Nicox Selects Development Candidate in a New Class of NO-mediated Intraocular Pressure (IOP) Lowering Agents
Press Release | ||
Nicox Selects Development Candidate in a New Class of NO-mediated Intraocular Pressure (IOP) Lowering Agents | ||
Sophia Antipolis, France |
Nicox SA (Euronext Paris: FR0013018124, COX), an international ophthalmology company, today announced that it has selected a new development candidate, NCX 1728, from its proprietary
research program focused on nitric oxide (NO)-mediated IOP lowering agents. An analog of this molecule has demonstrated1 positive results in ocular hypertensive non-human primates
compared to travoprost 0.1%, a prostaglandin analog. Prostaglandin analogs are the standard of care for IOP lowering therapies.
Nicox owns all exclusive worldwide rights to NCX 1728. Further optimization of the ophthalmic formulations of NCX 1728 will continue prior to initiating formal pre-Investigational New Drug (IND) tests required for the filing of an IND application.
Michele Garufi, Chairman and Chief Executive Officer of Nicox commented “We are very proud to announce the selection of this new drug candidate, NCX 1728, which becomes our third in-house development program. NCX 1728 is the first in a new class of molecules combining the clinically proven effects of nitric oxide with phosphodiesterase-5 inhibition, which has been shown to enhance the efficacy and the duration of nitric oxide-mediated effects.”
NCX 1728 was invented in Nicox’s Bresso (Milan, Italy) Research Laboratories using the Company’s proprietary NO-donating research platform, which has enabled the development of a leading scientific and strategic position in the therapeutic application of NO-donating compounds.
NO-mediated IOP lowering agents
It has been established that NO plays a key role in the regulation of IOP and can be linked with other pharmaceutical agents, as is the case with our lead clinical development candidate NCX 470, a second generation NO-donating prostaglandin analog, and the first generation product, VYZULTA (latanoprostene bunod ophthalmic solution), 0.024%. VYZULTA is exclusively licensed worldwide to our partner Bausch + Lomb, who is commercializing it in the U.S. and Canada. The effect of NO on IOP lowering may be further increased or prolonged by phosphodiesterase-5 (PDE5) inhibitors, which inhibit the degradation of cyclic guanosine monophosphate (cGMP), a key intracellular messenger that is produced as a result of stimulation by NO.
Nicox owns all exclusive worldwide rights to NCX 1728. Further optimization of the ophthalmic formulations of NCX 1728 will continue prior to initiating formal pre-Investigational New Drug (IND) tests required for the filing of an IND application.
Michele Garufi, Chairman and Chief Executive Officer of Nicox commented “We are very proud to announce the selection of this new drug candidate, NCX 1728, which becomes our third in-house development program. NCX 1728 is the first in a new class of molecules combining the clinically proven effects of nitric oxide with phosphodiesterase-5 inhibition, which has been shown to enhance the efficacy and the duration of nitric oxide-mediated effects.”
NCX 1728 was invented in Nicox’s Bresso (Milan, Italy) Research Laboratories using the Company’s proprietary NO-donating research platform, which has enabled the development of a leading scientific and strategic position in the therapeutic application of NO-donating compounds.
NO-mediated IOP lowering agents
It has been established that NO plays a key role in the regulation of IOP and can be linked with other pharmaceutical agents, as is the case with our lead clinical development candidate NCX 470, a second generation NO-donating prostaglandin analog, and the first generation product, VYZULTA (latanoprostene bunod ophthalmic solution), 0.024%. VYZULTA is exclusively licensed worldwide to our partner Bausch + Lomb, who is commercializing it in the U.S. and Canada. The effect of NO on IOP lowering may be further increased or prolonged by phosphodiesterase-5 (PDE5) inhibitors, which inhibit the degradation of cyclic guanosine monophosphate (cGMP), a key intracellular messenger that is produced as a result of stimulation by NO.
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