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  • Brand : BIOFRON

  • Catalogue Number : BF-T4009

  • Specification : 98%(HPLC)

  • CAS number : 2469-34-3

  • Formula : C30H45ClO6

  • Molecular Weight : 537.13

  • PUBCHEM ID : 12442762

  • Volume : 25mg

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Catalogue Number


Analysis Method






Molecular Weight



White crystalline powder

Botanical Source

Polygala tenuifolia,Polygala sibirica,Polygala fallax

Structure Type



Standards;Natural Pytochemical;API




Tennifolsaeure/(2S,3R,4S,4aR,6aR,8aS,12aS,13S,14aR,14bR)-13-(Chloromethyl)-2,3-dihydroxy-4,6a,11,11,14b-pentamethyl-2,3,4,4a,5,6,6a,7,8,9,10,11,12,12a,13,14,14a,14b-octadecahydro-4,8a(1H)-picenedicarboxylic acid/13-(Chloromethyl)-2,3-dihydroxy-4,6a,11,11,14b-pentamethyl-2,3,4,4a,5,6,6a,7,8,9,10,11,12,12a,13,14,14a,14b-octadecahydro-4,8a(1H)-picenedicarboxylic acid/4,8a(1H)-Picenedicarboxylic acid, 13-(chloromethyl)-2,3,4,4a,5,6,6a,7,8,9,10,11,12,12a,13,14,14a,14b-octadecahydro-2,3-dihydroxy-4,6a,11,11,14b-pentamethyl-/12-(Chloromethyl)-2,3-dihydroxy-27-norolean-13-ene-23,28-dioic acid,Tenuigenin/Senegenin/tenuifolic acid/(2b,3b,4a,12a)-12-(Chloromethyl)-2,3-dihydroxy-27-norolean-13-ene-23,28-dioic acid/4,8a(1H)-Picenedicarboxylic acid, 13-(chloromethyl)-2,3,4,4a,5,6,6a,7,8,9,10,11,12,12a,13,14,14a,14b-octadecahydro-2,3-dihydroxy-4,6a,11,11,14b-pentamethyl-, (2S,3R,4S,4aR,6aR,8aS,12aS,13S,14aR,14bR)-/Tenuifolsaeure/(2S,3R,4S,4aR,6aR,8aS,12aS,13S,14aR,14bR)-13-(Chloromethyl)-2,3-dihydroxy-4,6a,11,11,14b-pentamethyl-2,3,4,4a,5,6,6a,7,8,9,10,11,12,12a,13,14,14a,14b-octadecahydropicene-4,8a(1H)-dicarboxylic acid/Senegin


(2S,3R,4S,4aR,6aR,8aS,12aS,13S,14aR,14bR)-13-(chloromethyl)-2,3-dihydroxy-4,6a,11,11,14b-pentamethyl-2,3,4a,5,6,7,8,9,10,12,12a,13,14,14a-tetradecahydro-1H-picene-4,8a-dicarboxylic acid


1.3±0.1 g/cm3



Flash Point

361.5±31.5 °C

Boiling Point

674.1±55.0 °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#:2469-34-3) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Senegenin has been shown to inhibit neuronal apoptosis, thereby exerting a neuroprotective effect. In the present study, we established a rat model of spinal cord contusion injury using the modified Allen’s method. Three hours after injury, senegenin (30 mg/g) was injected into the tail vein for 3 consecutive days. Senegenin reduced the size of syringomyelic cavities, and it substantially reduced the number of apoptotic cells in the spinal cord. At the site of injury, Bax and Caspase-3 mRNA and protein levels were decreased by senegenin, while Bcl-2 mRNA and protein levels were increased. Nerve fiber density was increased in the spinal cord proximal to the brain, and hindlimb motor function and electrophysiological properties of rat hindlimb were improved. Taken together, our results suggest that senegenin exerts a neuroprotective effect by suppressing neuronal apoptosis at the site of spinal cord injury.


apoptosis; electrophysiology; motor function; nerve regeneration; neural regeneration; senegenin; spinal cord contusion; thinleaf milkwort root.


Senegenin Inhibits Neuronal Apoptosis After Spinal Cord Contusion Injury


Shu-Quan Zhang 1 , Min-Fei Wu 2 , Rui Gu 3 , Jia-Bei Liu 3 , Ye Li 3 , Qing-San Zhu 3 , Jin-Lan Jia

Publish date

2016 Apr




Neuronal apoptosis is an important event in hypoxia/reoxygenation (H/R)-induced neuronal injury. Senegenin (Sen), the predominant and most active component in Radix Polygalae root extracts, displays anti-apoptotic and anti-oxidative properties. Sen protects against H/R-induced neuronal apoptosis of highly differentiated PC12 cells and primary cortical neurons. Sen has also been investigated as a source of potential therapeutic targets. In this study, a proteomic approach was used to identify Sen-regulated proteins in PC12 cells. We found that Sen protected against H/R-induced neuronal apoptosis by upregulating RhoGDIα protein expression. The regulatory functions of RhoGDIα were investigated by knocking down RhoGDIα expression in PC12 cells using small interfering RNA (siRNA), followed by quantification of apoptosis and then altering the expression levels of apoptosis-related proteins. Our data show that after silencing RhoGDIα, the neuroprotective effects of Sen on H/R-induced PC12 cell apoptosis were absent. Furthermore, RhoGDIα silencing alleviated the Sen-mediated inhibition of the JNK pathway. Therefore, these findings indicated that Sen attenuates H/R-induced neuronal apoptosis by upregulating RhoGDIα expression and inhibiting the JNK pathway. In addition to the mechanism underlying neuroprotective effects of Sen, RhoGDIα was identified as a putative target of Sen based on a primary rat cortical neuron model of H/R-induced injury.


apoptosis; electrophysiology; motor function; nerve regeneration; neural regeneration; senegenin; spinal cord contusion; thinleaf milkwort root.


Senegenin Inhibits Hypoxia/Reoxygenation-Induced Neuronal Apoptosis by Upregulating RhoGDIα


Xuemin Li 1 2 , Yandong Zhao 1 , Panhong Liu 1 , Xiaoqing Zhu 1 3 , Minyi Chen 4 , Huadong Wang 1 , Daxiang Lu 1 , Renbin Qi 5

Publish date

2015 Dec




The purpose of this study was to assess the protective effect of senegenin on acute lung injury (ALI) in rats induced by sepsis. Rat ALI model was reproduced by cecal ligation and puncture (CLP). All rats were randomly divided into five groups: group 1 (control), group 2 (CLP), group 3 (CLP + senegenin 15 mg/kg), group 4 (CLP + senegenin 30 mg/kg), and group 5 (CLP + senegenin 60 mg/kg). CLP + senegenin groups received senegenin by gavage daily for consecutive 5 days, respectively, while the mice in control and CLP groups were given an equivalent volume of saline. We detected the lung wet/dry weight ratios and the histopathology of the lung. The levels of lung tissue myeloperoxidase (MPO), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH) were determined. Meanwhile, the nuclear factor-kappa B (NF-κB) activation, tumor necrosis factor-alpha (TNF-α), and interleukin-1β (IL-1β) levels were studied. The results demonstrated that senegenin treatment significantly attenuated CLP-induced lung injury, including reduction of lung wet/dry weight ratio, protein leak, infiltration of leukocytes, and MPO activity. In addition, senegenin markedly decreased MDA content and increased SOD activity and GSH level. Serum levels of TNF-α and IL-1β were also decreased by senegenin administration. Furthermore, senegenin administration inhibited the nuclear translocation of NF-κB in the lungs. These findings indicate that senegenin exerts protective effects on CLP-induced septic rats. Senegenin may be a potential therapeutic agent against sepsis.


acute lung injury; inflammation; oxidative stress; senegenin; sepsis.


Senegenin Ameliorate Acute Lung Injury Through Reduction of Oxidative Stress and Inhibition of Inflammation in Cecal Ligation and Puncture-Induced Sepsis Rats


Chun-Hong Liu 1 , Wei-Dong Zhang 2 , Jian-Jie Wang 3 , Shan-Dan Feng 4

Publish date

2016 Apr

Description :

Protective effect of senegenin on splenectomy-induced postoperative cognitive dysfunction in elderly rats. PUMID/DOI:24660030 Exp Ther Med. 2014 Apr;7(4):821-826. Epub 2014 Jan 24. These results suggest that Senegenin suppressed splenectomy-induced transient cognitive impairment in elderly rats, possibly by downregulating two signaling pathways involved in inflammation, TLR4/MyD88/NF-κB and TLR4/TRIF/NF-κB, to further inhibit the expression of key pro-inflammatory cytokines, specifically, TNF-α, IL-1β, IL-6 and IL-8, and ultimately the neuroinflammation in the hippocampal tissues. In conclusion, the present study revealed that Senegenin exhibited neuroprotective effects against splenectomy-induced transient cognitive impairment in elderly rats, which indicated that Senegenin may be a promising agent for the treatment of POCD. Senegenin attenuates hepatic ischemia-reperfusion induced cognitive dysfunction by increasing hippocampal NR2B expression in rats PUMID/DOI:23029109 PLoS One. 2012;7(9):e45575. Cognitive dysfunction induced by HIR is associated with reduction of NR2B expression. Senegenin plays a neuroprotective role in HIR via increasing NR2B expression in rat hippocampus. These findings suggest that Senegenin might be a potential agent for prevention and treatment of postoperative cognitive dysfunction (POCD) or other neurodegenerative diseases.