JWJ-01-306

JWJ-01-306 (10 μM; 5 h) potently degrades endogenous ZBTB11 in MIA PaCa-2 cells via a CRBN- and proteasome-dependent mechanism. As measured by HiBiT quantification, the D_max reaches 60%; whereas detected by immunoblotting, the D_max reaches 90%^[1].
JWJ-01-306 (10 μM; 1-14 days) acts synergistically with Sotorasib (HY-114277) to potently inhibit the proliferation of sotorasib-resistant MIA PaCa-2 cells, degrade ZBTB11, specifically impair cellular oxidative phosphorylation, reduce the basal oxygen consumption rate, maximal oxygen consumption rate and mitoATP/glycoATP ratio, downregulate ZBTB11-mediated transcription of mitochondrial ribosomal and complex I genes, disrupt tricarboxylic acid (TCA) cycle flux in cells, and induce reductive glutamine metabolism^[1].
JWJ-01-306 (10 μM; 1-6 days) potently inhibits the proliferation of parental and MRTX1133 (HY-134813)-resistant SUIT2 cells, enhances the antiproliferative effect of MRTX1133 in drug-resistant cells, impairs cellular oxidative phosphorylation, and reduces the basal oxygen consumption rate, maximum oxygen consumption rate, and mitoATP/glycoATP ratio^[1].
JWJ-01-306 (1 μM; 7 days) enhances the antiproliferative activity of MRTX1133 in pancreatic cancer organoids and deepens the response to K-Ras inhibition^[1].
JWJ-01-306 (5 h) potently degrades endogenous ZBTB11 in MOLT-4 cells with a DC₅₀ of 0.28 μM, reaching a maximum degradation rate of 72% after 5 h of treatment. It also degrades endogenous IKZF1 in Jurkat cells with a DC₅₀ of 0.03 μM, achieving a maximum degradation rate of 85% after 5 h of treatment^[2].
JWJ-01-306 (10 μM; 24 h) reduces oxidative phosphorylation (OxPhos) levels and mitochondrial ATP production in both parental and Dabrafenib (HY-14660)-resistant SK-MEL-5 melanoma cells^[2].
JWJ-01-306 (10 μM; 14 days) reduces the proliferative capacity of both parental and Dabrafenib-resistant SK-MEL-5 melanoma cells^[2].

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