N-(6-氨基己基)-5-氯-1-萘磺胺盐酸盐

IC50: 28 μM (Phosphodiesterase) and 51 µM (Myosin light chain kinase)

W-7 is distributed mainly in the cytoplasm, and inhibits proliferation of Chinese hamster ovary K1 (CHO-K1) cells. W-7 selectively blocks the phase of the cell cycle (G1/S boundary phase) in a manner. 25 μM W-7 arrests the growth of the cells at the G1/S boundary phase of the cell cycle.
W-7 (100 μM) exhibits a similar extent of antagonism between the contractile responses to carbachol and KCl. The increase in myosin light chain (P-LC) phosphate content in response to 1-min stimulation with 10 μM carbachol is inhibited by W-7. W-7 antagonizes the smooth muscle contraction through the inhibition of the initial increase in the P-LC phosphorylation.
Treatment with W-7 results in the dose-dependent inhibition of cell proliferation in various human multiple myeloma cell lines. W-7 induces G1 phase cell cycle arrest by downregulating cyclins and upregulating p21cip1. W-7 induces apoptosis via caspase activation; this occurred partly through the elevation of intracellular calcium levels and mitochondrial membrane potential depolarization and through inhibition of the STAT3 phosphorylation and subsequent downregulation of Mcl-1 protein.
W-7 competitively inhibits Ca ²⁺ /calmodulin-dependent phosphodiesterase with a K _i value of 300 μM.

W-7 (3 mg/kg; intraperitoneal injection; on 5 consecutive days per week; female BALB/c nu mice) treatment significantly reduces tumor growth in a murine MM model.