PRLX-93936 dihydrochloride

PRLX-93936 (72 h) dihydrochloride selectively inhibits the viability of human cancer cell lines, with the strongest activity observed in pancreatic and head and neck cancer cell lines, and reduces the survival rate of human cancer cell lines with high TRIM21 expression^[1].
PRLX-93936 (500 nM; 30 min-10 h) dihydrochloride induces TRIM21-dependent degradation of nuclear pore complex proteins and MCL1 in PANC-1 human pancreatic cancer cells^[1].
PRLX-93936 (500 nM; 30 min) dihydrochloride induces TRIM21-dependent ubiquitination of nuclear pore complex proteins in human pancreatic cancer cell line PANC-1 pretreated with MG132 (HY-13259)^[1].
PRLX-93936 (cells are pretreated with 1 μM MG132 for 30 min, followed by treatment with 500 nM PRLX-93936 for 30 min or 2 h, and co-treated with 100 nM biotin for 30 min) dihydrochloride induces the translocation of TRIM21 to the nuclear pore complex in human pancreatic cancer cell line PANC-1. Treatment with 500 nM PRLX-93936 dihydrochloride for 30 min or 2 h results in close proximity between TRIM21 and nucleoporins such as NUP98^[1].
PRLX-93936 (2 h) dihydrochloride acts as a molecular glue that induces a direct, dose-dependent interaction between TRIM21 and NUP98 in HEK293T cells^[1].
PRLX-93936 (for 5 days) dihydrochloride potently reduces the viability of cholangiopancreatic organoids with high TRIM21 expression, and induces TRIM21-dependent degradation of nuclear pore complex proteins.
PRLX-93936 (1-10 μM) dihydrochloride reduces HIF-1α protein accumulation under hypoxic conditions^[3].

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