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Tetramethylpyrazine

$78

  • Brand : BIOFRON

  • Catalogue Number : BF-T2001

  • Specification : 98%

  • CAS number : 1124-11-4

  • Formula : C8H12N2

  • Molecular Weight : 136.19

  • PUBCHEM ID : 14296

  • Volume : 20mg

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Catalogue Number

BF-T2001

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

136.19

Appearance

Colorless crystal

Botanical Source

rhizome of Ligusticum chuanxiong Hort.

Structure Type

Alkaloids

Category

Standards;Natural Pytochemical;API

SMILES

CC1=C(N=C(C(=N1)C)C)C

Synonyms

Pyrazine, 2,3,5,6-tetramethyl-/Chuanxingzine/Ligustrazine/2,3,5,6-Tetramethylpyrazine/2,3,5,6,-Tetramethyl-1,4-pyrazine/PPyrazine, tetramethyl-/Tetramethyl-1,4-diazine/Tetramethylpyrazine/2,3,5,6-TETRA METHYL PYRAZINE

IUPAC Name

2,3,5,6-tetramethylpyrazine

Density

1.0±0.1 g/cm3

Solubility

Chloroform; Ethyl Acetate

Flash Point

71.6±17.6 °C

Boiling Point

192.7±35.0 °C at 760 mmHg

Melting Point

77-80 °C(lit.)

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

2933990000

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:1124-11-4) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

31678281

Abstract

“The current study aimed to investigate the effects of tetramethylprazine (TMP) on myocardial ischemia/reperfusion (MI/R) injury and its underlying mechanisms. MI/R rat model and hypoxia/reoxygenation (H/R) cardiomyocytes model were established. CK level and LDH activity were detected to evaluate MI/R and H/R injury. Cell viability was determined by cell counting kit-8 (CCK-8) assay. Cell apoptosis were identified by flow cytometry and autophagy were detected by western blot. Treatment with TMP significantly reduced CK level and LDH activity and decreased myocardial infarct size in MI/R rats. TMP reduced autophagy dysfunction induced by MI/R. Moreover, TMP treatment decreased H/R-induced injury and attenuated autophagy dysfunction in cardiomyocytes. Inhibiting autophagic flux with chloroquine (CQ) decreased the cardioprotection exerted by TMP in vivo and in vitro. Additionally, the effects of TMP on the modulation of autophagy were inhibited by LY294002 (a PI3K inhibitor) in H/R cardiomyocytes. Our findings suggested TMP exerted cardioprotection against MI/R injury by decreasing Beclin-1 associated autophagy dysfunction through PI3K pathway.
Copyright © 2019 Elsevier Inc. All rights reserved.”

KEYWORDS

Autophagy; Cardioprotection; Ischemia/reperfusion; Tetramethylprazine

Title

Tetramethylprazine attenuates myocardial ischemia/reperfusion injury through modulation of autophagy.

Author

Zuo Z1, Zuo PF1, Sheng ZL1, Wang X1, Ding JD2, Ma GS3.

Publish date

2019 Dec 15

PMID

31607719

Abstract

“BACKGROUND:
Acute cerebral infarction threats human health and life safety. The edaravone is a new antioxidant and hydroxyl radical scavenger, which is the novel scavenger for clinical use, mainly for nervous system diseases.
OBJECTIVE:
The purpose of this study is to observe the clinical treatment effects of edaravone on the degree of improvement of neurological impairment and functional movement impairment in patients with acute cerebral infarction.
METHOD:
A total of 130 patients admitted to our hospital because of acute cerebral infarction from December 2015 to May 2017 were selected for group analysis. These patients were divided into a control group (n = 65) and a treatment group (n = 65) with a random odd-even method. The control group accepted conventional treatment, while the treatment group received edaravone treatment on top of the conventional treatment of the control group. After treatment, the differences in functional movement, living ability score, neurological score, treatment effect, and adverse reaction of these two groups were tested and compared.
RESULTS:
The total treatment efficiency of conventional treatment in the control group was significantly lower than the combination treatment in the treatment group (P < 0.05). The inter-group differences in the National Institutes of Health Stroke Scale, activities of daily living, and Fugl-Meyer assessment scores after the treatment were significant between these two groups (P < 0.05). The posttreatment effect on the treatment group was superior to that on the control group (P < 0.05). The adverse reaction rate of the treatment group did not significantly vary from that of the control group (P > 0.05).
CONCLUSION:
Edaravone can significantly improve the degree of neurological impairment during acute cerebral infarction, functional movement, and living quality with a definite effect and high safety. Thus, this drug has a good prospect in clinical treatment.

KEYWORDS

Acute cerebral infarction; clinical treatment effect; edaravone

Title

Clinical observation in edaravone treatment for acute cerebral infarction.

Author

Sun Z1, Xu Q2, Gao G3, Zhao M4, Sun C1.

Publish date

2019 Oct

PMID

31541868

Abstract

“As for complex brain diseases involved with multiple pathogenic factors, it is extremely difficult to achieve curative effect by acting on a single target. Multi-approach drugs provide a promising prospect in the treatment of complex brain diseases and have been attracting more and more interest. Enlightened by synergetic effect of combination in traditional herb medicines, forty-two novel cinnamic acid derivatives were designed and synthesized by introducing capsaicin and/or ligustrazine moieties to enhance biological activities in both neurological function and neurovascular protection. Elevated levels of cell viability on human brain microvascular endothelium cell line (HBMEC-2) and human neuroblastoma cell line (SH-SY5Y) against free radical injury were observed in most of compounds. Among them, compound 14a exhibited the most potent activities with a significant EC50 value of 3.26 ± 0.16 μM (HBMEC-2) and 2.41 ± 0.10 μM (SH-SY5Y). Subsequently, the results of morphological staining and flow cytometry analysis experiments on both cell lines showed that 14a had the potential to block apoptosis, maintain cell morphological integrity and protect physiological function of mitochondria. Moreover, 14a displayed specific angiogenesis effect in the chick chorioallantoic membrane (CAM) assay; and the results of RT-PCR suggested that the mechanism for angiogenesis effect was associated with the enhancement of the expressions of VEGFR2 mRNA in chick embryo. Preliminary structure-activity relationship was analyzed. The above evidences suggested that conjunctures gained by combining active ingredients in traditional herb medicines deserved further study and might provide references in discovering dual-effective lead compounds for brain diseases.
Copyright © 2019 Elsevier Masson SAS. All rights reserved.

KEYWORDS

Angiogenesis; Brain injury; Cinnamic acids; Dual effects; Neuroprotective

Title

Design, synthesis and biological evaluation of cinnamic acid derivatives with synergetic neuroprotection and angiogenesis effect.

Author

Zhang WX1, Wang H1, Cui HR1, Guo WB1, Zhou F1, Cai DS1, Xu B1, Jia XH1, Huang XM1, Yang YQ1, Chen HS1, Qi JC1, Wang PL2, Lei HM3.

Publish date

2019 Dec 1


Description :

Tetramethylpyrazine (Ligustrazine), an alkylpyrazine isolated from Ligusticum wallichii (Chuan Xiong)[1], is present in french fries, bread, cooked meats, tea, cocoa, coffee, beer, spirits, peanuts, filberts, dairy products and soy products as fragrance and flavouring ingredienexhibits. Tetramethylpyrazine (Ligustrazine) also has potential nootropic and anti-inflammatory activities in rats[2][3].