Cyasterone

• CAS: 17086-76-9
• Catalog Number: ACM17086769-1
• Category: Main Products
• Molecular Weight: 520.65
• Molecular Formula: C29H44O8
• Synonyms: cyasteron; Cyasterone
• IUPAC Name: (3S,4S,5R)-4-[(2R,3R)-2,3-dihydroxy-3-[(2S,3R,5R,9R,10R,13R,14S,17S)-2,3,14-trihydroxy-10,13-dimethyl-6-oxo-2,3,4,5,9,11,12,15,16,17-decahydro-1H-cyclopenta[a]phenanthren-17-yl]butyl]-3,5-dimethyloxolan-2-one
• SMILES: C[C@H]1[C@@H]([C@H](OC1=O)C)C[C@H]([C@@](C)([C@H]2CC[C@@]3([C@@]2(CC[C@H]4C3=CC(=O)[C@H]5[C@@]4(C[C@@H]([C@@H](C5)O)O)C)C)O)O)O
• InChI: InChI=1S/C29H44O8/c1-14-16(15(2)37-25(14)34)10-24(33)28(5,35)23-7-9-29(36)18-11-20(30)19-12-21(31)22(32)13-26(19,3)17(18)6-8-27(23,29)4/h11,14-17,19,21-24,31-33,35-36H,6-10,12-13H2,1-5H3/t14-,15+,16-,17-,19-,21+,22-,23-,24+,26+,27+,28+,29+/m0/s1
• InChI Key: NEFYSBQJYCICOG-YSEUJXISSA-N
• Boiling Point: 735.2±60.0 °C
• Melting Point: 164-166 °C
• Flash Point: 239.2ºC
• Density: 1.31±0.1 g/ml
• Appearance: White powder
• Exact Mass: 520.30400
• pKa: 14.12±0.70

Case Study

How Does Cyasterone Improve Sepsis-Related Acute Lung Injury

Lin, Miao, et al. Chinese medicine, 2023, 18(1), 136.

This study investigated cyasterone's impact and its underlying mechanisms in treating sepsis-related acute lung injury (ALI). Researchers established a mouse sepsis model using cecal ligation and puncture (CLP) before administering cyasterone intraperitoneally from day 1 to day 3 to evaluate its preventive effects against acute lung injury in sepsis. Besides, the research also analyzed the molecular mechanism of cyasterone using primary mouse peritoneal macrophages in vitro.
Key Findings
· Cyasterone pretreatment reduced lung histopathological injury and oxidative stress caused by CLP, decreased the secretion of inflammatory factors, and inhibited the activation of the NLRP3 inflammasome in mice with acute lung injury (ALI).
· Additionally, cyasterone enhanced the expression of antioxidant enzymes via AKT(Ser473)/GSK3β(S9)/Nrf2 pathway activation, lowered ROS levels, and consequently diminished the release of pro-inflammatory cytokines and NLRP3 inflammasome activation triggered by LPS in primary mouse peritoneal macrophages.
· Research results propose that cyasterone shows potential as a therapeutic agent to prevent sepsis-induced acute lung injury.

Cyasterone Accelerates Fracture Healing by Promoting MSCs Migration and Osteogenesis

Zhu, Junlang, et al. Journal of Orthopaedic Translation, 2021, 28, 28-38.

Mesenchymal stem cell (MSCs) therapy has become a hot topic in clinical research on regenerative medicine, but it is limited by the fact that only a few implanted MSCs can successfully reach the site of injury. This work studied the effects of cyasterone on in vitro MSCs migration and osteogenic differentiation, as well as the related potential mechanisms.
· Evaluation Methods
The migration and osteogenesis of MSCs were assessed using a transwell assay and Alizarin Red S staining. Gene and protein expression levels were measured through qPCR and Western Blot analysis. Furthermore, the enhanced migratory capacity of MSCs induced by Cyasterone was inhibited by CXCR4 siRNA. A rat model of femoral fracture was also established to investigate the impact of Cyasterone on fracture healing. Additionally, this study examined the influence of Cyasterone on the mobilization of MSCs in vivo.
· Evaluation Results
The findings indicated that Cyasterone increased the number of MSCs in peripheral blood. Serum levels of SDF-1α at various time points were assessed using ELISA. Micro-CT and histological analyses were conducted to evaluate the fractured femurs. The results demonstrated that Cyasterone effectively promoted the migration and osteogenic capabilities of MSCs. Treatment with Cyasterone led to faster healing of fractured femurs. Moreover, Cyasterone significantly elevated SDF-1α levels in rats with femoral fractures.

Anti-Osteoarthritic Application of Cyasterone via NF-κB and MAPK Pathway Modulation in Chondrocyte Models

Teng L, et al. Chinese Journal of Natural Medicines, 2023, 21(2), 99-112.

Cyasterone exhibits potent anti-inflammatory activity in osteoarthritis through targeted regulation of intracellular signaling. In this study, rat primary chondrocytes were stimulated with interleukin-1β (IL-1β) to model inflammatory conditions in vitro, while a monosodium iodoacetate (MIA)-induced rat model was used to mimic osteoarthritic progression in vivo. Treatment with cyasterone significantly reduced IL-1β-mediated chondrocyte apoptosis, increased extracellular matrix components (collagen II and aggrecan), and downregulated key inflammatory mediators including iNOS, COX-2, MMP-3, MMP-13, and ADAMTS-5. Mechanistically, Western blot and immunofluorescence analyses demonstrated that cyasterone inhibited the activation of the NF-κB and MAPK pathways, thereby reducing nuclear translocation of NF-κB p65 and phosphorylation of ERK, JNK, and p38 MAPKs. In vivo, oral administration of cyasterone notably suppressed synovial inflammation and protected cartilage integrity, comparable to the effects of dexamethasone. Histopathological assessments confirmed reduced cartilage degradation and inflammatory infiltration. These findings provide compelling experimental evidence supporting the therapeutic application of cyasterone in osteoarthritis, particularly through pathway-targeted modulation of chondrocyte inflammatory responses.