(+)-ferruginol structure
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Common Name | (+)-ferruginol | ||
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CAS Number | 514-62-5 | Molecular Weight | 286.452 | |
Density | 1.0±0.1 g/cm3 | Boiling Point | 388.1±31.0 °C at 760 mmHg | |
Molecular Formula | C20H30O | Melting Point | 56-57℃ | |
MSDS | N/A | Flash Point | 175.1±14.5 °C |
Use of (+)-ferruginolFerruginol ((+)-Ferruginol), a natural diterpenoid, is an inhibitor of the activation of Epstein-Barr virus early antigen (EBV-EA). Ferruginol inhibits the growth of thyroid cancer cells through the induction of mitochondrial Apoptosis. Ferruginol has antitumor, cardioprotective, antioxidant, gastroprotective, and neuroprotective activities[1][2][3]. |
Name | ferruginol |
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Synonym | More Synonyms |
Description | Ferruginol ((+)-Ferruginol), a natural diterpenoid, is an inhibitor of the activation of Epstein-Barr virus early antigen (EBV-EA). Ferruginol inhibits the growth of thyroid cancer cells through the induction of mitochondrial Apoptosis. Ferruginol has antitumor, cardioprotective, antioxidant, gastroprotective, and neuroprotective activities[1][2][3]. |
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Related Catalog | |
In Vitro | Ferruginol(0-160 μM;24 小时)对甲状腺癌细胞具有有效的抗增殖作用,对 MDA-T32 细胞系的 IC50 为 12 μM。Ferruginol 对正常细胞的毒性作用不太明显[1]。 Ferruginol(0-24 μM;24 小时)诱导 MDA-T32 细胞的凋亡性细胞死亡。Ferruginol 剂量依赖性地增加 Bax 表达并降低 Bcl-2 表达[1]。 Ferruginol(0-24 μM;24 小时)抑制 MDA-T32 细胞的 MAPK 和 PI3K/AKT 信号通路[1]。 Ferruginol(0-24 μM;24 小时)还会引起 ROS 介导的 MDA-T32 细胞基质金属蛋白酶改变[1]。 Cell Viability Assay[1] Cell Line: MDA-T32 cells Concentration: 0-160 μM Incubation Time: 24 hours Result: Exerted potent antiproliferative action against thyroid cancer cells. Apoptosis Analysis[1] Cell Line: MDA-T32 cells Concentration: 0 μM, 6 μM, 12 μM, and 24 μM Incubation Time: 24 hours Result: Induced apoptotic cell death of MDA-T32 cells Western Blot Analysis[1] Cell Line: MDA-T32 cells Concentration: 0 μM, 6 μM, 12 μM, and 24 μM Incubation Time: 24 hours Result: Blocked the MAPK and PI3K/AKT signaling pathway. |
In Vivo | Ferruginol(20 mg/kg;口服;每天;持续 4 周)发挥心脏保护作用,表现为增强的心脏功能和减少的结构损伤和细胞凋亡。转录组和其他结果表明,Ferruginol 通过增加 PGC-1α 的表达并同时促进 SIRT1 增强脱乙酰酶 SIRT1 去乙酰化和激活 PGC-1α 的表达,促进 PGC-1α 介导的线粒体生物发生和脂肪酸氧化 (MB 和 FAO)[3]。 Animal Model: Male C57BL/6 mice (20 g, 8-10 weeks old) with Doxorubicin (DOX)-induced cardiotoxicity (DIC)[3]. Dosage: 20 mg/kg Administration: Administered intragastrically; daily; for 4 weeks Result: Relieved Doxorubicin-induced cardiac structural and functional lesion. |
References |
Density | 1.0±0.1 g/cm3 |
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Boiling Point | 388.1±31.0 °C at 760 mmHg |
Melting Point | 56-57℃ |
Molecular Formula | C20H30O |
Molecular Weight | 286.452 |
Flash Point | 175.1±14.5 °C |
Exact Mass | 286.229675 |
PSA | 20.23000 |
LogP | 7.57 |
Vapour Pressure | 0.0±0.9 mmHg at 25°C |
Index of Refraction | 1.530 |
Precursor 0 | |
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DownStream 3 | |
3-Phenanthrenol, 4b,5,6,7,8,8a,9,10-octahydro-4b,8,8-trimethyl-2-(1-methylethyl)-, (4bS,8aS)- |
Abieta-9(11),8(14),12-trien-12-ol |
Abieta-8,11,13-triene-12-ol |
Ferruginol |
(4bS,8aS)-2-Isopropyl-4b,8,8-trimethyl-4b,5,6,7,8,8a,9,10-octahydro-phenanthren-3-ol |
Abieta-8,11,13-trien-12-ol |