HS-72

HS-72 acts as an allosteric inhibitor of Hsp70i. It only reduces the ATP-binding affinity of Hsp70i without inhibiting its intrinsic ATPase activity, and can induce conformational rearrangement of purified Hsp70 protein^[1].
HS-72 (0.001-0.1 mM) was identified via FLECS chemoproteomic screening. Biochemical tests including affinity pull-down, thermofluor melting assay and limited proteolysis-mass spectrometry verify that HS-72 selectively binds Hsp70i over constitutive Hsc70, while Hsp90 recovery is considered nonspecific in the affinity-resin assay^[1].
HS-72 (25, 50 μM; 48-72 h) inhibits proliferation of BT474, MCF-7 and SkBr3 breast cancer cells, while non-tumorigenic MCF10A and RWPE1 cells are relatively insensitive to HS-72^[1].
HS-72 (1-100 μM; 24 h) dose-dependently elevates caspase 3/7 apoptotic activity in BT474, HeLa, HepG2, T47D and LNCaP tumor cell lines^[1].
HS-72 (10, 50 μM; 24 h) promotes degradation of Hsp70 client proteins HER2 and Akt in BT474 and MCF-7 breast cancer cells, and shows stronger degradation activity when combined with HS-10^[1].
HS-72 (50, 100 μM; 18 h) induces accumulation of insoluble mutant HttQ74-GFP aggregates in PC12 neuronal cells^[1].
HS-72 (50-100 nmol/mL; 1 h pretreatment; 24 h post-infection) dose-dependently reduces DENV infection in U937+DC-SIGN cells while maintaining cell viability at concentrations below 90 nmol/mL^[2].
HS-72 reduces infectious DENV production in a foci forming assay, with an EC₅₀ of 22.8 nmol/mL^[2].
HS-72 (75 nmol/mL) inhibits DENV infection at the early stage of the viral life cycle, and significantly reduces viral RNA at the entry stage in U937+DC-SIGN cells^[2].
HS-72 (75 nmol/mL; 1 h pretreatment) disrupts the in situ interactions of Hsp70i with DENV E protein and DC-SIGN at 4 h post-infection, indicating inhibition of Hsp70i association with the DENV receptor complex^[2].

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