Tranilast sodium (MK-341 sodium) serves as an anti-atopic agent and is effective in suppressing the production of prostaglandin D2 (PGD2) with an IC50 of 0.1 mM. This compound is known for its anti-inflammatory and immunomodulatory effects[1]. Furthermore, Tranilast sodium counteracts the actions of angiotensin II and inhibits its biological effects on vascular smooth muscle cells[2].
体内研究
When administered orally at a dose of 300 mg/kg twice daily for three days, Tranilast dose-dependently suppresses angiogenesis in mice, further highlighting its potential therapeutic applications[5].
体外研究
Tranilast demonstrates significant immunomodulatory activities, notably inhibiting the formation of various inflammatory mediators. It effectively inhibits Endotoxin-induced production of prostaglandin E2 (PGE2) with IC50 values ranging from approximately 1 to 20 μM, thromboxane B2 with IC50 values between 10 and 50 μM, transforming growth factor beta 1 (TGF-β1) with IC50 values around 100 to 200 μM, and interleukin-8 (IL-8) with an IC50 of about 100 μM. Additionally, Tranilast suppresses A23187-induced monocyte leukotriene C4 and PGE2 formation with IC50 values ranging from 10 to 40 μM and 2 to 20 μM, respectively[3].
In vitro studies demonstrate that Tranilast exerts a dose-dependent anti-proliferative effect on MCF-7 and MDA-MB-231 breast cancer cell lines within the concentration range of 10 to 200 μM. It also enhances the anti-tumor effects of Tamoxifen, administered at concentrations of 1 to 20 μM, on these human breast cancer cells[4].
Additionally, Tranilast inhibits the proliferation of human dermal microvascular endothelial cells (HDMECs) at concentrations of 12.5, 25, 50, and 100 μg/mL over 72 hours[5].
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