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Polyphyllin I


  • Brand : BIOFRON

  • Catalogue Number : BF-P2021

  • Specification : 98%

  • CAS number : 50773-41-6

  • Formula : C44H70O16

  • Molecular Weight : 855.021

  • PUBCHEM ID : 11018329

  • Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight



White crystalline powder

Botanical Source

rhizomes of Paris yunnanensis Franch.

Structure Type



Standards;Natural Pytochemical;API




β-D-Glucopyranoside, (3β,25R)-spirost-5-en-3-yl O-α-L-arabinofuranosyl-(1->4)-O-[6-deoxy-α-L-mannopyranosyl-(1->2)]-/(3β,25R)-Spirost-5-en-3-yl α-L-arabinofuranosyl-(1->4)-[6-deoxy-α-L-mannopyranosyl-(1->2)]-β-D-glucopyranoside/Chonglou saponin I/Polyphyllin A/Polyphyllin Ⅰ




1.4±0.1 g/cm3


Methanol; DMF

Flash Point

Boiling Point

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#:50773-41-6) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Polyphyllin I has been reported to possess anticancer properties in various cancer types, including prostate cancer. However, little is known about the potential of Polyphyllin I in induction of prostate cancer cell cycle arrest and its underlying mechanisms.

The anti-proliferation activity of Polyphyllin I was tested using cell counting kit-8 assay. The cell cycle arrest effects of Polyphyllin I were confirmed by flow cytometry. Western blot was used to test the effect of Polyphyllin I on cell cycle-related protein expression. Reverse transcription-polymerase chain reaction was used to test the expression of genes regulating P21 expression.

Polyphyllin I induced prostate cancer cell cycle arrest in G0/G1 phase in concentration-dependent manner. Polyphyllin I induced cell cycle arrest by upregulating the expression of P21. Further studies showed that the upregulation of p21 expression induced by Polyphyllin I via the upregulation of IL6 expression.

Polyphyllin I could induce cell cycle arrest in G0/G1 phase in prostate cancer cells by upregulating the expression of P21 and IL6.


Polyphyllin I induces cell cycle arrest in prostate cancer cells via the upregulation of IL6 and P21 expression.


Zhang D1, Liu S1, Liu Z1, Ma C1, Jiang Y1, Sun C2, Li K2, Cao G3, Lin Z2, Wang P2, Zhang J4, Xu D5, Kong F2, Zhao S4,6.

Publish date

2019 Nov




The molecular mechanisms underlying the anti-breast cancer effects of polyphyllin I, a natural compound extracted from Paris polyphylla rhizomes, are not fully understood. In the present study, we found that polyphyllin I induces mitochondrial translocation of DRP1 by dephosphorylating DRP1 at Ser637, leading to mitochondrial fission, cytochrome c release from mitochondria into the cytosol and, ultimately apoptosis. Polyphyllin I also increased the stabilization of full-length PINK1 at the mitochondrial surface, leading to the recruitment of PARK2, P62, ubiquitin, and LC3B-II to mitochondria and culminating in mitophagy. PINK1 knockdown markedly suppressed polyphyllin I-induced mitophagy and enhanced polyphyllin I-induced, DRP1-dependent mitochondrial fission and apoptosis. Furthermore, suppression of DRP1 by mdivi-1 or shRNA inhibited PINK1 knockdown/polyphyllin I-induced mitochondrial fragmentation and apoptosis, suggesting that PINK1 depletion leads to excessive fission and, subsequently, mitochondrial fragmentation. An in vivo study confirmed that polyphyllin I greatly inhibited tumor growth and induced apoptosis in MDA-MB-231 xenografts, and these effects were enhanced by PINK1 knockdown. These data describe the mechanism by which PINK1 contributes to polyphyllin I-induced mitophagy and apoptosis and suggest that polyphyllin I may be an effective drug for breast cancer treatment.


DRP1; PINK1; mitochondrial fission; mitophagy; polyphyllin I


Polyphyllin I induces mitophagic and apoptotic cell death in human breast cancer cells by increasing mitochondrial PINK1 levels.


Li GB1,2, Fu RQ1, Shen HM3, Zhou J1, Hu XY1, Liu YX1, Li YN1, Zhang HW1, Liu X1, Zhang YH1, Huang C4, Zhang R2, Gao N1.

Publish date

2017 Feb 7




Vasculogenic mimicry (VM) is a functional microcirculation pattern formed by aggressive tumor cells and is related to the metastasis and poor prognosis of many cancer types, including hepatocellular carcinoma (HCC). Thus far, no effective drugs have been developed to target VM. In this study, patients with liver cancer exhibited reduced VM in tumor tissues after treatment with Rhizoma Paridis. Polyphyllin I (PPI), which is the main component of Rhizoma Paridis, inhibited VM formation in HCC lines and transplanted hepatocellular carcinoma cells. Molecular mechanism analysis showed that PPI impaired VM formation by blocking the PI3k-Akt-Twist1-VE-cadherin pathway. PPI also displayed dual effects on Twist1 by inhibiting the transcriptional activation of the Twist1 promoter and interfering with the ability of Twist1 to bind to the promoter of VE-cadherin, resulting in VM blocking. This study is the first to report on the clinical application of the VM inhibitor. Results may contribute to the development of novel anti-VM drugs in clinical therapeutics.


Polyphyllin I suppresses the formation of vasculogenic mimicry via Twist1/VE-cadherin pathway.


Xiao T1,2, Zhong W1,2, Zhao J3, Qian B4, Liu H1,5, Chen S1, Qiao K1,2, Lei Y1,2, Zong S1,2, Wang H1,2, Liang Y1,2, Zhang H2, Meng J1,2, Zhou H1,2, Sun T6,7, Liu Y8,9, Yang C10,11.

Publish date

2018 Sep 5

Description :

Polyphyllin I is a bioactive constituent extracted from Paris polyphylla, has strong anti-tumor activity. Polyphyllin I is an activator of the JNK signaling pathway and is an inhibitor of PDK1/Akt/mTOR signaling. Polyphyllin I induces autophagy, G2/M phase arrest and apoptosis[1][2][3].