Echothiophate is a potent, long-acting irreversible cholinesterase inhibitor used as an ocular hypertensive in the treatment of glaucoma. Occasionally used for accomodative esotropia. Echothiophate iodide for ophthalmic solution will depress both plasma and erythrocyte cholinesterase levels in most patients after a few weeks of eye drop therapy by binding irreversibly to cholinesterase, and thus long acting due to the slow rate of hydrolysis by cholinesterase. It causes miosis, increase in facility of outflow of aqueous humor, fall in intraocular pressure, and potentiation of accommodation.

Diclorphenamide, a carbonic anhydrase inhibitor, was initially developed for the treatment of glaucome, however, now it is used for patients suffering from primary hypokalemic and hyperkalemic periodic paralysis. The exact mechanism of diclorphenamide in periodic paralysis is unknown.

Acetazolamide, usually sold under the trade name Diamox in some countries. DIAMOX is used for adjunctive treatment of: chronic simple (open-angle) glaucoma, secondary glaucoma, and preoperatively in acute angle-closure glaucoma where delay of surgery is desired in order to lower intraocular pressure. DIAMOX is also indicated for the prevention or amelioration of symptoms associated with acute mountain sickness despite gradual ascent. DIAMOX is an enzyme inhibitor that acts specifically on carbonic anhydrase, the enzyme that catalyzes the reversible reaction involving the hydration of carbon dioxide and the dehydration of carbonic acid. In the eye, this inhibitory action of acetazolamide decreases the secretion of aqueous humor and results in a drop in intraocular pressure, a reaction considered desirable in cases of glaucoma and even in certain non-glaucomatous conditions. Evidence seems to indicate that DIAMOX has utility as an adjuvant in treatment of certain dysfunctions of the central nervous system (e.g., epilepsy). The diuretic effect of DIAMOX is due to its action in the kidney on the reversible reaction involving hydration of carbon dioxide and dehydration of carbonic acid. The result is renal loss of HCO3 ion, which carries out sodium, water, and potassium. It is on the World Health Organization's List of Essential Medicines, a list of the most important medications needed in a basic health system.

Neostigmine is a cholinesterase inhibitor used in the treatment of myasthenia gravis and to reverse the effects of muscle relaxants such as gallamine and tubocurarine. Neostigmine, unlike physostigmine, does not cross the blood-brain barrier. By inhibiting acetylcholinesterase, more acetylcholine is available in the synapse, therefore, more of it can bind to the fewer receptors present in myasthenia gravis and can better trigger muscular contraction. Neostigmine is used for the symptomatic treatment of myasthenia gravis by improving muscle tone.

Pilocarpine is an alkaloid extracted from plants of the genus Pilocarpus. The drug stimulates the muscarinic receptors (especially M3, which is expressed in smooth muscles and glands) and thus induces salivation, hypertension and water intake. Pilocarpine was appoved by FDA for the alleviation of symptoms of xerostomia in patients who have undergone radiation therapy to their head and neck cancer and in patients with Sjogren's Syndrome. Ophthalmic solution of the drug is prescribed for the treatment of glaucoma, ocular hypertension, postoperative elevated intraocular pressure, etc.

Unoprostone Isopropyl is a synthetic docosanoid and a structural analogue of an inactive biosynthetic cyclic derivative of arachidonic acid, 13,14-dihydro-15-keto-prostaglandin F 2a. Although the mechanism of action is unknown, unoprostone isopropyl is believed to reduce elevated intraocular pressure by increasing the outflow of aqueous humor through the trabecular meshwork. Unoprostone isopropyl (UI) may have a local effect on Big Potassium channels and ClC-2 chloride channels, but the exact mechanism is unknown at this time. Unoprostone is used for the management of open-angle glaucoma and ocular hypertension. The therapeutic efficacy of Unoprostone can be decreased when used in combination with Celecoxib, Diclofenac, Diflunisal, Etodolac and some other drugs. Unoprostone isopropyl ophthalmic solution may gradually increase the pigmentation of the iris, cause pigment changes (darkening) to periorbital pigmented tissues and eyelashes, exacerbate active intraocular inflammation (e.g., uveitis), and cause macular edema. In clinical studies, the most common ocular adverse reactions with use of Rescula were burning/stinging, burning/stinging upon drug instillation, dry eyes, itching, increased length of eyelashes, and injection. These were reported in approximately 10–25% of patients. Ocular adverse reactions occurring in approximately 5–10% of patients were abnormal vision, eyelid disorder, foreign body sensation, and lacrimation disorder. Other adverse reactions occurred more rarely.

Dapiprazole is an alpha-1 adrenergic receptors antagonist which was developed for for the treatment of drug induced mydriasis produced by adrenergic or parasympatholytic agents. The drug was marketed under the name Rev-Eyes, however it was withdrawn from market due to its slow effect.

Dipivefrin is a prodrug with little or no pharmacologically activity until it is hydrolyzed into epinephrine inside the human eye. The liberated epinephrine, an adrenergic agonist, appears to exert its action by stimulating α -and/or β2-adrenergic receptors, leading to a decrease in aqueous production and an enhancement of outflow facility. The dipivefrin prodrug delivery system is a more efficient way of delivering the therapeutic effects of epinephrine, with fewer side effects than are associated with conventional epinephrine therapy. Dipivefrin is used as initial therapy for the control of intraocular pressure in chronic open-angle glaucoma.

Demecarium (HUMORSOL®) is an indirect-acting parasympathomimetic agent, also known as a cholinesterase inhibitor and anticholinesterase. Cholinesterase inhibitors prolong the effect of acetylcholine, which is released at the neuroeffector junction of parasympathetic postganglion nerves, by inactivating the cholinesterases that break it down. Application of demecarium (HUMORSOL®) to the eye produces intense miosis and ciliary muscle contraction due to inhibition of cholinesterase, allowing acetylcholine to accumulate at sites of cholinergic transmission. These effects are accompanied by increased capillary permeability of the ciliary body and iris, increased permeability of the blood-aqueous barrier, and vasodilation. Myopia may be induced or, if present, may be augmented by the increased refractive power of the lens that results from the accommodative effect of the drug. Demecarium (HUMORSOL®) indirectly produces some of the muscarinic and nicotinic effects of acetylcholine as quantities of the latter accumulate.

Physostigmine (Phy) is one of the oldest drug isolated from Calabar beans and successfully used for the treatment of glaucoma in 1864. Since then, it has been widely employed for various therapeutic purposes. Recently, it has gained prominence because of its clinical trials in the treatment of Alzheimer's disease. Physostigmine was used to treat glaucoma. It can be applied topically to the conjunctiva. Phy is also considered to be a potent prophylactic antidote for organophosphate poisoning. It is a reversible cholinesterase (ChE) inhibitor and has a short duration of action. For the last 50 years, numerous authors have shown that pretreatment with Phy would rapidly improve the incapacitating effects of organophosphate intoxication in various animal species. Phy carbamylates to a portion of ChE enzyme and thus protects the enzyme from binding with organophosphate, which are irreversible ChE inhibitors. The carbamylated ChE enzyme decarbamylates to free the enzyme for normal functioning. The rates of decarbamylation of butyrylcholinesterase (BuChE) in plasma and ChE in brain and muscle are different and are related to the half-life of Phy in these tissues. In addition to ChE inhibition, Phy has a direct action on acetylcholine (ACh) receptor ionophore complex by interacting with the ACh-gated cation channels. A cholinesterase inhibitor that is rapidly absorbed through membranes. It also can cross the blood-brain barrier and is used when central nervous system effects are desired, as in the treatment of severe anticholinergic toxicity.