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  • Brand : BIOFRON

  • Catalogue Number : BF-B3004

  • Specification : 98%

  • CAS number : 10309-37-2

  • Formula : C18H24O

  • Molecular Weight : 256.38

  • PUBCHEM ID : 5468522

  • Volume : 100mg

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Catalogue Number


Analysis Method






Molecular Weight



Red liquid

Botanical Source

Cullen corylifolium

Structure Type



Standards;Natural Pytochemical;API




P-(3,7-dimethyl-3-vinylocta-trans-1,6-dimethyl) phenol/Phenol, 4-[(1E,3S)-3-ethenyl-3,7-dimethyl-1,6-octadien-1-yl]-/BACTRIS GASIPAES FRUIT JUICE/4-[(1E,3S)-3-ethenyl-3,7-dimethylocta-1,6-dien-1-yl]phenol/Backuchiol/Bakuchiol/4-[(1E,3S)-3,7-Dimethyl-3-vinyl-1,6-octadien-1-yl]phenol/Drupanol/4-[(1E,3S)-3,7-Dimethyl-3-vinylocta-1,6-dien-1-yl]phenol/(S)-bakuchiol/UP 256/Phenol, 4-[(1E,3S)-3-ethenyl-3,7-dimethyl-1,6-octadienyl]-




1.0±0.1 g/cm3


Methanol; Ethyl Acetate

Flash Point

176.6±11.7 °C

Boiling Point

391.4±21.0 °C at 760 mmHg

Melting Point


InChl Key

WGK Germany


HS Code Reference


Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:10309-37-2) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Bakuchiol (Bak), a monoterpene phenol isolated from the seeds of Psoralea corylifolia, has been widely used to treat a large variety of diseases in both Indian and Chinese folkloric medicine. However, the effects of Bak on cardiac hypertrophy remain unclear. Therefore, the present study was designed to determine whether Bak could alleviate cardiac hypertrophy. Mice were subjected to aortic banding (AB) to induce cardiac hypertrophy model. Bak of 1 ml/100 g body weight was given by oral gavage once a day from 1 to 8 weeks after surgery. Our data demonstrated for the first time that Bak could attenuate pressure overload-induced cardiac hypertrophy and could attenuate fibrosis and the inflammatory response induced by AB. The results further revealed that the effect of Bak on cardiac hypertrophy was mediated by blocking the activation of the NF-κB signaling pathway. In vitro studies performed in neonatal rat cardiomyocytes further proved that the protective effect of Bak on cardiac hypertrophy is largely dependent on the NF-κB pathway. Based on our results, Bak shows profound potential for its application in the treatment of pathological cardiac hypertrophy, and we believe that Bak may be a promising therapeutic candidate to treat cardiac hypertrophy and heart failure.


Bakuchiol; NF kappa B; aortic banding; cardiac hypertrophy; cardiomyocytes.


Bakuchiol Protects Against Pathological Cardiac Hypertrophy by Blocking NF-κB Signaling Pathway


Zheng Wang 1 , Lu Gao 1 , Lili Xiao 1 , Lingyao Kong 1 , Huiting Shi 1 , Xinyu Tian 1 , Luosha Zhao 2

Publish date

2018 Oct 31




The purpose of the present study was to evaluate the effects of bakuchiol on the inflammatory response and to identify the molecular mechanism of the inflammatory effects in a lipopolysaccharide (LPS)-stimulated BV-2 mouse microglial cell line and mice model. The production of prostaglandin E2 (PGE2), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) was measured by enzyme-linked immunosorbent assay. The mRNA expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), TNF-α, and IL-6 was measured using reverse transcription-polymerase chain reaction analysis. Mitogen-activated protein kinase (MAPK) phosphorylation was determined by western blot analysis. In vitro experiments, bakuchiol significantly suppressed the production of PGE2 and IL-6 in LPS-stimulated BV-2 cells, without causing cytotoxicity. In parallel, bakuchiol significantly inhibited the LPS-stimulated expression of iNOS, COX-2, and IL-6 in BV-2 cells. However, bakuchiol had no effect on the LPS-stimulated production and mRNA expression of TNF-α or on LPS-stimulated c-Jun NH2-terminal kinase phosphorylation. In contrast, p38 MAPK and extracellular signal-regulated kinase (ERK) phosphorylation were inhibited by bakuchiol. In vivo experiments, Bakuchiol reduced microglial activation in the hippocampus and cortex tissue of LPS-injected mice. Bakuchiol significantly suppressed LPS-injected production of TNF-α and IL-6 in serum. These results indicate that the anti-neuroinflammatory effects of bakuchiol in activated microglia are mainly regulated by the inhibition of the p38 MAPK and ERK pathways. We suggest that bakuchiol may be beneficial for various neuroinflammatory diseases.


MAPK phosphorylation; bakuchiol; inflammatory response; microglia; neuroinflammation.


Bakuchiol Suppresses Inflammatory Responses Via the Downregulation of the p38 MAPK/ERK Signaling Pathway


Hye-Sun Lim 1 2 , Yu Jin Kim 3 4 , Bu-Yeo Kim 3 , Soo-Jin Jeong 5

Publish date

2019 Jul 22




Psoralea corylifolia L. (Fructus Psoraleae) is widely used in Asia, but there are concerns about hepatotoxicity caused by constituents such as psoralens and bakukiol. Bakuchiol (BAK) has antiinflammatory, antipyretic, antibacterial antiviral, anticancer, and estrogenic activity but appears to be hepatotoxic in in vitro tests. This study investigated the hepatotoxicity in vivo in rats. Using intragastrically administered bakuchiol at doses of 52.5 and 262.5 mg/kg for 6 weeks. Bodyweight, relative liver weight, biochemical indicators, histopathology, mRNA expression of CYP7A1, HMG-CoA reductase, BSEP, PPARα, SREBP-2, and MRP3 were measured. Many abnormalities were observed in the bakuchiol-treated groups including suppression of weight gain and food intake, change of some parameters in serum biochemistry, and increased weight of liver. The mRNA expression of CYP7A1, HMG-CoA reductase, PPARα, and SREBP-2 decreased in bakuchiol-treated group, the expression of BSEP increased in bakuchiol-treated low dosage, and the expression of BSEP decreased in bakuchiol-treated high dosage. In conclusion, we provide evidence for the first time that bakuchiol can induce cholestatic hepatotoxicity, suggesting potential hepatotoxicity. The mechanism may be related to effects on liver lipid metabolism, but further investigation is necessary. Copyright © 2017 John Wiley & Sons, Ltd.


RNA expression; Sprague-Dawley rats; bakuchiol; blood biochemistry; chronic toxicity study; hepatotoxicity.


Bakuchiol Contributes to the Hepatotoxicity of Psoralea Corylifolia in Rats


Zhi-Jian Li 1 2 , Abudumijiti Abulizi 3 , Guo-Lin Zhao 1 , Tao Wang 1 , Fan Zhou 4 , Zhen-Zhou Jiang 1 , Silafu Aibai 2 , Lu-Yong Zhang 1

Publish date

2017 Aug

Description :

Bakuchiol is a phytoestrogen isolated from the seeds of Psoralea corylifolia L; has anti-tumor effects.IC50 value:Target:in vitro: Bakuchiol reduced mitochondrial membrane potential (Psim) of cells in a concentration- and time-dependent manner, showing a more potent effect than that of resveratrol. S phase arrest, caspase 9/3 activaton, p53 and Bax up-regulation, as well as Bcl-2 down-regulation were observed in bakuchiol-treated A549 cells [1]. UGT2B7 was inhibited by the strongest intensity. The noncompetitive inhibition was demonstrated by the results obtained from Dixon plot and Lineweaver-Burk plot. The Ki value was calculated to be 10.7 μM [2]. Bakuchiol was found to be naturally occurring potent inhibitors of hCE2, with low Ki values ranging from 0.62μM to 3.89μM [3]. After exposure to bakuchiol at 0.25-fold, 0.5-fold and 1-fold of minimum inhibitory concentration (MIC) (3.91 μg/ml) for 24h, the fungal conidia of T. mentagrophytes demonstrated a significant dose-dependent increase in membrane permeability. Moreover, bakuchiol at 1-fold MIC elicited a 187% elevation in reactive oxygen species (ROS) level in fungal cells after a 3-h incubation [4].in vivo: In combination with the reported concentration after an intravenous administration of bakuchiol (15 mg/kg) in rats, the high risk of in vivo inhibition of bakuchiol towards UGT2B7-catalyzed metabolism of drugs was indicated [2]. In a guinea pig model of tinea pedis, bakuchiol at 1%, 5% or 10% (w/w) concentration in aqueous cream could significantly reduce the fungal burden of infected feet (p<0.01-0.05) [4].