Table 4. Classes of Clinically Utilized Drugs for Treating Ocular Hypertension/POAG/NTGa.
| pharmacological class of drug | general name of approved drugs (brand name) | mode(s) of action | pertinent comments |
|---|---|---|---|
| Conventional AQH Outflow Promoting Drugs | |||
| cholinergic muscarinic receptor agonists | pilocarpine (Isopto Carpine); carbachol (Miostat) | enhancement of AQH via conventional outflow pathway | oldest drug therapy known for glaucoma; use limited by 4× daily topical ocular [t.o.] dosing and brow ache and meiosis |
| rho kinase (ROCK) inhibitors | ripasudil (Galanatec); netarsudil (Rhopressa) | increase conventional outflow of AQH (perhaps also enhancing episcleral venous outflow) | relatively efficacious IOP-lowering; increased propensity for hyperemia induction |
| AQH Production (Inflow) Inhibitor Drugs | |||
| carbonic anhydrase inhibitors | dorzolamide (Trusopt); brinzolamide (Azopt) | AQH Inflow inhibition at ciliary processes | oral acetazolamide and methazolamide were used in the past; currently used for acute IOP control instead of chronic therapy; 2x-t.o. daily dosing |
| beta-adrenergic receptor antagonists (“beta blockers”) | timolol (Timoptic); betaxolol (Betoptic); levobunolol (Betagan) | AQH Inflow inhibition at ciliary processes | widely utilized; 2×-t.o. daily dosing; can induce bradycardia; asthmatics treated very cautiously. |
| alpha2-adrenergic receptor agonists | brimonidine (Alphagan); apraclonidine (Iopidine) | AQH Inflow suppression at ciliary processes and enhancement of uveoscleral outflow of AQH | epinephrine and dipivefrin used historically; brimonidine widely used nowadays; 2×- daily t.o. dosing but propensity to cause ocular allergic reaction |
| Uveoscleral Outflow Promoting Drugs | |||
| prostaglandin analogs (FP-receptor agonists), a novel non-PG EP2-receptor agonist (OMDI)) | latanoprost (Xalatan); travoprost (Travatan); bimatoprost (Lumigan); tafluprost (Zioptan). omidenepag isopropyl (OMDI) (Eybelis) | enhancement of uveoscleral and also conventional outflow of AQH Enhancement of uveoscleral outflow of AQH | FP-receptor agonists are the most widely used most potent and most efficacious drug class enabling 1x-t.o. dosing; cosmetic side-effects in and around eyes (iridial color change; deepening of eyelid sulcus). OMDI approved in Japan does not have the aforementioned side-effects. |
| Multiple Modes of Action Drugs | |||
| prostaglandin conjugates | latanoprostene bunod (latanoprost conjugated to an nitric oxide [NO] donor) (Vyzulta) | increase uveoscleral and also conventional outflow of AQH | efficacious IOP-lowering using dual mechanisms of action; 1×-t.o. dosing; propensity for greater hyperemia induction due to NO |
| combination products | examples include: dorzolamide + timolol (Cosopt); brimonidine + brinzolamide (Simbrinza); travoprost + timolol (DuoTrav); latanoprost + netarsudil (Roclatan) | enhancement of outflow and suppression of inflow of AQH | efficacious IOP-lowering using dual modes of action; 1×-t.o. dosing; Patients who are refractory or poor responders to standards of care usually require combination products. |
a
While t.o. drugs are the mainstay treatment for OHT/POAG/NTG, some patients are recalcitrant to pharmaceutical agents. Thus, use of the above-mentioned drugs is often secondarily supplemented with implantation of AQH microshunts or surgeries to reduce the IOP down to or below the normal range in order to help preserve vision in these patients.5−7,13,99,116