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. Author manuscript; available in PMC: 2019 Jan 4.
Published in final edited form as: Expert Rev Ophthalmol. 2014 Jan 9;6(6):611–622. doi: 10.1586/eop.11.65

Table 2.

Overview of preclinical experiments and results for non-Rho kinase inhibitors that interact with the Rho GTPase pathway.

Non-ROCK inhibitors (target of inhibitor) Results
ML-7 (myosin light chain kinase) ↓ TM contraction
↓ MLC phosphorylation in TM cells
↓ Scar in cell model
GGTI-DU40 (geranylgeranyl-transferase-1) ↑ Outflow
↑ Cell separation and cell rounding in TM cells
↓ Actin bundles and focal adhesions in TM cells
↓ MLC phosphorylation in TM cells
↓ Membrane localization of isoprenylated small GTPases and Gβγ in TM cells
Lovastatin, compactin (HMG-CoA reductase) ↑ Outflow
↑ Cell rounding and actin depolymerization in CB and TM cells
↓ Focal adhesions in CB and TM cells
↓ MLC phosphorylation in TM and CB cells
↓ Membrane-bound Rho GTPase in TM cells
↓ Scar in cell model
Pyrrolopyrimidines (LIM kinase-2) ↓ IOP
↑ Outflow
H-7 (serine/threonine kinases) ↓ IOP
↑ Outflow
↑ Alterations in cell shape, actin cytoskeleton and focal adhesion complexes in TM cells
↑ Changes in morphology and contractility in SC and peri-SC cells

CB: Ciliary body; IOP: Intraocular pressure; MLC: Myosin light chain; ROCK: Rho kinase; SC: Schlemm’s canal; TM: Trabecular meshwork.