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    Novel glaucoma drugs close at hand

    Agents act on prostaglandin receptors; some combine this with other mechanisms of action

     

    At least seven new glaucoma drugs were in clinical trials and two others were approved by the FDA in 2017, according to Gary D. Novack, PhD.

    Many drugs that have progressed the most act on prostaglandin receptors, though some combine this with other mechanisms of action, explained Dr. Novack, professor of pharmacology, University of California, Davis. He highlighted the status of several glaucoma drug developments (as of May 2017) during the most recent meeting of the American Academy of Ophthalmology.

    Dr. Novack began his search on www.clinicaltrials.gov, looking under glaucoma as an indication and excluding devices and adjuncts. He then looked at all drugs in clinical trial phases I, II, or III submitted between Jan. 1, 2010 and May 31, 2017.

    He found 341 trials, and restricted these to “open” status, leaving him with 53 trials, and winnowed these down by using the criterion “new.” He also looked at applications for glaucoma drugs that were before the FDA as either new drug application (NDA) or biological licensing application (BLA).

     

    Newly approved

    The newly approved drugs are latanoprostene bunod ophthalmic solution 0.024% (Vyzulta, Bausch + Lomb and Nicox) and netarsudil ophthalmic solution 0.02% (Rhopressa, Aerie Pharmaceuticals).

    Latanoprostene bunod won approval from the FDA on Nov. 2. It is metabolized in the eye to latanoprost acid and butanediol mononitrate.

    An F2-alpha prostaglandin analog, latanoprost acid increases outflow of aqueous fluid primarily through the uveoscleral pathway. Butanediol mononitrate releases nitric oxide, which is reported to induce relaxation of cells in the trabecular meshwork and Schlemm’s
    canal, increasing outflow through them.

    Netarsudil won approval Dec. 18, 2017. According to Aerie, the drug inhibits both Rho-kinase (ROCK) and noreprinephrine transporters (NET). Inhibiting ROCK relaxes the trabecular meshwork cells, while inhibiting NET reduces production of aqueous fluid.

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