Terameprocol

Terameprocol is an inhibitor targeting the Sp1 transcription factor, which can selectively inhibit the transcription of Sp1-dependent genes. Terameprocol exerts its effects by inhibiting Sp1-mediated gene transcription, such as reducing the expression of genes like CDC2, survivin and HMGB1, thereby arresting the cell cycle, inducing apoptosis, and suppressing the inflammatory response. Terameprocol exhibits anti-proliferative, pro-apoptotic, and anti-inflammatory activities and is currently mainly used in the research of diseases such as cancer and pulmonary arterial hypertension[1][2][3]. In Vitro:Terameprocol (25 μM; 16 h) inhibited the production of prostaglandins (PGE2), some cytokines and chemokines induced by lipopolysaccharide (LPS) in RAW 264.7 cells, and also inhibited the expression and activity of COX-2, and inhibited the growth of RAW264.7 cells, but did not induce cell apoptosis^[1]. Terameprocol (10 μM; 24 h, 48 h) downregulated survivin transcription and protein expression in HCC2429 and H460 non-small cell lung cancer cell experiments, while enhancing the sensitivity of cells to radiotherapy, but did not induce cell apoptosis and did not affect the cell cycle^[2]. Terameprocol (0.1-20 μM; 24 h) inhibited cell proliferation in a dose-dependent manner in rat pulmonary artery smooth muscle cells (PASMCs) experiments, and induced cell apoptosis at 20 μM^[3]. In Vivo:Terameprocol (1 mg; intraperitoneal injection; 1 time; administered 1 hour before lipopolysaccharide (LPS) injection) reduces the levels of TNF-α and MCP-1 in the serum of C57BL6/J mice in the endotoxemia model^[1].
Terameprocol (166mg/kg; intraperitoneal injection; on days 7, 12, and 17; for 21 days) improves cardiac function, alleviates cardiac and pulmonary remodeling, inhibits the proliferation and induces the apoptosis of pulmonary artery smooth muscle cells in the monocrotaline (MCT)-induced pulmonary hypertension model of male Wistar rats (weighing 180-200g, age not mentioned)^[3].