Panaxatriol

Panaxatriol is an orally active dammarane-type tetracyclic triterpene sapogenin. Panaxatriol enhances the phosphorylation levels of Akt, insulin receptor and p70S6K in skeletal muscle. Panaxatriol reduces the mRNA expression level of Atrogin1 in skeletal muscle. Panaxatriol induces apoptosis, pre-G1 cell cycle arrest and increased intracellular ROS levels in prostate cancer cells, decreases mitochondrial membrane potential, inhibits cell migration and reduces colony formation. Panaxatriol can be used in research related to insulin resistance, myocardial ischemia/reperfusion injury and prostate cancer^[1][2][3]. In Vitro:Panaxatriol (15-60 μM; 48-72 h) exhibits concentration-dependent cytotoxicity against DU-15 human prostate cancer cells, with an IC₅₀ of 30 μM^[3].
Panaxatriol (15-60 μM; 6 days) concentration-dependently suppresses colony formation by DU-15 human prostate cancer cells^[3].
Panaxatriol (15-60 μM; 48 h) concentration-dependently induces apoptosis in DU-15 human prostate cancer cells, as detected by DAPI staining^[3].
Panaxatriol (15-60 μM; 72 h) concentration-dependently increases intracellular ROS production in DU-15 human prostate cancer cells^[3].
Panaxatriol (15-60 μM; 72 h) concentration-dependently reduces mitochondrial membrane potential in DU-15 human prostate cancer cells^[3].
Panaxatriol (15-60 μM; 24 h) concentration-dependently induces sub-G1 cell cycle arrest in DU-15 human prostate cancer cells, with 24.8% of cells arrested at 60 μM^[3].
Panaxatriol (30 μM; 48 h) inhibits the migration of DU-15 human prostate cancer cells in an in vitro wound healing assay^[3]. In Vivo:Panaxatriol (0.2% in standard diet; p.o.; daily; 6 weeks) supplementation alone improves insulin resistance markers and modulates muscle protein synthesis/degradation pathways in insulin-resistant KKAy mice, and when combined with aerobic exercise, it further reduces HOMA-R to 10.3, increases soleus muscle mass to 16.3 mg, and enhances Akt and p70S6K phosphorylation compared to exercise alone^[1].
Pretreatment with panaxatriol (5 mg/kg; p.o.; daily; 7 days) markedly ameliorates ischemia/reperfusion-induced myocardial damage in isolated rat hearts, as demonstrated by preserved cardiac contractile function, reduced myocardial enzyme leakage, attenuated oxidative stress, and delayed time to contracture^[2].