Information provided in the product description is from published literature. Due to the nature of scientific experimentation, your results (e.g., selectivity and effective concentrations) or specific application for this product may differ. If you have questions about how this product fits your application, please contact our technical support staff.
Visit our FAQ
Toll Free Phone (USA and Canada Only): (888) 526-5351
Direct Phone: (734) 975-3888
Provide batch numbers separated by commas to download or request available product inserts, QC sheets, certificates of analysis, data packs, and GC-MS data.

Discover high-quality research tools to investigate GLP-1 mechanisms and next-generation metabolic targets.
OBESITY RESEARCH SOLUTIONSLigustroflavone is an apigenin triglycoside originally isolated from L. vulgare that has diverse biological activities.1 It increases parathyroid hormone (PTH) release from rat primary parathyroid gland cells when used at a concentration of 1 µM and inhibits calcium influx in HEK293 cells.2 It increases serum PTH, as well as serum and bone calcium levels, in a streptozotocin-induced mouse model of diabetes with osteoporosis when administered at doses of 5 and 20 mg/kg three times per week. It also reduces increases in the expression and levels of the extracellular calcium sensing receptor (CaSR) in the kidney of diabetic osteoporotic mice. Ligustroflavone (10, 30, and 60 mg/kg) decreases infarct volume in a rat model of ischemic stroke and decreases the levels of the necroptosis-associated proteins RIPK3 and MLKL in the brain of ischemic rats when administered at a dose of 30 mg/kg.3
WARNING This product is not for human or veterinary use.
1. Isolation and structure elucidation of ligustroflavone, a new apigenin triglycoside from the leaves of Ligustrum vulgare L. Pharmazie 55(1), 78-80 (2000).
2. Protective effects of ligustroflavone, an active compound from Ligustrum lucidum, on diabetes-
3. Ligustroflavone reduces necroptosis in rat brain after ischemic stroke through targeting RIPK1/RIPK3/MLKL pathway. Naunyn Schmiedebergs Arch. Pharmacol. 392(9), 1085-1095 (2019).