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Proscillaridin A
Proscillaridin A
ChemFaces products have been cited in many studies from excellent and top scientific journals
Product Name Proscillaridin A
Price:
CAS No.: 466-06-8
Catalog No.: CFN70368
Molecular Formula: C30H42O8
Molecular Weight: 530.7 g/mol
Purity: >=98%
Type of Compound: Steroids
Physical Desc.: Powder
Source: The herbs of Drimia robusta
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
Download: COA    MSDS
Similar structural: Comparison (Web)  (SDF)
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According to end customer requirements, ChemFaces provide solvent format. This solvent format of product intended use: Signaling Inhibitors, Biological activities or Pharmacological activities.
Size /Price /Stock 10 mM * 1 mL in DMSO / Inquiry
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Related Screening Libraries
Size /Price /Stock 10 mM * 100 uL in DMSO / Inquiry / In-stock
10 mM * 1 mL in DMSO / Inquiry / In-stock
Related Libraries
Biological Activity
Description: Proscillaridin A is a cardiac glycoside, it has anticancer, analgesic effects and immunoreactivities. Proscillaridin A induces apoptosis in MDA-MB-231 cells by increasing free calcium concentration and by activating caspase-3. It exerts anti-tumor effects through GSK3β activation and alteration of microtubule dynamics in glioblastoma.
Targets: GSK3β | Topoisomerase | Caspase | STAT3 | JNK | TrxR1 | JNK | PARP | Src | eIF2α | ATPase | Bcl-2/Bax | Sodium Channel | Potassium Channel | DNA
In vitro:
Biological & Pharmaceutical Bulletin, 2008, 31(6):1131-1140.
Antiproliferative Activity of Derivatives of Ouabain, Digoxin and Proscillaridin A in Human MCF7 and MDA-MB-231 Breast Cancer Cells.[Reference: WebLink]
Three derivatives of ouabain, digoxin and Proscillaridin A containing the carboxylic group instead of the lactone moiety were synthesized and examined for cytotoxicity in human breast cancer cells.
METHODS AND RESULTS:
Evaluation of the cytotoxicity of these compounds employing an MTT assay and inhibition of [3H]thymidine incorporation into DNA in both MCF-7 and MDA-MB-231 breast cancer cells demonstrated that compound 3, the most active of the series, proved to be only slightly less potent than Proscillaridin A. We evaluated the effects of these compounds 1-3 on change in intracellular Ca2+, appearance of apoptosis, inhibition of DNA topoisomerase I and II, and the activity of caspase-3 in breast cancer cells. These studies indicate that the increase in potency for 3 may be related, in part, to an activation of caspase-3, increasing free calcium concentration and topoisomerase II inhibition.
CONCLUSIONS:
All these data emphasize the potential usefulness of these derivatives of cardiac glycosides as anticancer agents.
Clinical and Experimental Hypertension, 1998, 20(5-6):593-599.
Proscillaridin A Immunoreactivity: Its Purification, Transport in Blood By A Specific Binding Protein And Its Correlation With Blood Pressure.[Reference: WebLink]

METHODS AND RESULTS:
A material crossreacting with antibodies against the bufadienolide Proscillaridin A and inhibiting the sodium pump was found in human blood plasma. The concentration of the material with a retention time similar to ouabain in a reversed phase HPLC correlated to systolic blood pressure and pulse pressure. Affinity purification of this compound from bovine adrenals resulted in the isolation of a compound with molecular mass of 600 Da that was not identical with ouabain.
CONCLUSIONS:
Consistent with the postulate that endogenous ouabain and Proscillaridin A immunoreactivities may belong to a new class of cardiotonic steroid hormones, a protein of Mr = 60 kDa has been found in bovine serum by affinity-labeling with N-hydroxysuccimidyl digoxigenin-3-O-methylcarbonyl-epsilon-aminocaproate.
In vivo:
Digest Journal of Nanomaterials & Biostructures, 2010, 5(2):457-465.
Analgesic effects of scilliroside, proscillaridin-a and taxifolin from squill bulb (Urginea maritima) on pains.[Reference: WebLink]
The aim of the present study was to assess the clinical efficacy of Proscillaridin A (C30H42O8), taxifolin (C15H12O7) and scilliroside ( C32H44O12 ) and safety of squill bulb (Urginea maritima) (L.) Baker extract on various pains of spontaneous volunteer patients.
METHODS AND RESULTS:
In this study, 250 patients were monitored in coats. The average age of these patients were between 40 and 74 years old. Of these 100 were male and 150 female patients. Also, 60 % of proscillaridin-A (C30H42O8), taxifolin (C15H12O7) and scilliroside ( C32H44O12 ) solution in pure glycerin was applied as external on the pain area.ASO, CRP and RF higher values of patiens were significantly decreased ( p < 0.05 and p < 0.01). Knee, joint, calf, hip, shoulder, upper back, low back (lumbago), tailbone and fibromyalgia paints of patients were significantly reduced (p < 0.05 and p < 0.01).
CONCLUSIONS:
Squill bulb constituents can reduce the musculoskeletal pains.
Proscillaridin A Description
Source: The herbs of Drimia robusta
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

Cell. 2018 Jan 11;172(1-2):249-261.e12.
doi: 10.1016/j.cell.2017.12.019.
IF=36.216(2019)

PMID: 29328914

Cell Metab. 2020 Mar 3;31(3):534-548.e5.
doi: 10.1016/j.cmet.2020.01.002.
IF=22.415(2019)

PMID: 32004475

Mol Cell. 2017 Nov 16;68(4):673-685.e6.
doi: 10.1016/j.molcel.2017.10.022.
IF=14.548(2019)

PMID: 29149595

ACS Nano. 2018 Apr 24;12(4): 3385-3396.
doi: 10.1021/acsnano.7b08969.
IF=13.903(2019)

PMID: 29553709

Nature Plants. 2016 Dec 22;3: 16206.
doi: 10.1038/nplants.2016.205.
IF=13.297(2019)

PMID: 28005066

Sci Adv. 2018 Oct 24;4(10): eaat6994.
doi: 10.1126/sciadv.aat6994.
IF=12.804(2019)

PMID: 30417089
Calculate Dilution Ratios(Only for Reference)
1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 1.8843 mL 9.4215 mL 18.843 mL 37.6861 mL 47.1076 mL
5 mM 0.3769 mL 1.8843 mL 3.7686 mL 7.5372 mL 9.4215 mL
10 mM 0.1884 mL 0.9422 mL 1.8843 mL 3.7686 mL 4.7108 mL
50 mM 0.0377 mL 0.1884 mL 0.3769 mL 0.7537 mL 0.9422 mL
100 mM 0.0188 mL 0.0942 mL 0.1884 mL 0.3769 mL 0.4711 mL
* Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
Protocol
Kinase Assay:
Oxidative Medicine & Cellular Longevity, 2018, 2018:1-17.
Proscillaridin A Promotes Oxidative Stress and ER Stress, Inhibits STAT3 Activation, and Induces Apoptosis in A549 Lung Adenocarcinoma Cells.[Reference: WebLink]
Cardiac glycosides are natural compounds used for the treatment of cardiovascular disorders. Although originally prescribed for cardiovascular diseases, more recently, they have been rediscovered for their potential use in the treatment of cancer. Proscillaridin A (PSD-A), a cardiac glycoside component of Urginea maritima, has been reported to exhibit anticancer activity. However, the cellular targets and anticancer mechanism of PSD-A in various cancers including lung cancer remain largely unexplored.
METHODS AND RESULTS:
In the present study, we found that PSD-A inhibits growth and induces apoptosis in A549 lung adenocarcinoma cells. The anticancer activity of PSD-A was found to be associated with the activation of JNK, induction of ER stress, mitochondrial dysfunction, and inhibition of STAT3 activation. PSD-A induces oxidative stress as evidenced from ROS generation, GSH depletion, and decreased activity of TrxR1. PSD-A-mediated ER stress was verified by increased phosphorylation of eIF2α and expression of its downstream effector proteins ATF4, CHOP, and caspases-4. PSD-A triggered apoptosis by inducing JNK (1/2) activation, increasing bax/bcl-2 ratio, dissipating mitochondrial membrane potential, and inducing cleavage of caspases and PARP. Further study revealed that PSD-A inhibits both constitutive and inducible STAT3 activations and decreases STAT3 DNA-binding activity. Moreover, PSD-A-mediated inhibition of STAT3 activation was found to be associated with increased SHP-1 expression, decreased phosphorylation of Src, and binding of PSD-A with STAT3 SH2 domain. Finally, STAT3 knockdown by shRNA inhibited growth and enhanced apoptotic efficacy of PSD-A.
CONCLUSIONS:
Taken together, the data suggest that PSD-A could be developed into a potential therapeutic agent against lung adenocarcinoma.
Cell Death & Disease,2018,9(10):984.
Proscillaridin A exerts anti-tumor effects through GSK3β activation and alteration of microtubule dynamics in glioblastoma.[Reference: WebLink]
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.
METHODS AND RESULTS:
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.
CONCLUSIONS:
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.
Cell Research:
Archives of Pharmacal Research, 2007, 30(10):1216-1224.
Apoptosis-mediated cytotoxicity of ouabain, digoxin and proscillaridin A in the estrogen independent MDA-MB-231 breast cancer cells.[Reference: WebLink]

METHODS AND RESULTS:
We examined the effects of three cardiac glycosides, ouabain, digoxin and Proscillaridin A, on the proliferation of estrogen independent MDA-MB-231 breast cancer cells. In terms of reduction in cell viability, the compounds rank for both 24 h and 48 h of incubation in MDA-MB-231 cells in the order Proscillaridin A > digoxin > ouabain. Digoxin for 24 h and 48 h of incubation in MDA-MB-231 cells proved to be only slightly more potent than ouabain, with IC50 values of 122 +/- 2 and 70 +/- 2 nM, respectively, compared to 150 +/- 2 and 90 +/- 2 nM for ouabain. In contrast, Proscillaridin A, was much more active and showed a high level of cytotoxic potency, IC50 51 +/- 2 and 15 +/- 2 nM for 24 h and 48 h of incubation, respectively. The concentrations of digoxin, ouabain and Proscillaridin A needed to inhibit [3H]thymidine incorporation into DNA by 50% (IC50) in MDA-MB-231 cells for 24 h of incubation were found to be 124 +/- 2 nM, 142 +/- 2 nM, and 48 +/- 2 nM, respectively.
CONCLUSIONS:
In the present study, we demonstrated that ouabain, digoxin, and Proscillaridin A induce apoptosis in MDA-MB-231 cells by increasing free calcium concentration and by activating caspase-3.
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