Methyl 4-caffeoylquinate CAS NO.123372-74-7

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General tips：For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging：1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition：Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Chemical Properties of Methyl 4-caffeoylquinate

Source of Methyl 4-caffeoylquinate

The flowerbud of Lonicera japonica Thunb.

Protocol of Methyl 4-caffeoylquinate

Preparing Stock Solutions of Methyl 4-caffeoylquinate

References on Methyl 4-caffeoylquinate

6-Hydroxy-3-O-methyl-kaempferol 6-O-glucopyranoside potentiates the anti-proliferative effect of interferon alpha/beta by promoting activation of the JAK/STAT signaling by inhibiting SOCS3 in hepatocellular carcinoma cells.[Pubmed:29031523]

Toxicol Appl Pharmacol. 2017 Dec 1;336:31-39.

Suppressor of cytokine signaling 3 (SOCS3) is a key negative regulator of type I interferon (IFN alpha/beta) signaling. Inhibition of SOCS3 by small molecules may be a new strategy to enhance the efficacy of type I IFN and reduce its side effects. We established a cell-based screening assay using human hepatoma HepG2 cells stably transfected with a plasmid wherein the luciferase reporter activity was propelled by interferon alpha-stimulated response element (ISRE), which is a motif specifically recognized by type I IFN-induced activation of Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway. After screening our chemical library, 6-hydroxy-3-O-methyl-kaempferol 6-O-glucopyranoside (K6G) was identified to be a potent activator of type I IFN with EC50 value of 3.33+/-0.04muM. K6G enhanced the phosphorylation of JAK1, Tyk2, and STAT1/2 but decreased the phosphorylation of STAT3. K6G also promoted endogenous IFN-alpha-regulated genes expression. More interestingly, K6G significantly decreased the expression of SOCS3 without affecting the expression of SOCS1. Furthermore, K6G enhanced the anti-proliferative effect of IFN-alpha on hepatocellular carcinoma (HCC) cells. These results suggested that K6G potentiated the inhibitory effect of IFN-alpha on HCC cell proliferation through activation of the JAK/STAT signaling pathway by inhibiting SOCS3 expression. K6G warrants further investigation as a novel therapeutic method to enhance the efficacy of IFN-alpha/beta.

Highly selective and sensitive colorimetric determination of Cr(3+) ion by 4-amino-5-methyl-4H-1,2,4-triazole-3-thiol functionalized Au nanoparticles.[Pubmed:29032343]

Spectrochim Acta A Mol Biomol Spectrosc. 2018 Feb 15;191:189-194.

In this work, a rapid, selective naked eyes colorimetric chemical probe for the detection of Cr(3+) was developed based on functionalization of gold nanoparticles. For this purpose, surface of Au NPs was functionalized using 4-amino-5-methyl-4H-1,2,4-triazole-3-thiol (AMTT). Through colorimetric studies, it was found that in the presence of Cr(3+) ions, AMTT-Au NPs instantly aggregated and resulted in a color change of the solution from red to blue. The color change of AMTT-Au NPs due to the aggregation induced by Cr(3+) can be seen with even naked eyes and also by UV-Vis spectroscopy with a detection limit of 1.8muM and 0.1muM, respectively. AMTT-Au NPs showed excellent selectivity toward Cr(3+) compared to other cations tested, including K(+), Na(+), Cs(+), Fe(3+), Ni(2+), Cu(2+), Co(2+), Zn(2+), Ba(2+), Ca(2+), Mg(2+), Cd(2+), Pb(2+), Hg(2+) ions and especially all trivalent lanthanide ions. The absorbance ratio (A650/A525) was linear toward Cr(3+) concentrations in the range of 0.6-6.1muM (R(2)=0.996). The best response was achieved over a pH range of 3-5. Furthermore, the proposed colorimetric method based on AMTT-Au NPs was successfully used for Cr(3+) ion detection in plasma sample and some water samples.

Role of ethanolic extract of Bacopa monnieri against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induced mice model via inhibition of apoptotic pathways of dopaminergic neurons.[Pubmed:29032054]

Brain Res Bull. 2017 Oct;135:120-128.

Parkinson's disease (PD) is a neurodegenerative disease which causes rigidity, resting tremor and postural instability. The neuroprotective effects of an ethanolic extract of Bacopa monnieri (BM) were evaluated in a Parkinsonian mice model induced by the MPTP. The present study investigates the mechanisms of neuroprotection elicited by BM, an herb traditionally recognized by the Indian system of medicine, Ayurveda. An ethanolic extract of BM was co-treated with the MPTP induced mouse model of PD and was shown to significantly rescue the motor behaviour (Rotarod, Grip Strength and Foot Printing test). Furthermore, on biochemical parameters too BM significantly showed protective effect as Catalase, LPO, Nitrite, SOD, GR, GPx parameters showed marked improvement and levels of Dopamine, DOPAC and HVA were enhanced significantly. There was a significant reduction in tyrosine hydroxylase (TH) immunoreactivity in the substantia nigra (SN) in MPTP treated group, which was considerably restored by the use of BM extract. BM also facilitated neuroprotection by creating an anti-apoptotic environment indicated by reduced apoptotic (Bax and caspase-3) and increased levels of anti-apoptotic (Bcl2) protein expression, respectively. Altogether, the present study suggests that BM treatment provides nigrostriatal dopaminergic neuroprotection against MPTP induced Parkinsonism by the modulation of oxidative stress and apoptotic machinery possibly accounting for the behavioural effects.