Critical evaluation of latanoprostene bunod in the treatment of glaucoma

Garcia, Giancarlo A.; Ngai, Philip; Mosaed, Sameh; Lin, Ken

doi:10.2147/opth.s103985

Cited by 32 publications

(25 citation statements)

References 63 publications

(71 reference statements)

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“…BDMN is further metabolized to 1,4‐butanediol and NO (Krauss et al ., ). Latanoprost acid reduces IOP by increasing AH outflow primarily through the uveoscleral pathway (unconventional route), whereas NO facilitates AH outflow through the TM and SC pathways (conventional route) (Cavet et al ., ; Garcia et al ., ; Cavet and DeCory, ).…”

Section: Pg Analogues As Ocular Hypotensive Agentsmentioning

confidence: 97%

Prostaglandin analogues and nitric oxide contribution in the treatment of ocular hypertension and glaucoma

Impagnatiello

Bastia

Almirante

et al. 2018

British J Pharmacology

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In patients with ocular hypertension or glaucoma, all treatments aim to lower intraocular pressure (IOP) by modulating aqueous humour (AH) production and/or uveoscleral and trabecular meshwork/Schlemm's canal AH drainage. PG analogues are considered to be the 'gold standard' treatment and are the most frequently used IOP-lowering agents. Recent data support an important role for NO in regulating IOP. Thus, novel PG analogues carrying a NO-donating moiety were recently advanced. Latanoprostene bunod (LBN) and NCX 470, NO-donating derivatives of latanoprost and bimatoprost, respectively, are examples of such compounds. LBN ophthalmic solution, 0.024% (Vyzulta™), showed greater IOP-lowering efficacy compared with that of Xalatan (latanoprost ophthalmic solution, 0.005%) or 0.5% timolol maleate in clinical settings. NCX 470 was found to be more effective than bimatoprost in animal models of ocular hypertension and glaucoma. Selective EP receptor agonists (i.e. taprenepag isopropyl, omidenepag isopropyl and aganepag isopropyl) and non-selective prostanoid receptor agonists (i.e. ONO-9054, sepetaprost isopropyl) that concomitantly stimulate FP and EP receptors have also been shown to hold promise as effective IOP-lowering agents.

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Section: Pg Analogues As Ocular Hypotensive Agentsmentioning

confidence: 97%

Prostaglandin analogues and nitric oxide contribution in the treatment of ocular hypertension and glaucoma

Impagnatiello

Bastia

Almirante

et al. 2018

British J Pharmacology

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“…Interestingly, latanoprostene bunod has been shown effective as a monotherapy and is also being tested in combination with lantanoprost (clinical trial identifier: NCT02829996). [50][51][52][53] Latanoprostene bunod is a combination lantanoprost with nitric oxide donor from Valent Pharmaceuticals under Food and Drug Administration review. Clinical data have shown safety and lowering intraocular pressure, although approval is pending assessment of Food and Drug Administration concerns over good manufacturing practices.…”

Section: Current State Of New Drugs In Ophthalmology: a Case Study Onmentioning

confidence: 99%

“…These reactions lead to eumelanin, consisting of 5-6dihydroxyindole and 5-6-dihydroxyindole-2-carboxylic acid in Selected metabolic activation pathways of topical ocular therapies including (a) nepafenac, (b) levobunolol, and (c) latanoprostene bunod. Adapted from literature reports 5,18,50.…”

mentioning

confidence: 99%

Do We Need to Study Metabolism and Distribution in the Eye: Why, When, and Are We There Yet?

Argikar¹,

Dumouchel²,

Kramlinger³

et al. 2017

Journal of Pharmaceutical Sciences

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The liver is known to be the principal site of drug metabolism. Depending on the route of administration, especially in cases of topical and local delivery, evaluation of local drug metabolism in extrahepatic tissues is vital to assess fraction of the drug metabolized. This parameter becomes important from the point of view of drug availability or the contribution to overall clearance. Examples include fraction metabolized in the gut for oral drugs and contribution of pulmonary or renal clearance to total clearance of a drug. Diseases of the eye represent a rising unmet medical need and a number of therapeutics are currently being developed in the form of small molecules and biologics. Treatment of ocular diseases has expanded to explore various topical formulations and local short- and long-term therapies by ocular routes of administration. Until recently, metabolism in the eye for any species, including human, was not well documented, but this topic is gaining wide interest. Many in vitro-ex vivo models, each with separate pros and cons, are being used for studying ocular metabolism. This review is aimed at providing a perspective on the relevance and application of ocular metabolism, melanin binding, and the use of tissue- and cell-derived ocular models in discovery and preclinical development.

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“…Среди последних разработок новых препаратов следует выделить донатор оксида азота латанопростин-бунод, ингибиторы rho-киназы и переносчика норэпинефрина (ROCK/NET ингибиторы) и их комбинацию с латанопростом (Роклатан), некоторые из которых можно считать дальнейшей эволюцией латанопроста. Латанопростин-бунод -донатор оксида азота, молекула которого практически идентична молекуле латанопроста, но вместо изопропилового эфира содержит цепочку с молекулами азота и кислорода, которая после гидролиза в роговице обеспечивает поступление во влагу передней камеры, помимо кислоты латанопроста, также бутандиола мононитрата, метаболизирующего в дальнейшем до образования оксида азота, который, в свою очередь, способствует ремоделированию внеклеточного матрикса иным путём, чем кислота латанопроста, что может обеспечить дополнительный гипотензивный эффект [33].…”

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