Terrestrosin D

Terrestrosin D is an orally active apoptosis inducer. Terrestrosin D induces cell cycle arrest at the G1 and S phases, reduces mitochondrial membrane potential, and inhibits the growth of cancer cells and endothelial cells. Terrestrosin D is studied in castration-resistant prostate cancer and pulmonary fibrosis^[1][2][3]. In Vitro:Terrestrosin D (2.6-41.3 μM; 24 h) exerts significant cytotoxicity in human normal liver LO2 cells (IC₅₀ = 16.88 μM) and human embryonic kidney 293T cells (IC₅₀ = 21.80 μM) following 24 h of treatment^[1].
Terrestrosin D (1-5 μM; 24 h) potently inhibits the growth of PC-3, PC-3M, DU145, LNCaP, and 22RV1 human prostate cancer cells with an IC₅₀ below 5 μM after 24 h of treatment^[2].
Terrestrosin D (2-5 μM; 24 h) induces G₁ phase cell cycle arrest in PC-3 human prostate cancer cells after 24 h of treatment with 2 or 5 μM^[2].
Terrestrosin D (1-5 μM; 24 h) potently inhibits the growth of HUVECs and bladder-derived normal human microvascular endothelial cells with an IC₅₀ below 3 μM after 24 h of treatment^[2].
Terrestrosin D (2-3 μM; 24 h) induces S phase cell cycle arrest in HUVEC human endothelial cells after 24 h of treatment with 2 or 3 μM^[2].
Terrestrosin D (2-5 μM; 24 h) induces dose-dependent, caspase-independent apoptosis in PC-3 human prostate cancer cells, with 60.5% of cells undergoing apoptosis after 24 h of treatment with 5 μM^[2].
Terrestrosin D (5 μM; 24 h) does not activate caspase-3 and instead reduces its activity in PC-3 human prostate cancer cells after 24 h of treatment with 5 μM, confirming a caspase-independent apoptotic mechanism^[2].
Terrestrosin D (2-3 μM; 24 h) induces dose-dependent, caspase-independent apoptosis in HUVEC human endothelial cells, with 34.3% of cells undergoing apoptosis after 24 h of treatment with 3 μM^[2].
Terrestrosin D (3 μM; 24 h) does not activate caspase-3 and instead reduces its activity in HUVEC human endothelial cells after 24 h of treatment with 3 μM, confirming a caspase-independent apoptotic mechanism^[2].
Terrestrosin D (2-5 μM; 24 h) induces mitochondrial membrane potential depolarization in 53.8% of PC-3 human prostate cancer cells^[2].
Terrestrosin D (2-3 μM; 24 h) induces dose-dependent mitochondrial membrane potential depolarization in HUVEC human endothelial cells^[2].
Terrestrosin D (1-5 μM; 24 h) dose-dependently increases VEGF secretion in PC-3 human prostate cancer cells, causing a 1.86-fold increase after 24 h of treatment with 5 μM^[2].
Terrestrosin D (1-3 μM; 24 h) dose-dependently increases VEGF secretion in HUVEC human endothelial cells, causing an 11.21-fold increase after 24 h of treatment with 3 μM^[2]. In Vivo:Terrestrosin D (5-15 mg/kg; p.o.; daily; 28 days) induces reversible dose-dependent hepatorenal toxicity in male Sprague-Dawley rats^[1].
Terrestrosin D (50 mg/kg; i.p.; 3 times weekly; 4 weeks) significantly suppresses PC-3 xenograft tumor growth in BALB/c nude mice, increases tumor cell apoptosis, and reduces tumor angiogenesis, without causing significant body weight loss^[2].
Terrestrosin D (10 mg/kg; i.p.; daily for
6 weeks) significantly attenuates Bleomycin (HY-108345)-induced pulmonary inflammation and fibrosis in male KM mice^[3].