ACHP possesses oral bioavailability in both mice and rats, showing notable in vivo efficacy in models of inflammation (such as the arachidonic acid-induced mouse ear edema model). It has adequate water solubility (0.12 mg/mL in pH 7.4 isotonic buffer) and outstanding Caco-2 permeability (Papp 62.3×10^-7 cm/s), with oral bioavailability observed in mice (BA: 16%) and rats (BA: 60%). The improved bioavailability in rats is attributed to its low clearance rate (0.33 L/h/kg). ACHP is orally effective at a dose of 1 mg/kg, demonstrating dose-dependent activity in acute inflammation models^[1].

ACHP Hydrochloride demonstrates strong inhibition of IKK-β (IC50: 8.5 nM) and shows cellular efficacy (IC50=40 nM in A549 cells). It inhibits IKK-α moderately with an IC50 of 250 nM and maintains high selectivity against other kinases, such as IKK3, Syk, and MKK4 (IC50>20,000 nM). Additionally, ACHP exhibits significant effectiveness in various cell-based assays. It blocks NF-κB-dependent reporter gene activity in TNFα-stimulated HEK293 cells and PMA/calcium ionophore-activated Jurkat T cells. However, ACHP does not inhibit PMA-induced AP-1 activation in MRC-5 cells or PMA/calcium ionophore-induced NF-κB-dependent reporter gene expression in Jurkat cells at doses above 10 μM. ACHP specifically disrupts NF-κB signaling by targeting IKK-β in live cells^[1].

ACHP reduces cell proliferation in a dose-responsive manner. Cell lines active for Tax show greater sensitivity to ACHP compared to Tax-inactive cell lines and Jurkat cells (with IC50 values of 3.1±1.3 μM for Tax-active cell lines, 10.7±1.7 μM for Tax-inactive cell lines, and 23.6 μM for Jurkat, respectively), indicating a higher reliance on NF-κB for the growth of Tax-active cells than for Tax-inactive cells^[2].