HSP70-IN-6

HSP70-IN-6 (JL-15) (10 min) potently disrupts the Hsp70-Bim protein-protein interaction in a cell-free fluorescence polarization assay, with an IC₅₀ of 0.07 μM^[1].
HSP70-IN-6 (JL-15) (0-50 μM; 30 min preincubation, 10 min luciferin incubation) dose-dependently suppresses BimBH3-stimulated ATPase activity of Hsp70 in a cell-free assay, with an IC₅₀ of 4.89 μM, without affecting basal ATPase activity^[1].
HSP70-IN-6 (JL-15) (0.2 mM) directly binds to recombinant Hsp70 in a cell-free ITC assay, with a K_d of 123 nM^[1].
HSP70-IN-6 (compound 22) (200 μM; 2:1 compound-to-protein molar ratio) binds to the NBD domain of Hsc70 (highly homologous to Hsp70) within the same hydrophobic cleft targeted by the Hsp70-Bim interaction, as confirmed by H-¹⁵N TROSY-HSQC NMR^[1].
HSP70-IN-6 (JL-15) (0.5-3.0 μM; 12 h) dose-dependently and selectively disrupts the Hsp70-Bim protein-protein interaction in K562 CML cells, without affecting the Hsp70-Bag3 complex^[1].
HSP70-IN-6 (JL-15) (10 mg/mL; 24 h) has a water solubility of 29.42 μg/mL, representing a 4-fold improvement over the reference compound S1g-10^[1].
HSP70-IN-6 (JL-15) (48 h) potently induces apoptosis in TKI-sensitive (BV173, K562) and TKI-resistant (K562-R3) CML cell lines with sub-μM EC₅₀ values, while exhibiting no significant toxicity to normal HEK293 and BaF3 cells^[1].
HSP70-IN-6 (JL-15) (2 μM; 24 h)-induced apoptosis in K562 CML cells is dependent on the presence of Hsp70 and Bim, confirming on-target activity^[1].
HSP70-IN-6 (JL-15) (2 μM; 12 h) reduces the expression levels of oncogenic client proteins AKT, Raf-1, and eIF4E in K562 CML cells^[1].

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