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Catalogue Number : BF-I3007
Specification : 98%
CAS number : 489-32-7
Formula : C33H40O15
Molecular Weight : 676.65
PUBCHEM ID : 5318997
Volume : 25mg

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Catalogue Number


Analysis Method






Molecular Weight



Yellow crystalline powder

Botanical Source

Epimedium brevicornu

Structure Type



Standards;Natural Pytochemical;API




ICARRIN/ICARIN/Icariin/Ieariline/Icariil/ICARIINE/Epimedim P.E/Icariln/Icraiin/4'-O-methyl-8-γ,γ-dimethylallylkaempferol-3-rhamnoside-7-glucoside




1.6±0.1 g/cm3



Flash Point

300.9±27.8 °C

Boiling Point

948.5±65.0 °C at 760 mmHg

Melting Point



InChl Key

WGK Germany


HS Code Reference


Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:489-32-7) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Icariin, a flavonoid isolated from traditional oriental herbal medicines, has been demonstrated to exhibit several health benefits in animal models and in humans. The aim of the present study was to investigate the effect of Icariin on hyperglycemia in type 2 diabetes mellitus (T2DM) in rats. A model of diabetes was established in 50 Sprague Dawley rats using a high-sugar and high-fat diet and peritoneal injection of streptozotocin. Diabetic rats were divided into five groups: Diabetic control; metformin; and rats treated with three different doses of Icariin, 5, 10 and 20 mg/kg. Body weight and blood glucose levels were measured, and serum adiponectin levels, expression of phospho-AMP mediated protein kinase (p-AMPK) and glucose transporter isoform 4 (GLUT-4) were measured using ELISA, Realtime PCR and western blotting, respectively. Diabetic rats without drug treatment exhibited reduced body weight, increased blood glucose levels and decreased the number of islets. In T2DM rats treated with 10 or 20 mg/kg Icariin, the blood glucose levels were reduced, whereas serum adiponectin levels were not affected. Additionally, the mRNA and protein expression levels of p-AMPK and GLUT-4 protein were increased in the T2DM rats treated with Icariin. In conclusion, in the diabetes rat model, Icariin alleviated the severity of diabetes, and the effects may be associated with reduction of hyperglycemia by activating an AMPK/GLUT-4 pathway.
Copyright: © Li et al.


AMP-mediated protein kinase; Icariin; glucose transporter isoform 4; type 2 diabetes mellitus


Icariin treatment reduces blood glucose levels in type 2 diabetic rats and protects pancreatic function.


Li X1, Wang YX1, Shi P1, Liu YP1, Li T1, Liu SQ1, Wang CJ1, Wang LX2,3, Cao Y1.

Publish date

2020 Apr




Myocardial contractile dysfunction in diabetic cardiomyocytes is a significant promoter of heart failure. Herein, we investigated the effect of icariin, a flavonoid monomer isolated from Epimedium, on diabetic cardiomyopathy (DCM) and explored the mechanisms underlying its unique pharmacological cardioprotective functions. High glucose (HG) conditions were simulated in vitro using cardiomyocytes isolated from neonatal C57 mice, while DCM was stimulated in vivo in db/db mice. Mice and cardiomyocytes were treated with icariin, with or without overexpression or silencing of Apelin and Sirt3 via transfection with adenoviral vectors (Ad-RNA) and specific small hairpin RNAs (Ad-sh-RNA), respectively. Icariin markedly improved mitochondrial function both in vivo and in vitro, as evidenced by an increased level of mitochondrial-related proteins via western blot analysis (PGC-1α, Mfn2, and Cyt-b) and an increased mitochondrial membrane potential, as observed via JC-1 staining. Further, icariin treatment decreased cardiac fibrogenesis (Masson staining), and inhibited apoptosis (TUNEL staining). Together, these changes improved cardiac function, according to multiple transthoracic echocardiography parameters, including LVEF, LVSF, LVESD, and LVEDD. Moreover, icariin significantly activated Apelin and Sirt3, which were inhibited by HG and DCM. Importantly, when Ad-sh-Apelin and Ad-sh-Sirt3 were transfected in cardiomyocytes or injected into the heart of db/db mice, the cardioprotective effects of icariin were abolished and mitochondrial homeostasis was disrupted. Further, it was postulated that since Ad-Apelin induced different results following increased Sirt3 expression, icariin may have attenuated DCM development by preventing mitochondrial dysfunction through the Apelin/Sirt3 pathway. Hence, protection against mitochondrial dysfunction using icariin may prove to be a promising therapeutic strategy against DCM in diabetes.
Copyright © 2020 Ni, Lin, Huang, Lu, Sun, Zhang, Lin, Chi and Guo.


Apelin/Sirt3; cardiac dysfunction; diabetic cardiomyopathy, DCM; icariin; mitochondrial dysfunction


Icariin Ameliorates Diabetic Cardiomyopathy Through Apelin/Sirt3 Signalling to Improve Mitochondrial Dysfunction.


Ni T1, Lin N2, Huang X1, Lu W1, Sun Z3, Zhang J3, Lin H3, Chi J4, Guo H4.

Publish date

2020 Mar




Icariin has been identified to promote osteogenic differentiation of bone mesenchymal stem cells (BMSCs). However, whether icariin could enhance angiogenic factor expression of BMSCs, which may be vital for bone repair, needs to be explored. Moreover, how to construct a delivery system of icariin and its repair capability in bone defects are still unknown. In the present study, the effects of icariin on the osteogenic differentiation and angiogenic factor expression of BMSCs were firstly evaluated. Moreover, new micro/nano hybrid structured HAp (micro/nano HAp) granules were fabricated to construct the delivery system of icariin, and the osteogenesis and angiogenesis of icariin loaded on micro/nano HAp granules in a rat femoral plug defect model were evaluated by micro-CT measurements, sequential fluorescent labeling and the histological assay. The in vitro results showed that icariin significantly improved osteogenic differentiation of rat BMSCs demonstrated by the enhanced alkaline phosphatase (ALP) activity and gene expression of runt-related transcription factor-2 (Runx2), ALP, collagen type I (Col I), osteocalcin (OCN) and OCN protein secretion. Moreover, icariin induced the angiogenic genes expression of BMSCs, such as vascular endothelial growth factor (VEGF) and angiotensin 1 (ANG1). Furthermore, the activation of the AKT signaling pathway was observed in BMSCs upon treatment with icariin, and these enhancement effects could be blocked by LY294002, which suggested that the AKT signaling pathway was involved in the osteogenic differentiation and angiogenic factor expression of BMSCs induced by icariin. More importantly, micro/nano HAp granules with rod-like shapes were successfully fabricated and acted as delivery carriers for icariin. Consequently, icariin loaded on micro/nano HAp granules could promote new bone formation and blood vessel formation. These results demonstrated that icariin could enhance osteogenic differentiation and angiogenic factor expression of BMSCs via the AKT signaling pathway, moreover, the novel micro/nano HAp granules could act as carriers for icariin to repair bone defects via enhancing osteogenesis and angiogenesis.


Evaluation of osteogenesis and angiogenesis of icariin loaded on micro/nano hybrid structured hydroxyapatite granules as a local drug delivery system for femoral defect repair.


Wu Y 1, Xia L , Zhou Y , Ma W , Zhang N , Chang J , Lin K , Xu Y , Jiang X .

Publish date

2015 Jun