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10-Q – Quarterly report [Sections 13 or 15(d)]

G1 Therapeutics has filed a 10-Q – Quarterly report [Sections 13 or 15(d)] with the U.S. Securities and Exchange Commission .

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10-Q – Quarterly report [Sections 13 or 15(d)]

Lpath has filed a 10-Q – Quarterly report [Sections 13 or 15(d)] with the U.S. Securities and Exchange Commission .

10-Q – Quarterly report [Sections 13 or 15(d)]

Vical has filed a 10-Q – Quarterly report [Sections 13 or 15(d)] with the U.S. Securities and Exchange Commission .

NEOMED Institute partners with McGill University to identify small molecule inhibitors of a novel oncology target: Cut-Like Homeobox 1 (CUX1)

On May 3, 2018 The NEOMED Institute reported that it has entered into a development collaboration with McGill University (Press release, NEOMED, MAY 3, 2018, View Source [SID1234527387]). Kemal Payza, Senior Project Director at NEOMED Institute will collaborate with Professor Alain Nepveu, Professor at the Goodman Cancer Research Centre and Departments of Oncology, Biochemistry and Medicine at McGill University, to discover new therapeutic small molecules to inhibit the protein target, Cut-Like Homeobox 1 (CUX1).

"I am delighted that we have added this new drug discovery project into NEOMED’s pipeline and I look forward to working with Dr. Nepveu on this very exciting target. Dr. Nepveu is a renowned expert on the DNA repair function of CUX1, a mechanism upon which RAS-driven cancer cells are acutely dependent for their survival. This is very important, because currently there is no treatment that targets RAS-driven tumours," explains Payza.

"This academic/industrial collaboration that we have entered into with the NEOMED Institute will permit us to rapidly leverage our biological understanding of this important target to develop small molecule drug candidates. A drug capable of interfering with the ability of CUX1 to participate in DNA repair would target many types of cancers in which reactive oxygen species are produced as a consequence of mutation in a RAS gene or any oncogene that activates the RAS pathway; such activation is seen in 59% of pancreatic cancers and some 30% of human cancers overall," adds Professor Nepveu.

"This collaboration exemplifies, once again, the ability of NEOMED to deliver on its mission to help advance academic innovation and excellence by leveraging our industrial drug development experience and expertise. We look forward to collaborating with world-leading experts, like Professor Nepveu and Zubaidah Ramdzan, to translate their science into therapeutic options for patients within the Canadian ecosystem," concludes Donald Olds, President & CEO of NEOMED Institute.

About CUX1
Activation of the RAS pathway in cancer cells leads to higher production of reactive oxygen species, which cause DNA damage by oxidation. In turn, sustained DNA damage triggers cellular senescence. Cancer cells can adapt to such oxidative DNA damage by increasing their expression of CUX1, which stimulates the activities of two enzymes that repair oxidized bases in DNA. Knocking down the CUX1 protein has been found to kill all cancer cells that have high levels of reactive oxygen species (ROS). Thus, small molecules that inhibit the ability of CUX1 to stimulate those critical DNA repair enzymes would be expected to provide therapeutic benefit to patients with RAS-driven cancers. While therapeutic approaches targeting various aspects of the DNA damage response are strategically important in cancer, direct inhibition of base excision repair enzymes can cause severe adverse effects on normal cells. In contrast, CUX1 is not essential to normal cells, but is absolutely required for survival in situations of severe genotoxic stress such as that caused by reactive oxygen species in RAS-driven cancer cells or by DNA-damaging cancer treatments. Thus, small molecules that inhibit the ability of CUX1 to stimulate base excision repair enzymes are expected to treat RAS-driven cancers with an improved therapeutic window.

Nicox announces the presentation of scientific data for NCX 667 at ARVO 2018

On May 3, 2018 Nicox SA (Euronext Paris: FR0013018124, COX), an international ophthalmology company, reported a poster presentation highlighting scientific data for NCX 667, a novel nitric oxide (NO) donating compound, at the Association for Research in Vision and Ophthalmology (ARVO) 2018 Annual Meeting, one of the key scientific events in the ophthalmology calendar, being held on April 29 – May 3, 2018 in Honolulu, Hawaii, United States.

Synthesized and characterized by Nicox, NCX 667 is a lead molecule among the Company’s future generation of stand-alone NO-donors which are designed to optimize NO dosing and can be used alone or in combination with existing standard-of-care drugs, as either ophthalmic solutions or extended release formulations, to enable robust intraocular pressure (IOP)-lowering in patients with open-angle glaucoma or ocular hypertension.

The ARVO 2018 abstract by Francesco Impagnatiello, Ph.D., et al. describes results following single dose administration of various doses (0.1%, 0.3% and 1.0% solution) of NCX 667 in several ocular normotensive and ocular hypertensive animal models. These results demonstrate that NCX 667 lowers IOP in a dose-dependent manner. Furthermore, an in vitro bioengineered human trabecular meshwork/Schlemm’s canal (TM/SC) system was used to study the effects of NCX 667 on the conventional outflow facility. These data support the hypothesis that the IOP-lowering effects of NCX 667 are likely due to an increase in outflow facility via the TM/SC outflow pathway.

Michael Bergamini, Ph.D., Executive Vice President, Chief Scientific Officer of Nicox, commented: "The results presented at ARVO this year show a clear, dose-dependent, and meaningful lowering of IOP in both ocular normotensive and hypertensive models. These results, combined with the in vitro data, continue to build upon the growing body of scientific evidence supporting the development of NCX 667, a lead molecule among our future generation of stand-alone NO-donors. We are continuing to generate new compounds in this class and are testing multiple leads using topical and sustained release dosing."

An estimated 3.5% of the worldwide population between 40 and 80 years of age are affected by the most common forms of glaucoma1.

The ARVO 2018 abstracts have been published in the meeting website located at View Source and details for the poster presentation are as follows:

Title: NCX 667, a novel nitric oxide (NO) donor lowers intraocular pressure (IOP) via stimulation of trabecular meshwork/Schlemm’s canal outflow facility

Date and time: Wednesday, May 2, 2018 from 11:15 am to 1:00 pm HAST

Presenter: Francesco Impagnatiello, Ph.D. , Nicox Research Institute

Session n° 448, Title: Glaucoma – Trabecular Meshwork

Abstract n°: 4707 / Poster n°: B0131

Location: Hawaii Convention Center, Exhibit Hall