Typhaneoside

Typhaneoside is an orally active activator of PI3K/Akt/mTOR and farnesoid X receptor. Typhaneoside promotes the activation of AMPK and Caspase-3, induces apoptosis, ferroptosis, autophagy, ROS accumulation, cell cycle arrest at the G₂/M phase, and reduces cancer cell viability. Typhaneoside improves glucose and lipid metabolism, alleviates inflammatory responses, oxidative stress and hepatic lipid accumulation, and exerts hepatoprotective effects. Typhaneoside can be used in research related to heart failure after myocardial infarction, acute myeloid leukemia, non-alcoholic fatty liver disease and neurological disorders^[1][2][3][4]. In Vitro:Typhaneoside (0-50 μM; 12-48 h) significantly reduces the viability of Kas-1, HL60 and NB4 acute myeloid leukemia cells in a time- and dose-dependent manner, while exerts no significant effect on K562 acute myeloid leukemia cells or normal 293T cells^[2].
Typhaneoside (20-40 μM; 24 h) induces apoptosis in Kas-1, HL60 and NB4 acute myeloid leukemia cells in a dose-dependent manner, with the highest apoptosis rate induced by treatment at 40 μM^[2].
Typhaneoside (20-40 μM; 24 h) dose-dependently reduces the mRNA expression levels of genes associated with mitochondrial dysfunction (NDUFS3, SDHB, UQCRFS1, TFAM, ClpP) in Kas-1, HL60 and NB4 acute myeloid leukemia cells^[2].
The effects of typhaneoside (40 μM; 24 h) on inducing reactive oxygen species production and apoptosis in Kas-1, HL60 and NB4 acute myeloid leukemia cells are significantly reversed by pre-treatment with NAC or DFO^[2].
Typhaneoside (40 μM; 24 h) upregulates autophagy-related proteins (ATG5, ATG7, Beclin 1, LC3) in Kas-1, HL60, and NB4 acute myeloid leukemia cells, and this effect is reversed by pre-treatment with 5 mM NAC for 2 h^[2].
Typhaneoside (12.5-50 μM; 24 h) activates FXR-dependent BSEP promoter activity in HEK293T cells, with significant activation observed at the concentration of 50 μM after 24 h^[3].
Typhaneoside (12.5-50 μM; 24 h) alleviates OAPA-induced lipid accumulation, oxidative stress, inflammatory response and glucose metabolism disorder in HepG2 cells by activating the AKT/GSK3β signaling pathway^[3].
Typhaneoside (5-50 μM; 10 min) concentration-dependently inhibits 4-aminopyridine (HY-B0604)-induced glutamate release from rat cerebral cortical synaptosomes, with an IC₅₀ of 20 μM^[4].
Typhaneoside (20 μM; 10 min)-mediated inhibition of 4-aminopyridine-induced glutamate release from rat cerebral cortex synaptosomes targets Ca²⁺-dependent vesicular exocytosis, rather than reverse transport via Ca²⁺-independent glutamate transporters^[4].
Typhaneoside (20 μM) inhibits KCl-induced glutamate release from rat cerebral cortex synaptosomes^[4].
Typhaneoside (20 μM; 10 min)-mediated inhibition of 4-aminopyridine-induced glutamate release from rat cerebral cortex synaptosomes depends on N-type (Ca_v2.2) voltage-dependent Ca²⁺ channels, and does not involve intracellular Ca²⁺ release or mitochondrial Na⁺/Ca²⁺ exchange^[4].
The inhibitory effect of Typhaneoside (20 μM; 10 min) on 4-aminopyridine-induced glutamate release from rat cerebral cortex synaptosomes depends on the MAPK/ERK signaling pathway, and does not involve PKA or PKC^[4].
Typhaneoside (20 μM; 10 min) reduces the phosphorylation levels of 4-aminopyridine-induced ERK1/2 and its presynaptic target synapsin I in rat cerebral cortex synaptosomes, but exerts no such effect on JNK or p38^[4]. In Vivo:Typhaneoside (10-40 mg/kg; once daily; 4 weeks) improves cardiac function, normalizes hemodynamic parameters, reduces pro-inflammatory and cardiac remodeling biomarkers, and inhibits excessive autophagy via activation of the PI3K/Akt/mTOR pathway in a dose-dependent manner in rats with heart failure post-myocardial infarction^[1].
Typhaneoside (10-30 mg/kg; i.p.; daily; 30 days) dose-dependently suppresses AML tumor growth in BALB/c nude mice, with the 30 mg/kg dose achieving the greatest tumor volume reduction and the highest 30-day survival rate of ~50%, while showing no overt tissue toxicity^[2].
Typhaneoside (30 mg/kg; i.p.; daily; 30 days) causes no overt tissue toxicity in healthy BALB/c nude mice^[2].
Typhaneoside (15-60 mg/kg/day; p.o.; daily; 8 weeks) dose-dependently alleviates HFD-induced NAFLD in male C57BL/6 mice by activating FXR signaling, reducing body and adipose tissue weight, improving lipid and glucose homeostasis, mitigating liver injury, oxidative stress and inflammation, and enhancing BAT thermogenesis and energy expenditure^[3].