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Thapsigargin

Catalog No. TQ0302   CAS 67526-95-8

Thapsigargin is a natural product, an inhibitor of sarcoplasmic/endoplasmic reticulum Ca2+ ATPase (SERCA) and an endoplasmic reticulum stress inducer. Thapsigargin increases cytoplasmic calcium concentration by blocking the ability of cells to pump calcium into the sarcoplasmic and endoplasmic reticulum.

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Thapsigargin Chemical Structure
Thapsigargin, CAS 67526-95-8
Pack Size Availability Price/USD Quantity
1 mg In stock $ 82.00
1 mL * 10 mM (in DMSO) In stock $ 570.00
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Purity: 99.3%
Purity: 99.07%
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Biological Description
Chemical Properties
Storage & Solubility Information
Description Thapsigargin is a natural product, an inhibitor of sarcoplasmic/endoplasmic reticulum Ca2+ ATPase (SERCA) and an endoplasmic reticulum stress inducer. Thapsigargin increases cytoplasmic calcium concentration by blocking the ability of cells to pump calcium into the sarcoplasmic and endoplasmic reticulum.
In vitro METHODS: Human rheumatoid arthritis synoviocytes MH7A were treated with Thapsigargin (0.001-1 μM) for 2-4 days, and cell proliferation was detected using the SRB.
RESULTS: Thapsigargin inhibited the proliferation of MH7A cells in a time- and dose-dependent manner. [1]
METHODS: Human hepatocellular carcinoma cells HepG2 were treated with Thapsigargin (25-100 nM) for 24 h. Endoplasmic reticulum stress/UPR gene expression was detected by RT-qPCR.
RESULTS: Thapsigargin treatment consistently induced ER stress gene expression only at elevated concentrations of 50 and 100 nM. [2]
In vivo METHODS: To assay in vivo ER stress-inducing activity, Thapsigargin (0.25-1 μg/g in 150 mM dextrose containing 1% DMSO) was administered as a single intraperitoneal injection to Balb/c mice in order.
RESULTS: Thapsigargin treatment resulted in significant expression of the ER stress markers ATF6 and eIF2α in adipose tissue. thapsigargin treatment failed to induce the expression of most of the ER stress and UPR proteins in the liver. [2]
METHODS: To investigate the antiviral function in vivo, Thapsigargin (30 ng/mouse) was administered by gavage to PR8 virus-infected BALB/c mice once daily for seven days.
RESULTS: Oral administration of Thapsigargin to mice significantly reduced severity and viral shedding and improved survival during infection with the deadly influenza virus. [3]
Cell Research Cell Line: MH7A human rheumatoid arthritis synovial cells. Concentration: 0.001, 0.1, and 1?μM. Incubation Time: For 2 and 4 days [2]
Animal Research Animal Model: Male Balb/c mice (20-25g). Dosage: 0.25ug/g, 0.5ug/g and 1ug/g. Administration: Injection; 24 hours [4]
Molecular Weight 650.75
Formula C34H50O12
CAS No. 67526-95-8

Storage

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

Solubility Information

DMSO: 250 mg/mL (384.17 mM), sonification is recommended.

TargetMolReferences and Literature

1. Wang H, et al. Effects of thapsigargin on the proliferation and survival of human rheumatoid arthritis synovial cells. ScientificWorldJournal. 2014 Feb 9;2014:605416. 2. Abdullahi A, et al. Modeling Acute ER Stress in Vivo and in Vitro. Shock. 2017 Apr;47(4):506-513. 3. Goulding LV, et al. Thapsigargin at Non-Cytotoxic Levels Induces a Potent Host Antiviral Response that Blocks Influenza A Virus Replication. Viruses. 2020 Sep 27;12(10):1093. 4. Abdullahi A, et al. Modeling Acute ER Stress in Vivo and in Vitro. Shock. 2017 Apr;47(4):506-513.

Related compound libraries

This product is contained In the following compound libraries:
Natural Product Library Bioactive Compound Library Calcium Channel Compound Library NO PAINS Compound Library Anti-Hypertension Compound Library Bioactive Compounds Library Max Anti-Infection Compound Library Selected Plant-Sourced Compound Library Apoptosis Compound Library Neuronal Signaling Compound Library

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Keywords

Thapsigargin 67526-95-8 Apoptosis Membrane transporter/Ion channel Metabolism Microbiology/Virology SARS-CoV Calcium Channel Ca2+ channels stress inhibit unfolded Inhibitor Ca channels coronavirus protein ,response SARS coronavirus inhibitor

 

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