170950-29-5

TrxR1-IN-B19 Chemical Structure
170950-29-5

Chemical Structure

TrxR1-IN-B19

Synonym(s): GO-Y015

  • CAS No.: 170950-29-5
  • Formula:C21H22O5
  • Molecular Weight:354.40

IUPAC Name: (1E,4E)-1,5-bis(2,3-dimethoxyphenyl)penta-1,4-dien-3-one

InChIKey: LSNRKPCFLXRJGN-PHEQNACWSA-N

SMILES: COC(C(OC)=CC=C1)=C1/C=C/C(/C=C/C2=C(C(OC)=CC=C2)OC)=O

Biological Activity: TrxR1-IN-B19 (GO-Y015) is a Curcumin (HY-N0005) derivative and TrxR1 inhibitor. TrxR1-IN-B19 inhibits de novo selenoprotein synthesis, suppresses SeP and GPx expression, and impairs selenium incorporation into Sec-tRNA[Sec]. TrxR1-IN-B19 induces Nrf2 accumulation through Keap1 cysteine modification, HO-1 expression, GSH synthesis, ROS accumulation, ER stress, mitochondrial dysfunction, Apoptosis, and G2/M phase arrest. TrxR1-IN-B19 improves glucose tolerance and insulin sensitivity, lowers blood glucose, inhibits tumor growth, and reduces arsenic accumulation. TrxR1-IN-B19 can be used for research on type 2 diabetes, arsenite-induced toxicity, and gastric cancer[1][2][3][4].

Cat. No. Product Name Purity Description Pricing
HY-120914
TrxR1-IN-B19 TrxR1-IN-B19 (GO-Y015) is a Curcumin (HY-N0005) derivative and TrxR1 inhibitor. TrxR1-IN-B19 inhibits de novo selenoprotein synthesis, suppresses SeP and GPx expression, and impairs selenium incorporation into Sec-tRNA[Sec]. TrxR1-IN-B19 induces Nrf2 accumulation through Keap1 cysteine modification, HO-1 expression, GSH synthesis, ROS accumulation, ER stress, mitochondrial dysfunction, Apoptosis, and G2/M phase arrest. TrxR1-IN-B19 improves glucose tolerance and insulin sensitivity, lowers blood glucose, inhibits tumor growth, and reduces arsenic accumulation. TrxR1-IN-B19 can be used for research on type 2 diabetes, arsenite-induced toxicity, and gastric cancer.
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This product is a controlled substance and not for sale in your territory.

This product is not for sale in your territory.

This compound is listed in the SVHC (Substances of Very High Concern) candidate list of ECHA (European Chemicals Agency).

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References