Jatrorrhizine Hydrochloride

Jatrorrhizine Hydrochloride
Product Name Jatrorrhizine Hydrochloride
CAS No.: 6681-15-8
Catalog No.: CFN98108
Molecular Formula: C20H20ClNO4
Molecular Weight: 373.83 g/mol
Purity: >=98%
Type of Compound: Alkaloids
Physical Desc.: Powder
Targets: PPAR | Influenza virus
Source: The barks of Phellodendron chinense Schneid.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Price: $50/20mg
Jatrorrhizine hydrochloride has lipid lowering effects, it can ameliorate hyperlipidemia via the suppression of lipogenesis and the enhancement of lipid oxidation in the liver. It exhibits a potent inhibitory effect toward neuraminidase of the H7N9 (N9) avian influenza virus, it also can potentiate the neuraminidase inhibitory effect of oseltamivir towards H7N9 influenza. Jatrorrhizine hydrochloride is a potential new antimelanoma drug candidate, can inhibit the proliferation and neovascularization of C8161 metastatic melanoma cells with low toxicity.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Anticancer Drugs. 2013 Aug;24(7):667-76.
    Jatrorrhizine hydrochloride inhibits the proliferation and neovascularization of C8161 metastatic melanoma cells.[Pubmed: 23695011]
    Malignant melanoma is the most aggressive form of skin cancer. Although various antimelanoma approaches have been used in the clinics to treat the disease over the last three decades, none of the drugs significantly prolonged the survival of metastatic melanoma patients; hence, effective drugs against metastatic melanoma are highly desired.
    METHODS AND RESULTS:
    In this study, we explored an antimetastatic melanoma agent derived from traditional Chinese medicinal herbs and found that Jatrorrhizine Hydrochloride (JH), an active component of the traditional Chinese medicinal herb Coptis chinensis, inhibited the proliferation and neovascularization of C8161 human metastatic melanoma cells. JH suppressed C8161 cell proliferation in a dose-dependent manner, with a half-maximal inhibitory concentration of 47.4±1.6 μmol/l; however, it did not induce significant cellular apoptosis at doses up to 320 μmol/l. Mechanistic studies showed that JH-induced C8161 cell cycle arrest at the G0/G1 transition, which was accompanied by overexpression of the cell cycle-suppressive genes p21 and p27 at higher doses. Moreover, JH reduced C8161 cell-mediated neovascularization in vitro and in vivo and impeded the expression of the gene for VE-cadherin, a key protein in tumor vasculogenic mimicry and angiogenesis.
    CONCLUSIONS:
    Taken together, the effective inhibitory effects of JH on metastatic melanoma cell proliferation and neovascularization with low toxicity suggest that JH is a potential new antimelanoma drug candidate.
    Mol Med Rep. 2016 Oct;14(4):3277-84.
    Jatrorrhizine hydrochloride attenuates hyperlipidemia in a high-fat diet-induced obesity mouse model.[Pubmed: 27573054 ]
    Jatrorrhizine Hydrochloride (JH) is an active component of the traditional Chinese herb Coptis chinensis, which has been used to prevent and treat metabolic disorders. Hyperlipidemia is one of the principal factors underlying numerous metabolic diseases, including diabetes and obesity. Therefore, the aim of the present study was to investigate the lipid lowering effects of JH treatment in vivo in an obesity mouse model. JH-treated hyperlipidemic mice exhibited a reduction in body weight, as well as improved glucose tolerance and insulin sensitivity. In addition, JH‑treated hyperlipidemic mice exhibited reduced serum triglyceride, total cholesterol and low‑density lipoprotein cholesterol levels, as well as increased high‑density lipoprotein cholesterol levels compared with untreated mice fed a high‑fat diet. Notably, JH treatment ameliorated the pathophysiological changes observed in the livers of hyperlipidemic mice. At the molecular level, JH downregulated the hepatic mRNA expression levels of SREBP‑1c and FAS, and induced PPAR‑α and CPT1A mRNA expression in hyperlipidemic mice. These findings suggest that JH ameliorates hyperlipidemia via the suppression of lipogenesis and the enhancement of lipid oxidation in the liver.
    Rsc Adv., 2015, 5(80):64937-43.
    Jatrorrhizine Hydrochloride potentiates the neuraminidase inhibitory effect of oseltamivir towards H7N9 influenza[Reference: WebLink]
    A Chinese natural product, Jatrorrhizine Hydrochloride (JH), exhibited potent inhibitory effect toward neuraminidase of the H7N9 (N9) avian influenza virus.
    METHODS AND RESULTS:
    The interaction between JH and N9 was modeled using molecular docking software AutoDock. Similar to the control drug oseltamivir, JH bound into the active site of N9, but its position did not overlap with the position of oseltamivir. In addition, JH and oseltamivir were simultaneously docked into the active site of N9s (N9WT and N9R294K). By analyzing the docking result of the binding position, hydrogen bond interaction, and pi-pi interaction, N9 inhibition was likely enhanced by the combination of JH and oseltamivir. Molecular dynamics simulations using GROMACS were used to obtain trajectories of N9s and two compound complexes (JH was chosen from the docking result, whereas oseltamivir was directly extracted from the crystal structure) and to validate key interactions. The coordination between JH and oseltamivir to inhibit neuraminidase activity was further confirmed by the enzymatic assays of N9s.
    CONCLUSIONS:
    This study introduces novel treatment strategies to target N9 for a potential anti-H7N9 influenza drug.
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