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SML0873

Sigma-Aldrich

Y16

≥98% (HPLC)

Synonym(s):

4-[[3-[(3-Methylphenyl)methoxy]phenyl]methylene]-1-phenyl-3,5-pyrazolidinedione

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About This Item

Empirical Formula (Hill Notation):
C24H20N2O3
CAS Number:
Molecular Weight:
384.43
UNSPSC Code:
12352200
NACRES:
NA.77

Quality Level

Assay

≥98% (HPLC)

form

powder

color

, faint yellow to dark orange

solubility

DMSO: 5 mg/mL, clear (warmed)

storage temp.

2-8°C

Biochem/physiol Actions

Y16 blocks the binding of LARG, a DBL-family Rho guanine nucleotide exchange factor, with Rho (Kd = 80 nM). Y16 specifically inhibits LARG catalyzed activation of RhoA and RhoA signaling pathways. Y16 blocks the growth and migration of MCF7 breast cancer cells.

Features and Benefits

This compound is a featured product for Cyclic Nucleotide research. Click here to discover more featured Cyclic Nucleotide products. Learn more about bioactive small molecules for other areas of research at sigma.com/discover-bsm.
This compound is featured on the GTP Binding Proteins (Low Molecular Weight) page of the Handbook of Receptor Classification and Signal Transduction. To browse other handbook pages, click here.

Other Notes

Product is a racemic mixture of E/Z isomers.

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Bo Zhang et al.
Cells, 9(3) (2020-03-08)
Rho GTPases, including Rho, Cdc42, Rac and ROP subfamilies, are key signaling molecules in RNA polymerase II (Pol II) transcriptional control. Our prior work has shown that plant ROP and yeast Cdc42 GTPases similarly modulate Ser2 and Ser5 phosphorylation status
Sreeharsha Gurrapu et al.
Cell death and differentiation, 25(7), 1259-1275 (2018-03-21)
Semaphorin 4C (Sema4C) expression in human breast cancers correlates with poor disease outcome. Surprisingly, upon knock-down of Sema4C or its receptor PlexinB2 in diverse mammary carcinoma cells (but not their normal counterparts), we observed dramatic growth inhibition associated with impairment

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