White crystalline powder
Ampelopsis grossedentata （Hand-Mazz）W.T.Wang
4H-1-Benzopyran-4-one, 2,3-dihydro-3,5,7-trihydroxy-2-(3,4,5-trihydroxyphenyl)-, (2S,3S)-/Ampelopsin E/(2R,3R)-3,5,7-trihydroxy-2-(3,4,5-trihydroxyphenyl)-2,3-dihydrochromen-4-one/3,5,7,3',4',5'-hexahydroxy-2,3-dihydroflavone/(2R,3R)-dihydromyricetin/Dihydromyricetin/(2R,3R)-3,5,7-Trihydroxy-2-(3,4,5-trihydroxyphenyl)-2,3-dihydrochromen-4-one Ampelopsin DHM/Flavanone,3,3',4',5,5',7-hexahydroxy/3,5,7,3',4',5'-hexahydroxy-2,3-dihydroflavonol/(+)-Dihydromyricetin/(2S,3S)-3,5,7-Trihydroxy-2-(3,4,5-trihydroxyphenyl)-2,3-dihydro-4H-chromen-4-one/Ampelopsin/Ampeloptin/(+)-Ampelopsin/3,3',4',5,5',7-Hexahydroxy-2,3-dihydroflavanonol/rac-ampelopsin
Dihydromyricetin is a potent inhibitor with an IC50 of 48 μM on dihydropyrimidinase. Dihydromyricetin can activate autophagy through inhibiting mTOR signaling. Dihydromyricetin suppresses the formation of mTOR complexes (mTORC1/2).
780.7±60.0 °C at 760 mmHg
HS Code Reference
Personal Projective Equipment
For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:27200-12-0) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Dihydromyricetin is a flavonoid isolated from Ampelopsis grossedentata, which is traditionally used in China. Dihydromyricetin exhibits health-benefiting activities with minimum adverse effects. Dihydromyricetin has been demonstrated to show antioxidative, anti-inflammatory, anticancer, antimicrobial, cell death-mediating, and lipid and glucose metabolism-regulatory activities. Dihydromyricetin may scavenge ROS to protect against oxidative stress or potentiate ROS generation to counteract cancer cells selectively without any effects on normal cells. However, the low bioavailability of dihydromyricetin limits its potential applications. Recent research has gained positive and promising data. This review will discuss the versatile effects and clinical prospective of dihydromyricetin.
The Versatile Effects of Dihydromyricetin in Health
Hongliang Li 1 , Qisheng Li 2 , Zhaowen Liu 1 , Kai Yang 1 , Zhixi Chen 1 , Qilai Cheng 1 , Longhuo Wu 1
As the most abundant natural flavonoid in rattan tea, dihydromyricetin (DMY) has shown a wide range of pharmacological effects. In addition to the general characteristics of flavonoids, DMY has the effects of cardioprotection, anti-diabetes, hepatoprotection, neuroprotection, anti-tumor, and dermatoprotection. DMY was also applied for the treatment of bacterial infection, osteoporosis, asthma, kidney injury, nephrotoxicity and so on. These effects to some extent enrich the understanding about the role of DMY in disease prevention and therapy. However, to date, we still have no outlined knowledge about the detailed mechanism of DMY, which might be related to anti-oxidation and anti-inflammation. And the detailed mechanisms may be associated with several different molecules involved in cellular apoptosis, oxidative stress, and inflammation, such as AMP-activated protein kinase (AMPK), mitogen-activated protein kinase (MAPK), protein kinase B (Akt), nuclear factor-κB (NF-κB), nuclear factor E2-related factor 2 (Nrf2), ATP-binding cassette transporter A1 (ABCA1), peroxisome proliferator-activated receptor-γ (PPARγ) and so on. Here, we summarized the current pharmacological developments of DMY as well as possible mechanisms, aiming to push the understanding about the protective role of DMY as well as its preclinical assessment of novel application.
Recent Update on the Pharmacological Effects and Mechanisms of Dihydromyricetin
Jingyao Zhang 1 2 , Yun Chen 2 , Huiqin Luo 1 2 , Linlin Sun 1 2 , Mengting Xu 1 2 , Jin Yu 2 , Qigang Zhou 3 , Guoliang Meng 1 , Shengju Yang 1
2018 Oct 25
1. This study investigates the effects of verapamil on the pharmacokinetics of dihydromyricetin in rats and clarifies its main mechanism. 2. The pharmacokinetic profiles of oral or intravenous administration of dihydromyricetin in Sprague-Dawley rats with or without pretreatment with verapamil were investigated. In addition, the effects of verapamil on the transport and metabolic stability of dihydromyricetin were investigated using Caco-2 cell transwell model and rat liver microsomes. 3. In the oral group, verapamil could significantly increase Cmax, and decrease oral clearance of dihydromyricetin (p < 0.05). In the intravenous group, the Cmax also increased compared with the control group, but the difference was not significant. However, the t1/2 and clearance rate decreased than that of the control (p < 0.05). The oral bioavailability increased significantly (p < 0.05) from 3.84% to 6.84% with the pretreatment of verapamil. A markedly higher transport of dihydromyricetin across the Caco-2 cells was observed in the basolateral-to-apical direction and was abrogated in the presence of the P-gp inhibitor, verapamil. Additionally, the intrinsic clearance rate of dihydromyricetin was decreased by the pretreatment with verapamil (27.0 versus 32.5 μL/min/mg protein). 4. Those results indicated that verapamil could significantly change the pharmacokinetic profiles of dihydromyricetin in rats, and it might exert these effects through increasing the absorption of dihydromyricetin by inhibiting the activity of P-gp, or through inhibiting the metabolism of dihydromyricetin in rat liver.
CYP450; Caco-2 cells; P-gp; dihydromyricetin; oral bioavailability; verapamil.
Effects of Verapamil on the Pharmacokinetics of Dihydromyricetin in Rats and Its Potential Mechanism
Yixiang Huang 1 , Junyong Zhao 1 , Wei Jian 1 , Gang Wang 1