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利卡靈A

NMR下載 COA and HPLC MSDS下載
names：
Licarin A
CAS號：
23518-30-1
MDL Number： MFCD20260801
MF(分子式)： C20H22O4 MW(分子量)： 326.39
EINECS: Reaxys Number:
Pubchem ID:5281836 Brand:BIOFOUNT

利卡靈A (23518-30-1,Licarin A)是二氫苯并呋喃新木脂素，是異丁香酚與辣根過氧化物酶 (HRP) 的氧化偶聯(lián)反應的產(chǎn)物。利卡靈A在抵抗錐蟲的錐蟲行為表現(xiàn)出 58.7％的寄生蟲裂解作用，IC₅₀ 值為 100.8 µM。利卡靈A 在 200 µM 時顯示 100％的寄生蟲死亡率。

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YZM000841-5mg	5mg	>95%	￥ 0.00	￥ 0.00		Backorder	- +	￥ 0.00
YZM000841-1mg	1mg	>95%	￥ 0.00	￥ 0.00		Backorder	- +	￥ 0.00

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中文別名	利卡靈A (23518-30-1,Licarin A);里卡靈 A
英文別名	Licarin A(23518-30-1);(-)-Licarin A;(±)-Licarin A
CAS號	23518-30-1
Inchi	InChI=1S/C20H22O4/c1-5-6-13-9-15-12(2)19(24-20(15)18(10-13)23-4)14-7-8-16(21)17(11-14)22-3/h5-12,19,21H,1-4H3/b6-5+/t12-,19-/m0/s1
InchiKey	ITDOFWOJEDZPCF-FNINDUDTSA-N
分子式 Formula	C20H22O4
分子量 Molecular Weight	326.39
溶解度Solubility
性狀	白色結(jié)晶粉末
儲藏條件 Storage conditions	存放在陰涼干燥處，短期（數(shù)天至數(shù)周）在0-4℃，長期（數(shù)月至數(shù)年）在-20℃。

利卡靈A (23518-30-1,Licarin A)實驗注意事項：
1.實驗前需戴好防護眼鏡，穿戴防護服和口罩，佩戴手套，避免與皮膚接觸。
2.實驗過程中如遇到有毒或者刺激性物質(zhì)及有害物質(zhì)產(chǎn)生，必要時實驗操作需要手套箱內(nèi)完成以免對實驗人員造成傷害
3.實驗后產(chǎn)生的廢棄物需分類存儲，并交于專業(yè)生物廢氣物處理公司處理，以免造成環(huán)境污染

Licarin A(23518-30-1) Experimental considerations:
1. Wear protective glasses, protective clothing and masks, gloves, and avoid contact with the skin during the experiment.
2. The waste generated after the experiment needs to be stored separately, and handed over to a professional biological waste gas treatment company to avoid environmental pollution.

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產(chǎn)品說明	利卡靈A (23518-30-1,Licarin A)是二氫苯并呋喃新木脂素，是異丁香酚與辣根過氧化物酶 (HRP) 的氧化偶聯(lián)反應的產(chǎn)物
Introduction	Licarin A (23518-30-1,利卡靈A) is a dihydrobenzofuran neolignan, a product of the oxidative coupling reaction between isoeugenol and horseradish peroxidase (HRP)
Application1
Application2
Application3

警示圖
危險性	warning
危險性警示	Not available
安全聲明	H303吞入可能有害+H313皮膚接觸可能有害+H2413吸入可能對身體有害
安全防護	P264處理后徹底清洗+P280戴防護手套/穿防護服/戴防護眼罩/戴防護面具+P305如果進入眼睛+P351用水小心沖洗幾分鐘+P338取出隱形眼鏡（如果有）并且易于操作,繼續(xù)沖洗+P337如果眼睛刺激持續(xù)+P2393獲得醫(yī)療建議/護理
備注	實驗過程中防止吸入、食入，做好安全防護

Matrix Solid-Phase Dispersion Combined with HPLC-DAD for Simultaneous Determination of Nine Lignans in Saururus chinensis PMID 30272133; Journal of chromatographic science 2019 Feb; 57(2):186-193

[Lignans from Machilus robusta] PMID 24010288; Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica 2013 Jun; 38(11):1740-6

New neolignans and lignans from Vietnamese medicinal plant Machilus odoratissima NEES PMID 16508197; Chemical & pharmaceutical bulletin 2006 Mar; 54(3):380-3

Antimycobacterial neolignans isolated from Aristolochia taliscana PMID 20209328; Memorias do Instituto Oswaldo Cruz 2010 Feb; 105(1):45-51

Increase of caspase-3 activity by lignans from Machilus thunbergii in HL-60 cells PMID 15305043; Biological & pharmaceutical bulletin 2004 Aug; 27(8):1305-7

1.Meso-dihydroguaiaretic acid and licarin A of Machilus thunbergii protect against glutamate-induced toxicity in primary cultures of a rat cortical cells.
Ma CJ;Kim SR;Kim J;Kim YC Br J Pharmacol. 2005 Nov;146(5):752-9.
Abstract: We previously reported that four lignans isolated from the bark of Machilus thunbergii Sieb. et Zucc. (Lauraceae) protected primary cultures of rat cortical neurons from neurotoxicity induced by glutamate. 2 Among the lignans, meso-dihydroguaiarectic acid (MDGA) and licarin A significantly attenuated glutamate-induced neurotoxicity when added prior to or right after the excitotoxic glutamate challenge. 3 The neuroprotective activities of two lignans appeared to be more effective in protecting neurons against neurotoxicity induced by NMDA than that induced by kainic acid. 4 MDGA and licarin A diminished the calcium influx that routinely accompanies with the glutamate-induced neurotoxicity, and inhibited the subsequent overproduction of cellular nitric oxide and peroxide to the level of control cells. They also preserved cellular activities of antioxidative enzymes such as superoxide dismutase, glutathione peroxidase and glutathione reductase reduced in the glutamate-injured neuronal cells. 5 Thus, our results suggest that MDGA and licarin A significantly protect primary cultured neuronal cells against glutamate-induced oxidative stress, via antioxidative activities.

2.Theoretical prediction of the relationship between phenol function and COX-2/AP-1 inhibition for ferulic acid-related compounds.
Murakami Y;Ito S;Atsumi T;Fujisawa S In Vivo. 2005 Nov-Dec;19(6):1039-43.
Abstract:Ferulic acid-related compounds possess antioxidant activity. Dehydrodiisoeugenol and ferulic acid dimer (bis-FA), but not the parent monomers isoeugenol and ferulic acid, inhibit lipopolysaccharide (LPS)-induced cyclooxygenase-2 (COX-2) gene expression in RAW 264.7 cells. To clarify the mechanism of their inhibitory effects on COX-2 expression, the phenolic O-H bond dissociation enthalpy (BDE) and ionization potential (IP) of 8 ferulic acid-related compounds were calculated by both semi-empirical molecular orbital (AM1, PM3) and ab initio (3-21G* 6-31G*) and density function theory (DFT) (B3LYP) methods. COX-2 inhibition appeared in compounds with phenolic O-H BDE higher than 85.76 kcal/mol, as calculated by the density function theory (DFT) approach. The phenolic O-H BDEs of the most potent compounds, dehydrodiisoeugenol and bis-FA, were 85.99 and 85.76 kcal/mol, respectively. No causal relationship between COX-2 inhibition and IP was found. Neither dehydrodiisoeugenol nor bis-FA possessed significant scavenging activity against the 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical. The NSAID-like activity of dehydrodiisoeugenol and bis-FA appears to be related to their phenol function.

3.Analysis of anti-inflammatory dehydrodiisoeugenol and metabolites excreted in rat feces and urine using HPLC-UV.
Li F;Yang XW Biomed Chromatogr. 2012 Jun;26(6):703-7. doi: 10.1002/bmc.1717. Epub 2011 Sep 19.
Abstract:Dehydrodiisoeugenol (DDIE) is a lignan in the fruit of Myristica fragrans. It can be converted into several metabolites in in vitro and in vivo metabolism. In this study, the excretion of DDIE in urine and feces was investigated after intravenous (i.v.) and intragastric (i.g.) administration to rats. DDIE and its metabolites (M-1 and M-2) were measured using HPLC. The amount of DDIE and its metabolites excreted was higher in feces than in urine, suggesting that DDIE and its metabolites are eliminated primarily in the feces. Significant differences in the excretion levels of DDIE and its metabolites were seen between i.v. and i.g. administration. Greater amounts of DDIE and its metabolites were excreted following i.v. administration, suggesting that DDIE can exert a longer period of anti-inflammatory activity following i.g. administration. The accuracy, precision, recovery and stability of the analytical method in this study were satisfactory for the measurement of DDIE and its metabolites in rat urine and feces. Observations made in this study will contribute to understanding of the absorption, distribution, metabolism and excretion pathway of DDIE and will aid decision-making regarding the best mode of DDIE administration during treatment to maximize its anti-inflammatory effects.

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