Latanoprost

432.59

432.59

1806241-263-5

6Z5B6HVF6O

DTXSID1041057

C29151

S01EE|S - Sensory organs

2937500000

87

3.98

pale yellow oil

1.1±0.1 g/cm3

583.8°C at 760 mmHg

188.3±23.6 °C

1.538

DMSO: freely soluble

−20°C

D20 +31.57° (c = 0.91 in acetonitrile)

4.88None

4.88

NONH for all modes of transport

3

MJ9669550

|Danger|H300 (44.83%): Fatal if swallowed [Danger Acute toxicity, oral]|P201, P202, P264, P270, P280, P281, P301+P310, P305+P351+P338, P308+P313, P310, P321, P330, P405, and P501|Aggregated GHS information provided by 88 companies from 10 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

The oral LD50 in the rat is > 50 mg/kg. An overdose of latanoprost is not expected to result in dangerous patient outcomes, however, conjunctival or episcleral hyperemia may occur.An intravenous infusion of 3 μg/kg of latanoprost in healthy volunteers led to mean plasma concentrations of 200 times higher than a normally administered therapeutic dose and no adverse effects were noted. One study suggested that an overdose of latanoprost lead to cystoid macular edema after a large, unintended overdose. This resolved within 4 weeks after 4 weeks following treatment with nepafenac 0.3% eye drops in addition to oral acetazolamide. Contact the local poison control center for updated guidance on the management of a latanoprost overdose.

Latanoprost is about 90% plasma protein-bound.

Latanoprost is indicated for the reduction of elevated intraocular pressure in patients who have been diagnosed with open-angle glaucoma or ocular hypertension. Latanoprost may be combined in a product with [Netarsudil], a rho kinase inhibitor, for the same indications. In addition to the above indications, the Canadian monograph for this drug also approves latanoprost for the treatment of elevated intraocular pressure as a result of angle-closure glaucoma that has been treated with peripheral iridotomy or laser iridoplasty.|FDA Label|Treatment of glaucoma|Roclanda is indicated for the reduction of elevated intraocular pressure (IOP) in adult patients with primary open-angle glaucoma or ocular hypertension for whom monotherapy with a prostaglandin or netarsudil provides insufficient IOP reduction.

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.

Sterile solutions that are intended for instillation into the eye. It does not include solutions for cleaning eyeglasses or CONTACT LENS SOLUTIONS. (See all compounds classified as Ophthalmic Solutions.)

This drug is rapidly absorbed in the cornea as an isopropyl ester prodrug and is then activated by the process of hydrolysis. A small amount of this drug is systemically absorbed. The Cmax of latanoprost in the systemic circulation is reached after 5 minutes and is measured to be 53 pg/mL. The Cmax in the aqueous humor is attained within 2 hours after administration. and has been estimated to be 15-30 ng/mL.|After hepatic beta-oxidation, the metabolites of latanoprost are primarily found to be excreted by the kidneys. About 88% of the latanoprost dose is recovered in the urine after topical administration. About 15% of a dose is reported to be excreted in the feces.|The volume of distribution of latanoprost is 0.16 ± 0.02 L/kg. The activated acid form of latanoprost can be measured in aqueous humor in the initial 4 hours post-administration, and it is measured in the plasma only for 1 hour following ophthalmic administration. This drug is more lipophilic than its parent prostaglandin and easily penetrates the cornea. It has been shown to cross the placenta in rats.|The systemic clearance of latanoprost is 7 mL/min/kg.

After corneal uptake, this prodrug is hydrolyzed and activated by esterases to become a pharmacologically active drug. The small portion of this drug that is able to reach the circulation is found to be metabolized by the liver to the 1,2-dinor and 1,2,3,4-tetranor metabolites through fatty acid beta-oxidation.

The elimination half-life of latanoprost from the plasma is about 17 minutes. The elimination half-life of latanoprost from the eye is estimated at 2–3 hours.

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.

latanoprost

Human Drugs -> EU pediatric investigation plans|Human drugs -> Roclanda -> EMA Drug Category|Ophthalmologicals -> Human pharmacotherapeutic group|Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients