Pterosin B

Pterosin B is an orally active indanone. Pterosin B can be obtained from Pteridium aquilinum. Pterosin B is a Sik3 signaling inhibitor. Pterosin B inhibits Klf5 expression and reduces β-amyloid deposition. Pterosin B prevents chondrocyte hypertrophy and osteoarthritis in mice. Pterosin B inhibits cardiomyocyte hypertrophy, improves cognitive impairment, and lowers blood glucose. Pterosin B can be used in research on arthritis, Alzheimer's disease, pathological cardiac hypertrophy and diabetes^{[1][2][3][4][5]}. In Vitro:Pterosin B (300 μM; 5 days) reduces the amounts of Sik3, phosphorylated Hdac4, and phosphorylated Crtc1 in primary chondrocytes, similar to the effect of 4-OH tamoxifen^[2].
Pterosin B (10-50 μM; 48 h) inhibits Angiotensin II-induced cardiomyocyte hypertrophy in H9c2 cells, reducing hypertrophy-related gene expression, cell size, and protein synthesis^[3].
Pterosin B (1, 5 μM) promotes the phenotypic shift of lipopolysaccharide-induced BV-2 cells from M1 to M2, inhibits Klf5 expression, and attenuates Lipopolysaccharide-induced microglial glycolysis^[4].
Pterosin B (300 μM; 36 h) inhibits the SIK3 signaling pathway, suppressing the cytoplasmic localization of HDAC5 and CRTC2 in HEK293 cells^[5].
In Vivo:Pterosin B (900 μM; intra-articular injection; 3 times a week; 8-12 weeks) protects mice from the development of osteoarthritis and reduces the expression of Col10 in the non-calcified zone of articular cartilage in wild-type mouse knee osteoarthritis models^[2].
Pterosin B (5-20 mg/kg; p.o.; 8 weeks) ameliorates cognitive deficits, reduces β-amyloid deposition, and inhibits excessive microglia activation in APP/PS1 mice^[4].
Pterosin B (0.1% in diet; p.o.; 1 month) lowers blood glucose levels and enhances insulin responses in db/db mice^[5].