Netarsudil, a Rho kinase (ROCK) inhibitor, targets the underlying pathophysiology of elevated IOP (intraocular pressure), increased trabecular outflow resistance, and thereby increases trabecular outflow and reduces IOP (1):
- distinct mechanism of action of netarsudil has been demonstrated to involve increasing trabecular outflow by decreasing actomyocin-driven cellular contraction and reducing production of extracellular matrix proteins
Latanoprost, the most commonly prescribed prostaglandin analogue, has a complementary mechanism of action, lowering IOP by increasing uveoscleral outflow (1).
NICE states that (2):
- latanoprost–netarsudil is recommended as an option for reducing intraocular pressure (IOP) in adults with primary open-angle glaucoma or ocular hypertension when a prostaglandin analogue alone has not reduced IOP enough, only if:
- they have then tried a fixed-dose combination treatment and it has not reduced IOP enough, or
- a fixed-dose combination treatment containing beta-blockers is unsuitable
Reference:
- Asrani S et al. Fixed-Dose Combination of Netarsudil and Latanoprost in Ocular Hypertension and Open-Angle Glaucoma: Pooled Efficacy/Safety Analysis of Phase 3 MERCURY-1 and -2. Adv Ther. 2020 Apr;37(4):1620-1631.
- NICE (October 2024). Latanoprost–netarsudil for previously treated primary open-angle glaucoma or ocular hypertension