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Saikosaponin D ATPase inhibitor

Cat.No.S5454

Saikosaponin D, a calcium mobilizing agent (SERCA inhibitor), is a type of Saponin derivative, which is a component extracted from Bupleurum falactum. This compound has anti-cancer activities.
Saikosaponin D ATPase inhibitor Chemical Structure

Chemical Structure

Molecular Weight: 780.98

Quality Control

Chemical Information, Storage & Stability

Molecular Weight 780.98 Formula

C42H68O13

Storage (From the date of receipt) 3 years -20°C powder
CAS No. 20874-52-6 -- Storage of Stock Solutions

Synonyms N/A Smiles CC1OC(OC2CCC3(C)C(CCC4(C)C3C=CC56OCC7(CCC(C)(C)CC57)C(O)CC46C)C2(C)CO)C(O)C(OC8OC(CO)C(O)C(O)C8O)C1O

Solubility

In vitro
Batch:

DMSO : 100 mg/mL (128.04 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Water : Insoluble

Ethanol : Insoluble

Molarity Calculator

Mass Concentration Volume Molecular Weight

In vivo
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In vivo Formulation Calculator (Clear solution)

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Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

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Mechanism of Action

Targets/IC50/Ki
SERCA [1]
In vitro
Saikosaponin D is a novel autophagic inducer that induces autophagy in various types of cancer cells through the formation of autophagosomes as measured by GFP-LC3 puncta formation. This compound increases cytosolic calciumlevel via direct inhibition of sarcoplasmic/endoplasmic reticulum Ca2+ATPase pump, leading to autophagy induction through the activation of the Ca2+/calmodulin-dependent kinase kinase-AMP-activated protein kinase-mammalian target of rapamycin pathway. Its treatment causes the disruption of calcium homeostasis, which induces endoplasmic reticulum stress as well as the unfolded protein responses pathway[1]. It can exhibit anti-cancer activities, which is mediated by the induction of apoptosis and autophagic cell death regardless of p53 status. Low dose of this chemical is capable of sensitizing chremosensitive or chemoresistant lung and cervical cancer or hepatoma cells to anti-cancer drug- or radiation-induced apoptosis. It also down-regulates PPM1D content, leading to the activation of Chk1, phosphorylation of Cdc25c and Cdk1, and subsequent G2/M arrest and apoptosis[2].
References

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