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In cells, sarco/endoplasmic calcium ATPases (SERCAs) transport free calcium into the sarcoplasmic and endoplasmic reticula, lowering intracellular calcium levels to stop signaling through this cation. Thapsigargin is a non-competitive, cell permeable inhibitor of calcium transport by SERCAs (IC₅₀ values are cell type-dependent and range from ~2-80 nM). Inhibition of SERCAs leads to an increase in intracellular calcium, which has been linked to cell activation, release of histamine from mast cells, and increased proliferation of certain types of cancer cells. In vivo, thapsigargin and related sesquiterpene lactones have anti-inflammatory and anti-cancer effects.

THAPSIGARGIN is colourless film

Reagent for defining and manipulating intracellular calcium pools.

THAPSIGARGIN is a widely used inhibitor of the ubiquitous sarco-endoplasmic reticulum Ca(2+)-ATPases in mammalian cells. It acts as a potent, cell-permeable, IP3-independent intracellular calcium releaser that blocks the transient increase in intracellular Ca2+ induced by angiostatin and endostatin. It induces apoptosis by disrupting intracellular free Ca2+ levels.

THAPSIGARGIN is an organic heterotricyclic compound that is a hexa-oxygenated 6,7-guaianolide isolated fron the roots of Thapsia garganica L., Apiaceae. A potent skin irritant, it is used in traditional medicine as a counter-irritant. Thapsigargi inhibits Ca2+-transporting ATPase mediated uptake of calcium ions into sarcoplasmic reticulum and is used in experimentation examining the impacts of increasing cytosolic calcium concentrations.

Potent inhibitor of sarco-endoplasmic reticulum Ca 2+ -ATPases.

Thapsigargin is an effective inhibitor of calcium ion pumps located on sarcoplasmic reticulum (SR) and endoplasmic reticulum (ER) microsomes of skeletal, cardiac, muscle and brain tissues. The inhibition of calcium ion pumps causes intracellular increase of calcium ion levels. It was found that thapsigargin at 100 nM concentration effectively inhibited the SR Ca2+- adenosine triphosphatase (ATPase) in cardiac and skeletal muscles. Thapsigargin was also reported to be effective in blocking autophagy by interfering with the autophagosome-lysosome fusion.

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The actual mechanism of action of thapsigargin is thought actually to block calcium channels in an open conformation that results in excess calcium entry from outside the cell. Excess calcium activates DNAses and precipitates the natural death sequence of the cells.Scientists are now thinking of modifying thapsigargin in such a way thatit will kill prostate cells preferentially and will not penetrate healthy cells elsewhere in the body.At the same time, they are determining whether this drug can also induce cell death in breast cancer cells.

1) Treiman et al. (1998), A tool coming of age: thapsigargin as an inhibitor of sarco-endoplasmic reticulum Ca(2+)-ATPases; Trends Pharmacol. Sci., 19 131 2) Zhou et al. (2009), Autophagy-mediated insulin receptor down-regulation contributes to endoplasmic reticulum stress-induced insulin resistance; Mol. Pharmacol., 76 596