ArticleInvestigative ophthalmology & visual science2021
NCX 667, a Novel Nitric Oxide Donor, Lowers Intraocular Pressure in Rabbits, Dogs, and Non-Human Primates and Enhances TGFβ2-Induced Outflow in HTM/HSC Constructs.
Article in Investigative ophthalmology & visual science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Promising Glaucoma Medication: A Comprehensive Translational Evaluation.Pharmaceutics · 2026Article
- Bioengineered 3D Human Trabecular Meshwork Models for Outflow Physiology and Glaucoma Research.Bioengineering (Basel, Switzerland) · 2026Review
- The protecting role of Ganoderma lucidum polysaccharides on the retinal neurovascular units in rats with retinal ischemia-reperfusion injury.Scientific reports · 2025Article
- Nimodipine Nanoparticles: A Promising Approach for Glaucoma Management.Pharmaceutics · 2025Article
- Glaucoma animal models in rabbits: State of the art and perspectives-A review.Animal models and experimental medicine · 2025Review
- Lasamide Containing Sulfonylpiperazines as Effective Agents for the Management of Glaucoma Associated Symptoms.ChemMedChem · 2024Article
- Evaluation of Pregabalin bioadhesive multilayered microemulsion IOP-lowering eye drops.Journal of controlled release : official journal of the Controlled Release Society · 2024Article
- ANGPTL7 and Its Role in IOP and Glaucoma.Investigative ophthalmology & visual science · 2024Article
- Recreating the Trabecular Outflow Tissue on Implantable, Micropatterned, Ultrathin, Porous Polycaprolactone Scaffolds.Bioengineering (Basel, Switzerland) · 2023Article
- Recently Approved Drugs for Lowering and Controlling Intraocular Pressure to Reduce Vision Loss in Ocular Hypertensive and Glaucoma Patients.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Protocol for laser-induced chronic ocular hypertension and intracameral injection in nonhuman primates.STAR protocols · 2022Article
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: NCX 667, a novel nitric oxide (NO) donor with an isomannide core, was characterized for its IOP-lowering ability in animal models of ocular hypertension and glaucoma. Bioengineered human trabecular meshwork/Schlemm's canal (HTM/HSC) constructs were used to explore the mode of action. Methods: Ocular normotensive New Zealand white (NZW) rabbits (ONT-rabbits), spontaneously ocular hypertensive pigmented Dutch-belted rabbits (sOHT-rabbits), hypertonic saline (5%)-induced transient ocular hypertensive NZW rabbits (tOHT-rabbits), ocular normotensive Beagle dogs (ONT-dogs), and laser-induced ocular hypertensive cynomolgus monkeys (OHT-monkeys) were used. NCX 667 or vehicle (30 µL) was instilled in a crossover, masked fashion and intraocular pressure (IOP) measured before dosing (baseline) and for several hours thereafter. The ONT-rabbits were used for cyclic guanosine monophosphate (cGMP) determination in ocular tissues after ocular dosing with NCX 667. Transforming growth factor-beta2 (TGFβ2) (2.5 ng/mL, six days)-treated HTM/HSC constructs were used to address changes in outflow facility. Results: NCX 667 resulted in robust and dose-dependent IOP decrease in all models used. Maximal IOP-lowering efficacy at 1% was -4.1 ± 0.6, -12.2 ± 2.7, -10.5 ± 2.0, -5.3 ± 0.8, and -6.6 ± 1.9 mmHg, respectively, in ONT-dogs, sOHT-rabbits, tOHT-rabbits, ONT-rabbits, and OHT-monkeys. In ONT-rabbits NCX 667 (1%) increased cGMP in aqueous humor (AH) but not in retina and iris/ciliary body. NCX 667 concentration-dependently increased outflow facility in TGFβ2-treated HTM/HSC constructs (outflow facility, 0.10 ± 0.06 and 0.30 ± 0.10 µL/min/mmHg/mm2, respectively, in vehicle- and NCX 667-treated constructs). Conclusions: NCX 667 leads to robust IOP lowering in several animal models. Evidence in HTM/HSC constructs indicate that the IOP reduction likely results from NO-mediated increase of the conventional outflow pathway. Other mechanisms including changes in AH production and episcleral vein pressure may not be excluded at this time.
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