IKarisoside A (Icarisoside-A)
(Synonyms: 大花淫羊藿苷 A; Icarisoside-A; Baohuoside II) 目录号 : GC33863
Ikarisoside A (Icarisoside-A) (Icarisoside-A) 是一种天然黄酮醇苷，具有抗炎特性。
Cas No.:55395-07-8
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
IKarisoside A(Icarisoside-A) is a natural compound isolated from Epimedium koreanum (Berberidaceae); has anti-inflammatory properties.IC50 value:Target: in vitro: Ikarisoside A inhibited the expression of LPS-stimulated inducible nitric oxide synthase (iNOS) and the production of nitric oxide (NO) in LPS-stimulated RAW 264.7 cells and mouse bone marrow-derived macrophages (BMMs) in a concentration-dependent manner. In addition, Ikarisoside A reduced the release of pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta). Furthermore, Ikarisoside A inhibited the activity of p38 kinase and nuclear factor-kappaB (NF-kappaB) [1]. Ikarisoside A is a potent inhibitor of osteoclastogenesis in RANKL-stimulated RAW 264.7 cells as well as in bone marrow-derived macrophages.The inhibitory effect of Ikarisoside A resulted in decrease of osteoclast-specific genes like matrix metalloproteinase 9 (MMP9), tartrate-resistant acid phosphatase (TRAP), receptor activator of NF-kappaB (RANK), and cathepsin K. Moreover, Ikarisoside A blocked the resorbing capacity of RAW 264.7 cells on calcium phosphate-coated plates. Ikarisoside A also has inhibitory effects on the RANKL-mediated activation of NF-kappaB, JNK, and Akt [2].
[1]. Choi HJ, et al. Ikarisoside A inhibits inducible nitric oxide synthase in lipopolysaccharide-stimulated RAW 264.7 cells via p38 kinase and nuclear factor-kappaB signaling pathways. Eur J Pharmacol. 2008 Dec 28;601(1-3):171-8. [2]. Choi HJ, eta l. Inhibition of osteoclastogenic differentiation by Ikarisoside A in RAW 264.7 cells via JNK and NF-kappaB signaling pathways. Eur J Pharmacol. 2010 Jun 25;636(1-3):28-35.
| Cas No. | 55395-07-8 | SDF | |
| 别名 | 大花淫羊藿苷 A; Icarisoside-A; Baohuoside II | ||
| Canonical SMILES | OC1=CC(O)=C2C(OC(C3=CC=C(O)C=C3)=C(O[C@H](O[C@@H](C)[C@H](O)[C@H]4O)[C@@H]4O)C2=O)=C1C/C=C(C)\C | ||
| 分子式 | C26H28O10 | 分子量 | 500.49 |
| 溶解度 | Soluble in DMSO | 储存条件 | 4°C, protect from light |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 1.998 mL | 9.9902 mL | 19.9804 mL |
| 5 mM | 0.3996 mL | 1.998 mL | 3.9961 mL |
| 10 mM | 0.1998 mL | 0.999 mL | 1.998 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
A simple and selective LC-MS/MS method for quantification of IKarisoside A in rat plasma and its application to a pharmacokinetic study
Biomed Chromatogr 2018 Aug;32(8):e4245.PMID:29575004DOI:10.1002/bmc.4245.
IKarisoside A is a natural flavonoid isolated from Epimedium plants. To further evaluate its medicinal potential, a sensitive and robust LC-MS/MS method was developed and validated for the assay of IKarisoside A in rat plasma. Orientin was used as an internal standard. The electrospray ionization was operated in its negative ion mode while IKarisoside A and IS were measured by selected reaction monitoring using precursor-to-product ion transitions of m/z 499.1 → 353.0 and m/z 446.9 → 327.6, respectively. This LC-MS/MS method had good sensitivity (LLOQ = 1.5 ng/mL), accuracy (both intra- and inter-day RE ≤ ±11.9%) and precision (both intra- and inter-day RSD ≤8.5%). The pharmacokinetics of IKarisoside A was subsequently profiled in Sprague-Dawley rats. Following oral administration (35 mg/kg), IKarisoside A reached maximum plasma concentration (Cmax , 207.6 ± 96.7 ng/mL) attained at 1.10 ± 0.42 h. Following oral administration, the clearance and terminal half-life were 42.9 ± 26.5 L/h/kg and 3.15 ± 0.80 h by oral route, respectively.
IKarisoside A inhibits acetylcholine-induced catecholamine secretion and synthesis by suppressing nicotinic acetylcholine receptor-ion channels in cultured bovine adrenal medullary cells
Naunyn Schmiedebergs Arch Pharmacol 2015 Dec;388(12):1259-69.PMID:26257152DOI:10.1007/s00210-015-1161-y.
IKarisoside A is a natural flavonol glycoside derived from plants of the genus Epimedium, which have been used in Traditional Chinese Medicine as tonics, antirheumatics, and aphrodisiacs. Here, we report the effects of IKarisoside A and three other flavonol glycosides on catecholamine secretion and synthesis in cultured bovine adrenal medullary cells. We found that IKarisoside A (1-100 μM), but not icariin, epimedin C, or epimedoside A, concentration-dependently inhibited the secretion of catecholamines induced by acetylcholine, a physiological secretagogue and agonist of nicotinic acetylcholine receptors. IKarisoside A had little effect on catecholamine secretion induced by veratridine and 56 mM K(+). IKarisoside A (1-100 μM) also inhibited (22)Na(+) influx and (45)Ca(2+) influx induced by acetylcholine in a concentration-dependent manner similar to that of catecholamine secretion. In Xenopus oocytes expressing α3β4 nicotinic acetylcholine receptors, IKarisoside A (0.1-100 μM) directly inhibited the current evoked by acetylcholine. It also suppressed (14)C-catecholamine synthesis and tyrosine hydroxylase activity induced by acetylcholine at 1-100 μM and 10-100 μM, respectively. The present findings suggest that IKarisoside A inhibits acetylcholine-induced catecholamine secretion and synthesis by suppression of nicotinic acetylcholine receptor-ion channels in bovine adrenal medullary cells.
IKarisoside A inhibits inducible nitric oxide synthase in lipopolysaccharide-stimulated RAW 264.7 cells via p38 kinase and nuclear factor-kappaB signaling pathways
Eur J Pharmacol 2008 Dec 28;601(1-3):171-8.PMID:18929556DOI:10.1016/j.ejphar.2008.09.032.
This study examined the anti-inflammatory properties of IKarisoside A, isolated from Epimedium koreanum (Berberidaceae), in lipopolysaccharide (LPS)-stimulated macrophages. IKarisoside A inhibited the expression of LPS-stimulated inducible nitric oxide synthase (iNOS) and the production of nitric oxide (NO) in LPS-stimulated RAW 264.7 cells and mouse bone marrow-derived macrophages (BMMs) in a concentration-dependent manner. In addition, IKarisoside A reduced the release of pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta). Furthermore, IKarisoside A inhibited the activity of p38 kinase and nuclear factor-kappaB (NF-kappaB), which are signaling molecules involved in NO production. NO production was inhibited when the cells were treated with LPS and either SB 203580 (a p38 inhibitor) or Bay 11-7082 (an inhibitory kappaB kinase 2 inhibitor). These results suggest that IKarisoside A inhibits the production of NO by inhibiting the activity of p38 MAPK and NF-kappaB. As a result of these properties, IKarisoside A has the potential to be used as an effective anti-inflammatory agent.
Inhibition of osteoclastogenic differentiation by IKarisoside A in RAW 264.7 cells via JNK and NF-kappaB signaling pathways
Eur J Pharmacol 2010 Jun 25;636(1-3):28-35.PMID:20353769DOI:10.1016/j.ejphar.2010.03.023.
Osteoclasts are specialized bone-resorbing cells derived from multipotent myeloid progenitor cells. They play a crucial homeostatic role in skeletal modeling and remodeling and destroy bone in many pathologic conditions. Receptor activator of NF-kappaB ligand (RANKL) is essential to osteoclastogenesis. In this study, we investigated the effects of IKarisoside A, isolated from Epimedium koreanum (Berberidaceae), on osteoclastogenesis in RANKL-treated murine monocyte/macrophage RAW 264.7 cells. The results indicate that IKarisoside A is a potent inhibitor of osteoclastogenesis in RANKL-stimulated RAW 264.7 cells as well as in bone marrow-derived macrophages. The inhibitory effect of IKarisoside A resulted in decrease of osteoclast-specific genes like matrix metalloproteinase 9 (MMP9), tartrate-resistant acid phosphatase (TRAP), receptor activator of NF-kappaB (RANK), and cathepsin K. Moreover, IKarisoside A blocked the resorbing capacity of RAW 264.7 cells on calcium phosphate-coated plates. IKarisoside A also has inhibitory effects on the RANKL-mediated activation of NF-kappaB, JNK, and Akt. Finally, IKarisoside A clearly decreased the expression of c-Fos and nuclear factor of activated T cells c1 (NFATc1) as well as the transcriptional activity of NFATc1, the master regulator of osteoclast differentiation. The data indicate that IKarisoside A has potential for use in treatment of diseases involving abnormal bone lysis such as osteoporosis, rheumatoid arthritis, and periodontal bone erosion.
Flavonoids from Epimedium wanshanense
Phytochemistry 1996 Sep;43(2):527-30.PMID:8862041DOI:10.1016/0031-9422(96)00187-2.
A novel flavonol glycoside named wanepimedoside A was isolated from the whole plant of Epimedium wanshanense, along with fifteen known flavonoids, anhydroicaritin, desmethylanhydroicaritin, icarisid I and II, quercetin, IKarisoside A and B, sagittatoside B, 2"-O-rhamnosylicarisid II, icariin, 2"-O-rhamnosylikarisoside A, epimedin B, epimedin C, and diphylloside A and B.