Thapsigargin (0.001-?1 μM; for 2 and 4 days) arrests cell proliferations in MH7A human rheumatoid arthritis synovial cells in a time- and dose-dependent manner.
Thapsigargin (0.001-?1 μM; for 2 and 4 days) induces cell apoptosis in MH7A cells in a time- and dose-dependent manner.
Thapsigargin (0.001-?1 μM; for 2 and 4 days) impairs mTOR activity and leads to cyclin D1 expressions in MH7A cells.
Thapsigargin inhibits Ca ²⁺ entry into human neutrophil granulocytes.
Thapsigargin inhibits the carbachol-evoked [Ca ²⁺ ]i-transients with (IC ₅₀ =0.353 nM) or without (IC ₅₀ =0.448 nM) a KCl-prestimulation, but an additional small component, with a much lower sensitivity (IC ₅₀ =4814 nM), is observed in the absence of a KCl-prestimulation. In contrast, the KCl-evoked [Ca ²⁺ ]i-transients displayed only one component with a very low sensitivity to Thapsigargin in both absence (IC ₅₀ =3343 nM) and presence (IC ₅₀ =6858 nM) of a carbachol-prestimulation.

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.