PinA1

PinA1 (up to 100 µM; 1 h) effectively promotes the assembly of the ternary complex between CRBN and CK1α in a fully defined biochemical system, with an EC₅₀ of 2.09 µmol/L^[1].
PinA1 (16 h) is a highly potent and cell-preferential CK1α degrader in engineered Jurkat cells, with a DC₅₀ of 46.9 nmol/L against CK1α, and it does not induce significant IKZF1 degradation^[1].
PinA1 (at concentrations up to 1 or 100 µM; for 48-120 h) selectively inhibits the proliferation of TP53 wild-type FLT3-ITD AML cell lines with IC₅₀ values below 0.5 µM, whereas TP53-mutant AML cells exhibit tolerance to its antiproliferative effect ^[1].
PinA1 (1 µM; 24-72 h) induces sustained G1-phase cell cycle arrest in TP53 wild-type MOLM-14 and MV4-11 AML cells, while the cell cycle progression of TP53-mutant AML cells remains largely unaffected^[1].
PinA1 (0.1-10 µM) selectively degrades CK1α and strongly activates the p53 signaling pathway exclusively in primary acute myeloid leukemia cells with wild-type TP53, while exhibiting no significant p53-inducing effect in normal hematopoietic cells or primary acute myeloid leukemia cells with mutant TP53^[1].
PinA1 selectively degrades CK1α and specifically induces p53-dependent apoptosis in TP53 wild-type acute myeloid leukemia cell lines and in vitro cultured primary acute myeloid leukemia cells, while exhibiting extremely low toxicity to normal human hematopoietic cells^[2].

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