Additionally, Dynasore significantly mitigates motor dysfunction at 3, 7, and 10 days following spinal cord injury (SCI) in rats. This enhancement in motor function is attributed to Dynasore's inhibition of the activation of the neuronal mitochondrial apoptotic pathway and the proliferation of astrocytes post-SCI^[4].

Dynasore impedes the GTPase activities of dynamin1, dynamin2, and Drp1 (mitochondrial dynamin) specifically, without affecting other small GTPases. It serves as an effective suppressor of endocytic pathways that rely on dynamin, by promptly obstructing the formation of coated vesicles immediately following its introduction. Throughout the treatment with Dynasore, an accumulation of two distinct forms of coated pit intermediates occurs: g-shaped, partially formed pits, and O-shaped, completely formed pits, observed at the moment of detachment^[1].

Furthermore, Dynasore effectively blocks the infection of human epithelial and neuronal cells by HSV-1 and HSV-2, encompassing cells from the primary genital tract as well as human fetal neurons and astrocytes. It diminishes the quantity of viral capsids reaching the nuclear pore when administered at the initiation of viral entry, and, if applied up to 8 hours after entry, Dynasore obstructs the transport of newly synthesized viral proteins from the nucleus to the cytosol^[2].

In the context of ischemia/reperfusion, Dynasore prevents the elevation of left ventricular end-diastolic pressure and curtails cardiac troponin I release during reperfusion, contributing to a reduction in infarct size. When adult mouse cardiomyocytes are exposed to oxidative stress, Dynasore enhances cell survival and viability^[3].