Thapsigargin

67526-95-8

650.75

DMSO : 250 mg/mL (384.17 mM; Need ultrasonic)

Apoptosis; Membrane Transporter/Ion Channel; Neuronal Signaling

Thapsigargin is an inhibitor of microsomal Ca²⁺-ATPase. Thapsigargin is a well characterized Endoplasmic Reticulum (ER) stress inducing agent^[1][2][3][4]. IC50 & Target: Ca²⁺-ATPase^[1] In Vitro: Thapsigargin (0.001-?1 uM; for 2 and 4 days) arrests cell proliferations in MH7A human rheumatoid arthritis synovial cells in a time- and dose-dependent manner^[2].
Thapsigargin (0.001-?1 uM; for 2 and 4 days) induces cell apoptosis in MH7A cells in a time- and dose-dependent manner^[2].
Thapsigargin (0.001-?1 uM; for 2 and 4 days) impairs mTOR activity and leads to cyclin D1 expressions in MH7A cells^[2].
Thapsigargin inhibits Ca²⁺ entry into human neutrophil granulocytes^[1].
Thapsigargin inhibits the carbachol-evoked [Ca²⁺]i-transients with (IC₅₀=0.353 nM) or without (IC₅₀=0.448 nM) a KCl-prestimulation, but an additional small component, with a much lower sensitivity (IC₅₀=4814 nM), is observed in the absence of a KCl-prestimulation. In contrast, the KCl-evoked [Ca²⁺]i-transients displayed only one component with a very low sensitivity to Thapsigargin in both absence (IC₅₀=3343 nM) and presence (IC₅₀=6858 nM) of a carbachol-prestimulation^[3].
In Vivo: Thapsigargin (Injection; 0.25 ug/g, 0.5 ug/g and 1 ug/g; 24 hours) significant increases of 2 to 5-fold in chemokine and pro-inflammatory expression. Thapsigargin is more sensitive to inducing a systemic immune response^[4].