacology Research & Perspectives (2022). PMID: 36029006 DOI: 10.1002/prp2.999 Source material

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