Blebbistatin is a Selective Non-Muscle Myosin II (NMII) Inhibitor

Blebbistatin is a selective non-muscle myosin II (NMII) inhibitor, promotes directional migration of corneal endothelial cells (CECs) and accelerates wound healing, and better preserves cell junctional integrity and barrier function.

Meanwhile, Blebbistatin acts as a recently discovered inhibitor of nonmuscle myosin II function. Additionally, it appears to be specific for class II myosins. Also, it potently inhibits the function of these myosins in cells. On the basis of these early results, blebbistatin appears to be a promising reagent for dissecting the specific roles of myosin II molecules in cells.

Moreover, the therapeutic potential of targeting NMII to enhance CEC migration is investigated using bovine corneal endothelial cells (BCECs). Blebbistatin, a direct myosin motor inhibitor, promotes migration and directional persistence in CECs through decreasing actin retrograde flow and increasing lamellipodial protrusion persistence to accelerate wound healing in vitro.

In addition, Blebbistatin (100 µM) completely inhibited the movement of rhodamine phalloidin-labeled actin by skeletal muscle HMM in the in Vitro motility assay. A. The blebbistatin-inhibited myosin interacted weakly with actin and did not interfere with the ongoing movement of the remaining uninhibited myosin.

Blebbistatin was most sensitive to 458 nm light, but light at 488 and 351 nm also easily inactivated the molecule as measured by the percentage of actin filaments sliding. In contrast, a much higher power of 514 nm light was required for photoinactivation, and virtually no inactivation occurred with 543 nm light even at 1.3 mW/µm<sup>2</sup>.

On the other hand,, Blebbistatin (0.05 mL, 20 μM; intracameral injection; daily; for 6 days; New Zealand white rabbits) treatment promotes wound healing in rabbit corneal endothelial scraping model.

To sum up, Blebbistatin, a myosin II inhibitor, can be photoinactivated by Blue Light.


Ho WT, et al. Targeting non-muscle myosin II promotes corneal endothelial migration through regulating lamellipodial dynamics. J Mol Med (Berl). 2019 Sep;97(9):1345-1357.

Takeshi Sakamoto, et al. 2005 Jan 18;44(2):584-8.