JRN73958  (Synonyms: Reduced scytonemin)

JRN73958 is a PI3K/Akt, MAPK, and NF-κB inhibitor. JRN73958 decreases LPS/IFNγ-induced PI3K/Akt, MAPK, and NF-κB activity. JRN73958 can be used for the research of leukemia^[1][2].

JRN73958 (0.5-2.5 μM; 2 h pretreatment, followed by 24 h LPS/IFNγ stimulation) suppresses LPS/IFNγ-induced NO production in murine macrophage RAW264 cells in a concentration-dependent manner, with the strongest inhibition observed at 2.5 μM^[1].
JRN73958 (2.5 μM; 2 h pretreatment, followed by LPS/IFNγ stimulation) significantly reduces LPS/IFNγ-induced iNOS and COX-2 mRNA and protein expression in murine macrophage RAW264 cells^[1].
JRN73958 (2.5 μM; 2 h pretreatment) inhibits LPS/IFNγ-mediated activation of p38 MAPK, ERK, SAPK/JNK, IκB, and STAT1 in murine macrophage RAW264 cells^[1].
JRN73958 (2.5 μM; 2 h pretreatment) increases HO-1 expression 3.5-fold in murine macrophage RAW264 cells, and this induction is required for JRN73958's inhibitory effect on LPS/IFNγ-induced NO production^[1].
JRN73958 (2.5 μM; 0, 15, 30, 60, 120 min) transiently increases intracellular ROS levels in murine macrophage RAW264 cells, reaching a 1.8-fold peak at 30 min^[1].
JRN73958 (2.5 μM; 24 h) activates Nrf2/ARE signaling in murine macrophage RAW264 cells, increasing ARE enhancer activity to 1.35-fold relative to untreated cells^[1].
JRN73958 (2.5 μM; 2 h incubation, following inhibitor pretreatment) has its induced HO-1 expression in murine macrophage RAW264 cells suppressed by pretreatment with the antioxidant NAC or the kinase inhibitors SB203580 and LY294002^[1].
JRN73958 (2.5 μM; 0, 5, 15, 30, 60, 120 min pretreatment) activates p38 MAPK and PI3K/Akt signaling in murine macrophage RAW264 cells, with peak phosphorylation observed at 30 min^[1].
Reduced scytonemin (R-scy) (1.0-5.0 μM; 24, 48, 72 h) inhibits the growth of human T-lymphoid Jurkat cells with an IC₅₀ of 1.8 μM^[2].
Reduced scytonemin (R-scy) (2.5 μM; 3, 6, 12 h) induces nuclear swelling, nuclear fragmentation, and reduced mitochondrial membrane potential in human T-lymphoid Jurkat cells over 3, 6, and 12 h^[2].
Reduced scytonemin (R-scy) (2.5-5.0 μM; 6, 12, 24 h) induces only marginal nucleosomal DNA fragmentation in human T-lymphoid Jurkat cells after 6, 12, and 24 h of treatment^[2].
Reduced scytonemin (R-scy) (2.5 μM; 72 h) induces human T-lymphoid Jurkat cell death that is resistant to caspase-8, caspase-9, and pan-caspase inhibitors after 72 h of treatment^[2].
Reduced scytonemin (R-scy) (2.5 μM; 12 h) induces the formation of multiple vacuoles and autophagosomes in human T-lymphoid Jurkat cells after 12 h of treatment^[2].
Reduced scytonemin (R-scy) (2.5 μM; 6, 12, 24 h) induces the conversion of LC3-I to LC3-II, a marker of autophagy, in human T-lymphoid Jurkat cells after 6, 12, and 24 h of treatment^[2].
Reduced scytonemin (R-scy) (2.5 μM; 12 h) induces colocalization of LC3 and lysosomes, marking autophagosome/autolysosome formation, in human T-lymphoid Jurkat cells after 12 h of treatment^[2].
Reduced scytonemin (R-scy) (2.5 μM; 48 h) induces autophagic cell growth inhibition in human T-lymphoid Jurkat cells after 48 h of treatment, which is reversible by the autophagy inhibitor 3-MA^[2].
Reduced scytonemin (R-scy) (2.5 μM; 48 h) induces human T-lymphoid Jurkat cell growth inhibition after 48 h of treatment, which is reversible by the antioxidant NAC^[2].
Reduced scytonemin (R-scy) (2.5 μM; 0.5, 1, 3, 6, 12, 24 h) inhibits Akt phosphorylation in a time-dependent manner in human T-lymphoid Jurkat cells over 0.5, 1, 3, 6, 12, and 24 h of treatment^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

548.59

C₃₆H₂₄N₂O₄

171773-95-8

O=C1/C(C2NC3=C(C2=C1C(C/4=O)=C5C6=C(C=CC=C6)NC5C4=C\C7=CC=C(C=C7)O)C=CC=C3)=C\C8=CC=C(C=C8)O

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Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Itoh T, et al. Reduced scytonemin isolated from Nostoc commune suppresses LPS/IFNγ-induced NO production in murine macrophage RAW264 cells by inducing hemeoxygenase-1 expression via the Nrf2/ARE pathway. Food Chem Toxicol. 2014;69:330-338.  [Content Brief]

  [2]. Itoh T, et al. Reduced scytonemin isolated from Nostoc commune induces autophagic cell death in human T-lymphoid cell line Jurkat cells. Food Chem Toxicol. 2013;60:76-82.  [Content Brief]