Adhibin

Adhibin (25 µM; 6 h) reduces active RhoA in cultured cancer cells by approximately 25-95%^[1].
Adhibin alters the expression of PXN, VASP, and KEAP1 in cultured cancer cells without affecting other tested cytoskeleton- and metastasis-related genes^[1].

Adhibin (up to 25 µM; 18 h/long-term) shows no toxicity to A549, MLE-12, and B16-F1 cancer cells at concentrations up to 25 µM, but long-term exposure delays growth and cell cycle progression and promotes cell detachment^[1].

Adhibin (low micromolar concentration; 20 min) selectively inhibits mammalian and invertebrate class-IX myosin ATPase and motor function, with IC₅₀ values of 2.5 µM and 2.6 µM, respectively, while having no effect on skeletal muscle, cardiac muscle, class-V, and non-muscle myosin-2 motors^[1].
Adhibin (submicromolar concentration; overnight) reduces the attachment, spreading, and migration of A549, MLE-12, and B16-F1 cells, and at submicromolar concentrations causes loss of polarity and an approximately 2-fold reduction in migration in B16-F1 cells^[1].
Adhibin (5-25 µM; 6 h/overnight) disrupts actin structures, focal adhesions, and pMLC2/NM2 cortical localization in B16-F1, A549, MLE-12, and NIH-3T3 cells^[1].
Adhibin (25 µM; up to 10 h) reduces focal adhesion movement and accelerates focal adhesion disassembly in A549 cells^[1].
Adhibin (10-25 µM; 18-24 h) reduces pMLC2 and phosphorylated MLCP in A549 and MLE-12 cells without altering total NM2A/B levels^[1].
Adhibin (5 µM; 3 h) impairs the contractile ring pMLC2 and increases multinucleation in B16-F1 cells^[1].
Adhibin (2-40 µM; 48 h) disrupts epithelial junctions in MLE-12 and Caco-2 cells, leading to mislocalization of ZO-1 and connexin-43 and loss of TEER^[1].
Adhibin (5-25 µM; 72 h) completely blocks the 3D migration of NIH-3T3 spheroids at 10 µM and 25 µM concentrations, and inhibits spheroid assembly at higher concentrations^[1].
Adhibin (25 µM; days 2-8) reduces budding and eccentricity in human colon organoids without affecting survival or proliferation markers^[1].