24699-16-9
Chemical Structure
Isomangiferin
- CAS No.: 24699-16-9
- Formula:C19H18O11
- Molecular Weight:422.34
IUPAC Name: 1,3,6,7-tetrahydroxy-4-((2S,3R,4R,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)tetrahydro-2H-pyran-2-yl)-9H-xanthen-9-one
InChIKey: CDYBOKJASDEORM-HBVDJMOISA-N
SMILES: OC1=CC(O)=C2C(OC3=CC(O)=C(O)C=C3C2=O)=C1[C@@H]([C@@H]([C@@H](O)[C@@H]4O)O)O[C@@H]4CO
Biological Activity: Isomangiferin is an orally active xanthone C-glucoside, and its chemical structure is similar to Mangiferin (HY-N0290). Isomangiferin is an effective VEGFR-2 kinase inhibitor, which can induces cell apoptosis, inhibit the growth, metastasis and angiogenesis of breast cancer. Isomangiferin exerts anti-inflammatory effects by inhibiting the HMGB1/NLRP3/NF-κB signaling pathway, thereby improving the renal function indicators of diabetic mice. Isomangiferin exhibits inhibitory effects on various bacteria and herpes simplex virus type 1 (HSV-1). Isomangiferin promotes the migration and osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) and reduces cell apoptosis and the production of ROS by activating the AMPK/ACC pathway, thereby facilitating fracture healing[1][2][3][4][5].
| Cat. No. | Product Name | Purity | Description | Pricing | |||||||||||||||||||
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Isomangiferin | 99.60% | Isomangiferin is an orally active xanthone C-glucoside, and its chemical structure is similar to Mangiferin (HY-N0290). Isomangiferin is an effective VEGFR-2 kinase inhibitor, which can induces cell apoptosis, inhibit the growth, metastasis and angiogenesis of breast cancer. Isomangiferin exerts anti-inflammatory effects by inhibiting the HMGB1/NLRP3/NF-κB signaling pathway, thereby improving the renal function indicators of diabetic mice. Isomangiferin exhibits inhibitory effects on various bacteria and herpes simplex virus type 1 (HSV-1). Isomangiferin promotes the migration and osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) and reduces cell apoptosis and the production of ROS by activating the AMPK/ACC pathway, thereby facilitating fracture healing. | ||||||||||||||||||||
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Isomangiferin (Standard) | ≥98% | Isomangiferin (Standard) is the analytical standard of Isomangiferin (HY-N0772). This product is intended for research and analytical applications. Isomangiferin is an orally active xanthone C-glucoside, and its chemical structure is similar to Mangiferin (HY-N0290). Isomangiferin is an effective VEGFR-2 kinase inhibitor, which can induces cell apoptosis, inhibit the growth, metastasis and angiogenesis of breast cancer. Isomangiferin exerts anti-inflammatory effects by inhibiting the HMGB1/NLRP3/NF-κB signaling pathway, thereby improving the renal function indicators of diabetic mice. Isomangiferin exhibits inhibitory effects on various bacteria and herpes simplex virus type 1 (HSV-1). Isomangiferin promotes the migration and osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) and reduces cell apoptosis and the production of ROS by activating the AMPK/ACC pathway, thereby facilitating fracture healing. | ||||||||||||||||||||
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- [1]. Zheng MS, et al. Antiviral effect of mangiferin and isomangiferin on herpes simplex virus. Chin Med J (Engl). 1990 Feb;103(2):160-5. [Content Brief]
- [2]. Ishaque M, et al. Xanthone C-glycosides isomers purified from Dryopteris ramosa (Hope) C. Chr. with bactericidal and cytotoxic prospects. Saudi J Biol Sci. 2022 Feb;29(2):1191-1196. [Content Brief]
- [3]. Gao B, et al. Isomangiferin promotes the migration and osteogenic differentiation of rat bone marrow mesenchymal stem cells. Open Life Sci. 2024 Jul 20;19(1):20220884. doi: 10.1515/biol-2022-0884. PMID: 39035458; PMCID: PMC11259999. [Content Brief]
- [4]. Yue S, et al. Isomangiferin Attenuates Renal Injury in Diabetic Mice via Inhibiting Inflammation. Diabetes Metab Syndr Obes. 2020 Nov 10;13:4273-4280. [Content Brief]
- [5]. Wang B, et al. Isomangiferin, a Novel Potent Vascular Endothelial Growth Factor Receptor 2 Kinase Inhibitor, Suppresses Breast Cancer Growth, Metastasis and Angiogenesis. J Breast Cancer. 2018 Mar;21(1):11-20. [Content Brief]
