Clinical data
Pronunciation la-TAN-oh-prost
Trade names Xalatan
AHFS/ Monograph
MedlinePlus a697003
  • US: C (Risk not ruled out)
Routes of
Topical (eye drops)
ATC code S01EE01 (WHO)
Legal status
Legal status
Pharmacokinetic data
Metabolism Activation by ester hydrolysis, deactivation by beta oxidation
Onset of action 3–4 hours
Biological half-life 17 minutes (plasma)
Duration of action ≥ 24 hours
Excretion Mainly via kidney
CAS Number 130209-82-4 YesY
PubChem (CID) 5311221
DrugBank DB00654 YesY
ChemSpider 4470740 YesY
KEGG D00356 YesY
ECHA InfoCard 100.162.178
Chemical and physical data
Formula C26H40O5
Molar mass 432.593 g/mol
3D model (Jmol) Interactive image

Latanoprost eye solution is a medication administered into the eyes to control the progression of glaucoma or ocular hypertension by reducing intraocular pressure (IOP). It is a prostaglandin analogue (more specifically an analogue of prostaglandin F[1]) that lowers the pressure by increasing the outflow of aqueous fluid from the eyes through the uveoscleral tract.[2] Latanoprost is an isopropyl ester prodrug, meaning it is inactive until it is hydrolyzed by esterases in the cornea to the biologically active acid.[3]

Latanoprost was invented by Johan W. Stjernschantz and Bahram Resul, employees of the Pharmacia Corporation of Uppsala, Sweden.[4] It is on the World Health Organization's List of Essential Medicines, a list of the most important medication needed in a basic health system.[5] It is also known by the brand name of Xalatan manufactured by Pfizer. Annual sales are approximately $1.6 billion. The patent for latanoprost expired in March 2011, and at least one generic version is now widely available in the U.S.

Medical uses

Open-angle glaucoma, ocular hypertension


In well-controlled clinical trials including patients with open-angle glaucoma or ocular hypertension (IOP ≥21 mm Hg), monotherapy with latanoprost reduced IOP levels by 22 to 39% over 1 to 12 months’ treatment. Latanoprost was significantly more effective than timolol 0.5% twice daily in 3 of 4 large (n = 163 to 267) randomised, double-blind trials. Latanoprost demonstrated a stable long-term IOP-lowering effect in 1- or 2-year continuations of these trials, with no sign of diminishing effect during prolonged treatment.[6]

Meta-analysis suggests that latanoprost is more effective than timolol in lowering IOP. However, it often causes iris pigmentation. While current evidence suggests that this pigmentation is benign, careful lifetime evaluation of patients is still justified.[7]

Closed-angle glaucoma

Patients who had elevated IOP despite iridotomy and/or iridectomy (including patients of Asian descent), latanoprost was significantly more effective than timolol in two double-blind, monotherapy trials (8.2 and 8.8 mm Hg vs 5.2 and 5.7 mm Hg for latanoprost vs timolol at 12 and 2 weeks, respectively).[8]

Adverse effects

Listed from most to least common:[9][10]


Use in pregnant women is limited due to high incidence of abortion shown in animal experiments. Because of this, latanoprost is classified as risk factor C (adverse events were observed in animal reproduction studies at maternally toxic doses) according to United States Food and Drug Administration's use-in-pregnancy ratings.[12] Drug excretion in breast milk is unknown.[2]


Interactions are similar to other prostaglandin analogs. Paradoxically, the concomitant use of latanoprost and bimatoprost or other prostaglandins may result in increased intraocular pressure. Non-steroidal anti-inflammatory drugs (NSAIDs) can reduce or increase the effect of latanoprost.[9][10]


Mechanism of action

Like tafluprost and travoprost, latanoprost is an ester prodrug that is activated to the free acid in the cornea. Also like the related drugs, latanoprost acid is an analog of prostaglandin F that acts as a selective agonist at the prostaglandin F receptor. Prostaglandins increase the sclera's permeability to aqueous fluid. So, an increase in prostaglandin activity increases outflow of aqueous fluid thus lowering intraocular pressure.[9][10]


Latanoprost is absorbed well through the cornea and completely hydrolysed to the active latanoprost acid. Highest concentrations of the acid in the aqueous humour are reached two hours after application, lowering of intraocular pressure starts after 3 to 4 hours, the highest effect is found after 8 to 12 hours, and its action lasts at least 24 hours. When latanoprost acid reaches the circulation, it is quickly metabolised in the liver by beta oxidation to 1,2-dinor- and 1,2,3,4-tetranor-latanoprost acid; blood plasma half life is only 17 minutes. The metabolites are mainly excreted via the kidney.[9][10]

The activation and deactivation pathway is analogous to the one of tafluprost; see Tafluprost#Pharmacokinetics for chemical formulae.



Latanoprost exhibits thermal and solar instability. The concentration of latanoprost stored at 50 °C will decrease by 10% every 8.25 days. When stored at 70 °C the concentration will decrease by 10% every 1.32 days. Ultraviolet light, for example in sunlight, causes rapid degradation of latanoprost.[13]


  1. Ishikawa H, Yoshitomi T, Mashimo K, Nakanishi M, Shimizu K (February 2002). "Pharmacological effects of latanoprost, prostaglandin E2, and F2alpha on isolated rabbit ciliary artery". Graefes Arch. Clin. Exp. Ophthalmol. 240 (2): 120–5. doi:10.1007/s00417-001-0412-4. PMID 11931077.
  2. 1 2 Patel SS, Spencer CM (1996). "Latanoprost. A review of its pharmacological properties, clinical efficacy and tolerability in the management of primary open-angle glaucoma and ocular hypertension". Drugs Aging. 9 (5): 363–378. doi:10.2165/00002512-199609050-00007. PMID 8922563.
  3. Huttunen, KM; Raunio, H; Rautio, J (2011). "Prodrugs—from serendipity to rational design". Pharmacol Rev. 63 (3): 750–71. doi:10.1124/pr.110.003459. PMID 21737530.
  4. "Patent US5296504 - Prostaglandin derivatives for the treatment of glaucoma or ocular hypertension - Google Patents".
  5. "WHO Model List of EssentialMedicines" (PDF). World Health Organization. October 2013. Retrieved 22 April 2014.
  6. Perry CM, McGavin JK, Culy CR, Ibbotson T (2003). "Latanoprost. An Update of its Use in Glaucoma and Ocular Hypertension". Drugs & Aging. 20 (8): 597–630. doi:10.2165/00002512-200320080-00005. PMID 12795627.
  7. Zhang WY, Wan Po AL, Dua HS, Azuara-Blanco A (2001). "Meta-analysis of randomised controlled trials comparing latanoprost with timolol in the treatment of patients with open angle glaucoma or ocular hypertension". British Journal of Ophthalmology. 85: 983–990. doi:10.1136/bjo.85.8.983. PMC 1724079Freely accessible. PMID 11466259.
  8. Aung T; Wong HT; Yip CC; et al. (2000). "Comparison of the intraocular pressure-lowering effect of latanoprost and timolol in patients with chronic angle closure glaucoma: a preliminary study.". Ophthalmology. 107 (6): 1178–83. doi:10.1016/s0161-6420(00)00073-7. PMID 10857840.
  9. 1 2 3 4 Latanoprost Professional Drug Facts.
  10. 1 2 3 4 Haberfeld, H, ed. (2015). Austria-Codex (in German). Vienna: Österreichischer Apothekerverlag.
  11. Amano S, Nakai Y, Ko A, Inoue K, Wakakura M (2008). "A case of keratoconus progression associated with the use of topical latanoprost". Japanese Journal of Ophthalmology. 52 (4): 334–6. doi:10.1007/s10384-008-0554-6. PMID 18773275.
  12. De Santis, M; Lucchese, A; Carducci, B; Cavaliere, A. F.; De Santis, L; Merola, A; Straface, G; Caruso, A (2004). "Latanoprost exposure in pregnancy". American Journal of Ophthalmology. 138 (2): 305–6. doi:10.1016/j.ajo.2004.03.002. PMID 15289149.
  13. Morgan PV, Proniuk S, Blanchard J, Noecker RJ (2001). "Effect of temperature and light on the stability of latanoprost and its clinical relevance". Journal of Glaucoma. 10 (5): 401–405. doi:10.1097/00061198-200110000-00007. PMID 11711838.
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