Thapsigargin是内质网应激诱导剂， 是一种微粒体Ca2+-ATPase抑制剂，可抑制不同细胞类型的冠状病毒复制。

Thapsigargin is a microsomal Ca2+-ATPase inhibitor and Endoplasmic Reticulum stress-inducing agent.

Thapsigargin inhibits Ca2+ entry into human neutrophil granulocytes[1]. Thapsigargin (0.001-?1 μM; for 2 and 4 days) arrests cell proliferation in MH7A human rheumatoid arthritis synovial 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 [2]. 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 very low sensitivity to Thapsigargin in both absence (IC50: 3343 nM) and presence (IC50: 6858 nM) of a carbachol-prestimulation [3].

Thapsigargin (Injection; 0.25ug/g, 0.5ug/g, and 1ug/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].

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 Model: Male Balb/c mice (20-25g). Dosage: 0.25ug/g, 0.5ug/g and 1ug/g. Administration: Injection; 24 hours [4]

67526-95-8

C34H50O12

650.75

毒胡萝卜素

DMSO:250 mg/mL (384.17 mM),Need ultrasonic
Powder: -20°C for 3 years
In solvent: -80°C for 2 years