Myricetin

Discontinued Product

6189 has been discontinued.

View all Thioredoxin Reductases products.
Description: Irreversible TrxR inhibitor
Chemical Name: 3,5,7-Trihydroxy-2-(3,4,5-trihydroxyphenyl)-4H-1-benzopyran-4-one
Purity: ≥97% (HPLC)
Datasheet
Citations
Reviews
Literature (2)

Biological Activity for Myricetin

Myricetin is an irreversible TrxR inhibitor (IC50 = 0.62 μM). Exhibits concentration-, time- and NADH-dependent TrxR inhibition. Results in the oxidation of Trx and reduced TrxR activity in vitro in addition to the accumulation of cells in sub-G1 phase. Reduces neoplastic transformation and induces cell death in cancer cell lines. Chemotherapeutic. Myricetin binds to the CAG motif of the mutant RNA from the HTT gene in Huntington's disease (HD). It prevents the translation of mutant huntingtin protein as well as sequestration of MBNL1. Myricetin alleviates proteotoxicity of expanded polyglutamine proteins in Cos-7 cells. Myricetin also improves neurobehavioral deficits in the HD mouse model.

Technical Data for Myricetin

M. Wt 318.24
Formula C15H10O8
Storage Store at -20°C
Purity ≥97% (HPLC)
CAS Number 529-44-2
PubChem ID 5281672
InChI Key IKMDFBPHZNJCSN-UHFFFAOYSA-N
Smiles OC1=CC(O)=C2C(OC(C3=CC(O)=C(C(O)=C3)O)=C(C2=O)O)=C1

The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.

Tocris products are intended for laboratory research use only, unless stated otherwise.

References for Myricetin

References are publications that support the biological activity of the product.

Lu et al (2006) Inhibition of mammalian thioredoxin reductase by some flavonoids: implications for myricetin and quercetin anticancer activity. Cancer.Res. 66 4410 PMID: 16618767

Lu & Holmgren et al (2009) Selenoproteins. J.Biol.Chem. 284 723 PMID: 18757362

Ko et al (2005) Mitochondrial-dependent, reactive oxygen species-independent apoptosis by myricetin: roles of protein kinase C, cytochrome c, and caspase cascade. Biochem.Pharmacol. 69 913 PMID: 15748703

Devi et al (2015) Molecular mechanisms underlying anticancer effects of myricetin. Life.Sci. 142 19 PMID: 26455550

Ong & Khoo et al (1997) Biological effects of myricetin. Gen.Pharmacol. 29 121 PMID: 9251891

Khan et al (2018) Myricetin reduces toxic level of CAG repeats RNA in Huntington's Disease (HD) and Spino Cerebellar Ataxia (SCAs). ACS Chem.Biol. 13 180 PMID: 29172480

View Related Products by Product Action

View all Thioredoxin Reductase Inhibitors

Keywords: Myricetin, Myricetin supplier, Myricetin, TrxR, Thioredoxin, reductase, irreversible, inhibitors, inhibits, chemotherapeutic, cancer, cell, death, CAG, motif, mutant, RNA, HTT, gene, in, Huntingtons, disease, Reductases, DNA,, and, Protein, Synthesis, 6189, Tocris Bioscience

Citations for Myricetin

Citations are publications that use Tocris products.

Currently there are no citations for Myricetin.

Reviews for Myricetin

There are currently no reviews for this product. Be the first to review Myricetin and earn rewards!

Have you used Myricetin?

Submit a review and receive an Amazon gift card.

$50/€35/£30/$50CAN/¥300 Yuan/¥5000 Yen for first to review with an image

$25/€18/£15/$25CAN/¥75 Yuan/¥2500 Yen for a review with an image

$10/€7/£6/$10 CAD/¥70 Yuan/¥1110 Yen for a review without an image

Submit a Review

Literature in this Area

Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!

*Please note that Tocris will only send literature to established scientific business / institute addresses.


Autophagy Poster

Autophagy Poster

Autophagy is a cellular process used by cells for degradation and recycling. Written by Patricia Boya and Patrice Codogno, this poster summarizes the molecular machinery, physiology and pathology of autophagy. Compounds available from Tocris are listed.

Programmed Cell Death Poster

Programmed Cell Death Poster

There are two currently recognized forms of programmed cell death: apoptosis and necroptosis. This poster summarizes the signaling pathways involved in apoptosis, necroptosis and cell survival following death receptor activation, and highlights the influence of the molecular switch, cFLIP, on cell fate.