Latanoprost

3.98

4.4

This chemical does not meet GHS hazard criteria for 0.7% (1 of 145) of reports.

Danger

H300 (63.4%): Fatal if swallowed [Danger Acute toxicity, oral]；H301 (11%): Toxic if swallowed [Danger Acute toxicity, oral]；H361 (62.1%): Suspected of damaging fertility or the unborn child [Warning Reproductive toxicity]

P203, P264, P270, P280, P301+P316, P318, P321, P330, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 145 reports by companies from 16 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.；Reported as not meeting GHS hazard criteria per 1 of 145 reports by companies.；There are 15 notifications provided by 144 of 145 reports by companies with hazard statement code(s).；Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website.

The primary adverse effects of latanoprost include eyelid edema, blurred vision, dry eyes, itching, redness, the growth of eyelashes, change in eyelid pigmentation (may become darker), iris, and eyelash. Other adverse effects of latanoprost include contact dermatitis/allergic conjunctivitis and an iris cyst. See specific adverse effects listed below.；Conjunctival hyperemia: Conjunctival hyperemia is among the most common side effects noted in 5% to 15% of patients, more than in timolol-treated eyes. Latanoprost with a preservative (benzalkonium chloride) may reduce the goblet cell density. The conjunctival redness usually appears within 2 to 3 days of initiation of the topical treatment, reduces within 1 month, and is typically mild with prolonged use.；Hypertrichosis: Hypertrichosis is an increase in the thickness, length, and number of eyelashes. Although this is preferred from a cosmetic point of view in some patients, the unilateral occurrence can be undesirable. The changes in the eyelashes are usually reversible after discontinuing the drug; this is due to the stimulation of the growth phase of the hair cycle.；Pigmentation: The pigmentation is due to increased melanin in the melanocytes, but the number of melanocytes does not increase. There is an upregulation of the tyrosinase activity in the melanocytes. The pigmentation may increase for the duration of drug use. The brownish color change of the iris after latanoprost use is permanent, but the pigmentation of the eyelid, periorbital tissue, and eyelash may be reversible. The pigmentation of the iris usually starts around the pupillary margin and then spreads towards the peripheral iris. Iris nevi and freckles are not affected by latanoprost. The pigmentation of the iris usually begins within 1 year of therapy and continues to increase with the use of the drug. Patients should receive counsel regarding the possible change in iris color, which may be more evident if using the medicine in only 1 eye. The iris pigmentation is more common in light-colored rides but may also occur in dark or brown rides. Darkening of the iris occurs in up to 10% of cases. Pigmentation of periocular tissue is reducible by removing the excess latanoprost drop from around the eye.；Intraocular inflammation: Latanoprost may worsen intraocular inflammation (uveitis) and should be avoided in the actively inflamed eye.；Macular edema: Latanoprost may induce or aggravate macular edema, including cystoid macular edema. Patients with aphakia and pseudophakia with open posterior capsules are at higher risk of developing cystoid macular edema (CME). Prostaglandin analogs (PGA) related to CME can be treated with discontinuation of the PGA. The most commonly used treatment strategy in pseudophakic CME is to suppress postsurgical inflammation using topical NSAIDs or corticosteroids, separately or combined. Corticosteroids are frequently used to treat pseudophakic CME because of their well-known anti-inflammatory effects.；Reactivation of herpetic keratitis: This may occur with latanoprost, and patients with active herpetic keratitis should avoid latanoprost. A contaminated multidose vial of latanoprost may cause bacterial keratitis in patients with a corneal epithelial defect or other corneal diseases.；Superficial punctate keratopathy: Damage to the ocular surface, including reduced tear break-up time, superficial punctate keratopathy may occur due to the preservative in latanoprost (benzalkonium), and the ocular surface toxicity has been noted to be less with preservative-free tafluprost.

S01EE01

S - Sensory organs；S01 - Ophthalmologicals；S01E - Antiglaucoma preparations and miotics；S01EE - Prostaglandin analogues；S01EE01 - Latanoprost

QS - Sensory organs；QS01 - Ophthalmologicals；QS01E - Antiglaucoma preparations and miotics；QS01EE - Prostaglandin analogues；QS01EE01 - Latanoprost

S01EE01

Latanoprost effectively decreases intraocular pressure by increasing uveoscleral outflow. A decrease in intraocular pressure has been measured within 3–4 hours post-administration, reaches a maximum decrease at 8–12 hours, and can be maintained for a period of 24 hours. **A note on eye and periorbital changes** Between 3 to 10% of patients taking latanoprost have experienced iris pigmentation after about 3-4 months of latanoprost use. Patients should be notified of this risk before initiating treatment. It may occur in both patients with light-colored irides (green-brown or blue/grey-brown) or dark-colored (brown) irides, but is less pronounced in the latter group. This drug may also cause other ocular effects including infrequent conjunctival hyperemia, pigmentation of periocular tissues, eyelash changes, hypertrichosis, and ocular irritation.

Elevated intraocular pressure leads to an increased risk of glaucomatous visual field loss. The higher the intraocular pressure, the higher the risk of damage to the optic nerve and loss of visual field. Latanoprost selectively stimulates the prostaglandin F2 alpha receptor and this results in a decreased intraocular pressure (IOP) via the increased outflow of aqueous humor, which is often implicated in cases of elevated intraocular pressure. Possible specific mechanisms of the abovementioned increased aqueous outflow are the remodeling of the extracellular matrix and regulation of matrix metalloproteinases. These actions result in higher tissue permeability related to humor outflow pathways, which likely change outflow resistance and/or outflow rates.