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Proscillaridin A


  • Brand : BIOFRON

  • Catalogue Number : BN-O1854

  • Specification : 98%(HPLC)

  • CAS number : 466-06-8

  • Formula : C30H42O8

  • Molecular Weight : 530.65

  • Volume : 20mg

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Catalogue Number


Analysis Method





Molecular Weight



Botanical Source

Structure Type








1.3±0.1 g/cm3


Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.

Flash Point

232.6±26.4 °C

Boiling Point

716.7±60.0 °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#:466-06-8) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.




Compounds with specific cytotoxic activity in senescent cells, or senolytics, support the causal involvement of senescence in aging and offer therapeutic interventions. Here we report the identification of Cardiac Glycosides (CGs) as a family of compounds with senolytic activity. CGs, by targeting the Na+/K+ATPase pump, cause a disbalanced electrochemical gradient within the cell causing depolarization and acidification. Senescent cells present a slightly depolarized plasma membrane and higher concentrations of H+, making them more susceptible to the action of CGs. These vulnerabilities can be exploited for therapeutic purposes as evidenced by the in vivo eradication of tumors xenografted in mice after treatment with the combination of a senogenic and a senolytic drug. The senolytic effect of CGs is also effective in the elimination of senescence-induced lung fibrosis. This experimental approach allows the identification of compounds with senolytic activity that could potentially be used to develop effective treatments against age-related diseases.


Identification and characterization of Cardiac Glycosides as senolytic compounds


Francisco Triana-Martinez 1 2, Pilar Picallos-Rabina 1, Sabela Da Silva-alvarez 1, Federico Pietrocola 3, Susana Llanos 4, Veronica Rodilla 5, Enrica Soprano 6, Pablo Pedrosa 1, Alba Ferreiros 1, Marta Barradas 7, Fernanda Hernandez-Gonzalez 3 8, Marta Lalinde 5, Neus Prats 3, Cristina Bernado 5, Patricia Gonzalez 9, Maria Gomez 9, Maria P Ikonomopoulou 10, Pablo J Fernandez-Marcos 7, Tomas Garcia-Caballero 11, Pablo Del Pino 6, Joaquin Arribas 5 12, Anxo Vidal 13, Miguel Gonzalez-Barcia 14, Manuel Serrano 3 12, Maria I Loza 2, Eduardo Dominguez 15, Manuel Collado 16

Publish date

2019 Oct 21;




Background: Cardiac glycosides are approved for the treatment of heart failure as Na+/K+ pump inhibitors. Their repurposing in oncology is currently investigated in preclinical and clinical studies. However, the identification of a specific cancer type defined by a molecular signature to design targeted clinical trials with cardiac glycosides remains to be characterized. Here, we demonstrate that cardiac glycoside proscillaridin A specifically targets MYC overexpressing leukemia cells and leukemia stem cells by causing MYC degradation, epigenetic reprogramming and leukemia differentiation through loss of lysine acetylation.

Methods: Proscillaridin A anticancer activity was investigated against a panel of human leukemia and solid tumor cell lines with different MYC expression levels, overexpression in vitro systems and leukemia stem cells. RNA-sequencing and differentiation studies were used to characterize transcriptional and phenotypic changes. Drug-induced epigenetic changes were studied by chromatin post-translational modification analysis, expression of chromatin regulators, chromatin immunoprecipitation, and mass-spectrometry.

Results: At a clinically relevant dose, proscillaridin A rapidly altered MYC protein half-life causing MYC degradation and growth inhibition. Transcriptomic profile of leukemic cells after treatment showed a downregulation of genes involved in MYC pathways, cell replication and an upregulation of hematopoietic differentiation genes. Functional studies confirmed cell cycle inhibition and the onset of leukemia differentiation even after drug removal. Proscillaridin A induced a significant loss of lysine acetylation in histone H3 (at lysine 9, 14, 18 and 27) and in non-histone proteins such as MYC itself, MYC target proteins, and a series of histone acetylation regulators. Global loss of acetylation correlated with the rapid downregulation of histone acetyltransferases. Importantly, proscillaridin A demonstrated anticancer activity against lymphoid and myeloid stem cell populations characterized by MYC overexpression.

Conclusion: Overall, these results strongly support the repurposing of proscillaridin A in MYC overexpressing leukemia.


Cardiac glycosides; Chromatin remodelling; Leukemia; Leukemia stem cells; Lysine acetylation; Lysine acetyltransferase; MYC; Proscillaridin A.


Heart failure drug proscillaridin A targets MYC overexpressing leukemia through global loss of lysine acetylation


Elodie M Da Costa 1 2, Gregory Armaos 1 2, Gabrielle McInnes 1 2, Annie Beaudry 2, Gaël Moquin-Beaudry 1 2, Virginie Bertrand-Lehouillier 2 3, Maxime Caron 2, Chantal Richer 2, Pascal St-Onge 2, Jeffrey R Johnson 4, Nevan Krogan 4, Yuka Sai 5, Michael Downey 5, Moutih Rafei 1 6 7, Meaghan Boileau 8, Kolja Eppert 8, Ema Flores-Diaz 9, Andre Haman 9, Trang Hoang 1 9, Daniel Sinnett 2 10, Christian Beausejour 1 2, Serge McGraw 2 3 11, Noël J-M Raynal 12 13

Publish date

2019 Jun 13




Glioblastoma (GBM) is characterized by highly aggressive growth and invasive behavior. Due to the highly lethal nature of GBM, new therapies are urgently needed and repositioning of existing drugs is a promising approach. We have previously shown the activity of Proscillaridin A (ProA), a cardiac glycoside inhibitor of the Na(+)/K(+) ATPase (NKA) pump, against proliferation and migration of GBM cell lines. ProA inhibited tumor growth in vivo and increased mice survival after orthotopic grafting of GBM cells. This study aims to decipher the mechanism of action of ProA in GBM tumor and stem-like cells. ProA displayed cytotoxic activity on tumor and stem-like cells grown in 2D and 3D culture, but not on healthy cells as astrocytes or oligodendrocytes. Even at sub-cytotoxic concentration, ProA impaired cell migration and disturbed EB1 accumulation at microtubule (MT) plus-ends and MT dynamics instability. ProA activates GSK3β downstream of NKA inhibition, leading to EB1 phosphorylation on S155 and T166, EB1 comet length shortening and MT dynamics alteration, and finally inhibition of cell migration and cytotoxicity. Similar results were observed with digoxin. Therefore, we disclosed here a novel pathway by which ProA and digoxin modulate MT-governed functions in GBM tumor and stem-like cells. Altogether, our results support ProA and digoxin as potent candidates for drug repositioning in GBM.


Proscillaridin A exerts anti-tumor effects through GSK3β activation and alteration of microtubule dynamics in glioblastoma


Raphael Berges 1, Emilie Denicolai 1, Aurelie Tchoghandjian 1, Nathalie Baeza-Kallee 1, Stephane Honore 1, Dominique Figarella-Branger 1, Diane Braguer 2

Publish date

2018 Sep 24;

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