We Offer Worldwide Shipping
Login Wishlist



  • Brand : BIOFRON

  • Catalogue Number : BF-P3010

  • Specification : 98%

  • CAS number : 18642-23-4

  • Formula : C20H16O5

  • Molecular Weight : 336.338

  • PUBCHEM ID : 5281806

  • Volume : 25mg

In stock

Checkout Bulk Order?

Catalogue Number


Analysis Method






Molecular Weight



Light yellow crystalline powder

Botanical Source

Cullen corylifolium

Structure Type



Standards;Natural Pytochemical;API




6H-Benzofuro[3,2-c][1]benzopyran-6-one, 3,9-dihydroxy-2-(3-methyl-2-buten-1-yl)-/Psoralidin/3,9-dihydroxy-2-(3-methylbut-2-enyl)-[1]benzofuro[3,2-c]chromen-6-one/3,9-Dihydroxy-2-prenylcoumestan/3,9-Dihydroxy-2-(3-methyl-2-buten-1-yl)-6H-[1]benzofuro[3,2-c]chromen-6-one/3,9-Dihydroxy-2-(3-methyl-2-butenyl)-6H-benzofuro[3,2-c][1]benzopyran-6-one/6H-Benzofuro(3,2-c)(1)benzopyran-6-one, 3,9-dihydroxy-2-(3-methyl-2-butenyl)-/3,9-Dihydroxy-2-(3-methyl-2-butenyl)-6H-benzofuro(3,2-c)(1)benzopyran-6-one/6-(3-Methylbut-2-enyl)coumestrol/3,9-Dihydroxy-2-(3-methylbut-2-en-1-yl)-6H-[1]benzofuro[3,2-c]chromen-6-one




1.4±0.1 g/cm3



Flash Point

231.3±25.7 °C

Boiling Point

458.8±34.0 °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#:18642-23-4) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Traditional Chinese medicines (TCM) have been proven to prevent osteoporosis, but their clinical applications are not widely recognized due to their complicated ingredients. Psoralidin, a prenylated coumestan, has been reported to prevent bone loss of ovariectomized rats, but detailed mechanisms are still not clear. In current study, we found that both psoralidin and coumestrol promoted osteoblast proliferation and differentiation, as evidenced by improvements in cell proliferation and alkaline phosphatase activity; increased formation of ALP colonies and calcified nodules; enhanced secretion of collagen-I, BMP-2, osteocalcin and osteopontin; and stimulation of the expression of IGF-1, β-catenin, Runx-2, Osterix, and OPG, as well as the mRNA ratio of OPG/RANKL, while significantly decreasing the expression of RANKL. In addition, both psoralidin and coumestrol inhibited osteoclast formation and osteoclastic bone resorption, as demonstrated by the lower tartrate-resistant acid phosphatase activity and smaller area, with fewer resorption pits formed. Interestingly, psoralidin showed much stronger effects than coumestrol at enhancing osteoblast proliferation/differentiation or inhibiting osteoclast differentiation and bone resorption. Moreover, we found that both psoralidin and coumestrol suppressed COX-2 and ROS production in rat osteoblastic calvarias cells, and psoralidin showed stronger effects than coumestrol. Furthermore, we detected that by blocking estrogen receptors with ICI 182.780 (an estrogen receptor antagonist), the osteoprotective effects of psoralidin and coumestrol were also blocked. Our findings demonstrated that psoralidin and coumestrol exert their bone-protective effects by enhancing bone formation of osteoblasts and inhibiting bone resorption of osteoclasts. These roles might be mediated by their antioxidant activity and transduced through estrogen receptor signaling.


Coumestrol; Isopentenyl group; Osteoblasts; Osteoclasts; Psoralidin.


Psoralidin, a Prenylated Coumestan, as a Novel Anti-Osteoporosis Candidate to Enhance Bone Formation of Osteoblasts and Decrease Bone Resorption of Osteoclasts


Yuankun Zhai 1 , Yingying Li 2 , Yanping Wang 3 , Jiawei Cui 2 , Kun Feng 4 , Xijian Kong 2 , Li Chen 5

Publish date

2017 Apr 15




Psoralidin is a metabolic product from the seed of psoraleacorylifolia, possessed anti-inflammatory and immunomodulatory effects. We speculated that psoralidin might impact osteoclastogenesis and bone loss. By using both in vitro and in vivo studies, we observed psoralidin strongly inhibited RANKL induced osteoclast formation during preosteoclast cultures, suggesting that it acts on osteoclast precursors to inhibit RANKL/RANK signaling. At the molecular level, by using MAPKs specific inhibitors (U-0126, SB-203580 and SP-600125) we demonstrated that psoralidin markedly abrogated the phosphorylation of p38, ERK, JNK. Moreover, the RANKL induced NF-κB/p65 phosphorylation and I-κB degradation were significantly inhibited by psoralidin. Further, psoralidin significantly suppressed osteoclastogenesis marker genes of TRAP, Cathepsin K and OSCAR. These were accompanied by the decreased expression of c-Fos and NFATc1 transcription factors. Consistent with in vitro results, our in vivo and serologic studies showed psoralidin inhibited lipopolysaccharide induced bone resorption by suppressing the inflammatory cytokines: TNF-α and IL-6 expression, as well as the ratio of RNAKL : OPG. These results collectively suggested that psoralidin could represent a novel therapeutic strategy for osteoclast-related disorders, such as rheumatoid arthritis and postmenopausal osteoporosis.


Coumestrol; Isopentenyl group; Osteoblasts; Osteoclasts; Psoralidin.


Psoralidin Suppresses Osteoclastogenesis in BMMs and Attenuates LPS-mediated Osteolysis by Inhibiting Inflammatory Cytokines


Lingbo Kong 1 , Rui Ma 2 , Xiaobin Yang 3 , Ziqi Zhu 3 , Hua Guo 3 , Baorong He 3 , Biao Wang 4 , Dingjun Hao 5

Publish date

2017 Oct




Upon synaptic stimulation and glutamate release, glutamate receptors are activated to regulate several downstream effectors and signaling pathways resulting in synaptic modification. One downstream intracellular effect, in particular, is the expression of immediate-early genes (IEGs), which have been proposed to be important in synaptic plasticity because of their rapid expression following synaptic activation and key role in memory formation. In this study, we screened a natural compound library in order to find a compound that could induce the expression of IEGs in primary cortical neurons and discovered that psoralidin, a natural compound isolated from the seeds of Psoralea corylifolia, stimulated synaptic modulation. Psoralidin activated mitogen-activated protein kinase (MAPK) signaling, which in turn induced the expression of neuronal IEGs, particularly Arc, Egr-1, and c-fos. N-methyl-D-aspartate (NMDA) receptors activation and extracellular calcium influx were implicated in the psoralidin-induced intracellular changes. In glutamate dose-response curve, psoralidin shifted glutamate EC50 to lower values without enhancing maximum activity. Interestingly, psoralidin increased the density, area, and intensity of excitatory synapses in primary hippocampal neurons, which were mediated by NMDA receptor activation and MAPK signaling. These results suggest that psoralidin triggers synaptic remodeling through activating NMDA receptor and subsequent MAPK signaling cascades and therefore could possibly serve as an NMDA receptor modulator.


Immediate-early genes; Learning and memory; NMDA receptor modulator; Psoralidin; Synaptic plasticity.


Psoralidin Stimulates Expression of Immediate-Early Genes and Synapse Development in Primary Cortical Neurons


Seojin Hwang 1 , Seong-Eun Lee 1 , Sang-Gun Ahn 2 , Gum Hwa Lee 3

Publish date

2018 Dec

Description :

Psoralidin, a natural furanocoumarin, is isolated from Psoralea corylifolia L. possessing anti-cancer properties.IC50 value:Target: Anticancer natural compoundin vitro: PSO dramatically decreased the cell viabilities in dose- and time-dependent manner. Autophagy inhibitor 3-MA blocked the production of LC3-II and reduced the cytotoxicity in response to PSO. Furthermore, PSO increased intracellular ROS level which was correlated to the elevation of LC3-II [1]. Psoralidin at 10 μM was able to induce the maximum reporter gene expression corresponding to that of E2-treated cells and such activation of the ERE-reporter gene by psoralidin was completely abolished by the cotreatment of a pure ER antagonist, implying that the biological activities of psoralidin are mediated by ER [2]. Psoralidin enhanced TRAIL-induced apoptosis in HeLa cells through increased expression of TRAIL-R2 death receptor and depolarization of mitochondrial membrane potential [3]. Psoralidin inhibited the IR-induced COX-2 expression and PGE(2) production through regulation of PI3K/Akt and NF-κB pathway. Also, psoralidin blocked IR-induced LTB(4) production, and it was due to direct interaction of psoralidin and 5-lipoxygenase activating protein (FLAP) in 5-LOX pathway. IR-induced fibroblast migration was notably attenuated in the presence of psoralidin [4].in vivo: Moreover, in vivo results from mouse lung indicate that psoralidin suppresses IR-induced expression of pro-inflammatory cytokines (TNF-α, TGF-β, IL-6 and IL-1 α/β) and ICAM-1[4].