Icariin

SKU: orb1304925

Description

Icariin is a flavonol glycoside that acts as a PDE5/PDE4 inhibitor and PPARα activator. It is utilized in research areas such as cardiovascular function, bone metabolism, and neuroprotection, with studies conducted in both cellular and animal models.

Research Area

Cell Biology, Metabolism Research, Molecular Biology

Key Properties

• CAS Number: 489-32-7
• MW: 676.66
• Purity: 98.49%
• Formula: C₃₃H₄₀O₁₅
• SMILES: COC1=CC=C(C=C1)C1=C(O[C@@H]2O[C@@H](C)[C@H](O)[C@@H](O)[C@H]2O)C(=O)C2=C(O)C=C(O[C@@H]3O[C@H](CO)[C@@H](O)[C@H](O)[C@H]3O)C(CC=C(C)C)=C2O1
• Target: Autophagy,PPAR,PDE
• Solubility: H2O:< 1 mg/mL (insoluble or slightly soluble);Ethanol:< 1 mg/mL (insoluble or slightly soluble);DMSO:245 mg/mL (362.07 mM);10% DMSO+40% PEG300+5% Tween 80+45% Saline:6 mg/mL (8.87 mM)

Bioactivity

• Target IC50:
  PDE4:73.5 μM|PDE5:0.432 μM
• In Vivo:
  METHODS: To investigate the protective effects against traumatic brain injury (TBI), Icariin (3-30 mg/kg) was administered orally twice daily for seven days to a mouse model of TBI induced by controlled cortical impact. RESULTS: The Icariin 30 mg/kg and 10 mg/kg treatment groups showed enhanced sensorimotor function 8 days after TBI in the rotating bar and balance beam tests.The Icariin treatment group showed an increase in recognition indices in the novel object recognition test at all doses, and an increase in spontaneous alternation in the Y maze test in the 30 mg/kg group.Icariin upregulated the expression of brain-derived neurotrophic factor, synaptophysin, and postsynaptic density protein 95. However, no protective effect against brain injury or neuronal death was observed.
• In Vitro:
  METHODS: Osteoarthritic fibroblast-like synoviocytes OA-FLSs were treated with Icariin (0.1-10 µM) for 12 h, and cell viability was measured using MTS assay. RESULTS: No cytotoxic effect of Icariin at 0.1-1 µM was observed in OA-FLSs. At a concentration of 10 µM, Icariin showed low cytotoxicity to OA-FLSs, which significantly inhibited the proliferation of OA-FLSs after 12 h. The results showed that Icariin was not effective in inhibiting the proliferation of OA-FLSs after 12 h of treatment. METHODS: Fibroblast-like synoviocyte FLSs were treated with Icariin (1-5 µM) for 24-36 h. Cell migration was detected using the Wounding migration assay and Transwell chamber assay. RESULTS: Wound closure was significantly slowed in FLS treated with Icariin, and Transwell chamber assay showed that Icariin inhibited FLS migration in a concentration-dependent manner.

Storage & Handling

• Storage: Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice/Shipping at ambient temperature.
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

Alternative Names

Autophagy, Inhibitor, Ieariline, Icariin, inhibit, PDE5, PPAR, Peroxisome proliferator-activated receptors, phosphodiesterase, Phosphodiesterase (PDE)

Compound Identifiers

PubChem CID

5318997