FTO

SYDNEY, July 10, 2023 /PRNewswire/ -- Race Oncology Limited ("Race") is pleased to announce execution of an exclusive licence agreement ("Agreement") to access U.S. cancer research and treatment organisation City of Hope's intellectual property ("IP) which highlights bisantrene as a potent inhibitor of the human fat mass and obesity-associated protein, or FTO. City of Hope, one of the largest cancer research and treatment centres in the United States and a leading research centre for diabetes and other life-threatening illnesses, encourages the use of its inventions, discoveries and intellectual property for the benefit of the public. These rights granted under the Agreement include the exclusive license of IP potentially arising from a patent application (PCT Application No. PCT/US2020/043294) ("Patent Application") as filed by City of Hope and know-how relating to data included in the Patent Application ("Know-How"). The Agreement ensures Race's exclusive access to that IP, which the Company believes will construct a transparent path for collaborative research and the downstream commercialisation of FTO inhibitory applications. A summary of the material terms of the Agreement can be found on page 3 of the ASX Announcement here. CEO and Managing Director, Damian Clarke-Bruce commented: "In 2020, City of Hope published research highlighting bisantrene as a potent inhibitor of FTO. This exclusive worldwide agreement secures access for Race to important IP associated with that work and opens exciting opportunities for us to collaborate closely with Professor Jianjun Chen and his research group. With the agreement in place, collaborative discussions regarding Race-sponsored research are now easier to facilitate. Moreover, this agreement secures a clear path for Race's FTO research agenda. We are excited about further validating this targeted application for bisantrene through preclinical and clinical studies and anticipate that FTO inhibition may offer a high-impact, personalised medicine solution for cancer patients." SOURCE Race Oncology

Scientists have discovered an unknown contributor to harmful blood vessel growth in the eye that could lead to new treatments for blinding macular degeneration and other common causes of vision loss. UVA Health scientists have discovered an unknown contributor to harmful blood vessel growth in the eye that could lead to new treatments for blinding macular degeneration and other common causes of vision loss. UVA's Jayakrishna Ambati, MD, and Shao-bin Wang, PhD, and their colleagues have identified a new target to prevent the formation of abnormal tangles of blood vessels associated with eye conditions such as neovascular age-related macular degeneration, proliferative diabetic retinopathy and ischemic retinal vein occlusion. "Our study has opened up the possibility of mitigating aberrant blood vessel growth in eye diseases by targeting the epigenetic machinery," said Ambati, the founding director of UVA's Center for Advanced Vision Science and a member of the University of Virginia School of Medicine's Department of Ophthalmology. "Through local targeting of the epigenetic regulator, we have gained a deeper understanding of how ocular immune cells can cause a loss of control over blood vessel growth under the retina. This approach also offers a new direction for the development of more effective, cost-efficient and accessible interventions, thereby avoiding issues such as drug resistance, which is a growing concern with conventional anti-VEGF therapies used in clinical treatments." Understanding Vision Loss Scientists have known that abnormal vessel overgrowth in the eye is fueled by excessive amounts of a substance called "vascular endothelial growth factor-A," or VEGF, that plays an important role in blood vessel formation. There are now treatments available that target VEGF to prevent vessel overgrowth, and they often provide dramatic benefits at first. Unfortunately, these benefits can fade with time. That leaves doctors in need of better treatments to help preserve patients' eyesight. Ambati and Wang's new research identifies a key protein that determines VEGF levels. Blocking this protein in lab mice reduced their VEGF levels significantly, and it did so in a targeted way, without unwanted side effects. The scientists noted, for example, that they observed no toxic effects on the retina, the light-sensing portion of the eye where the vessel overgrowth occurs. "This fat mass and obesity-associated (FTO) protein was previously shown to be correlated with obesity in humans. Unexpectedly, we found it also play important roles in regulating ocular neovascularization through an epigenetic mechanism," Ambati said. "This exciting discovery finally answers a longstanding question about how ocular immune cells, such as macrophages, contribute to abnormal blood vessel growth under the retina. This question was first investigated by our team 20 years ago, and we're thrilled to have found an answer." In addition to identifying a promising target for the development of new treatments for vision loss, the discovery sheds important light on the fundamental mechanisms responsible for the blood vessel overgrowth that robs millions of people of their sight. Neurovascular age-related macular degeneration alone affects more than 200 million people worldwide. While much more research and testing will be needed before the new finding could be translated into a treatment, the UVA scientists are excited about the potential of the discovery. "Current strategies for treating ocular neovascular disorders, which primarily focus on regulating the protein levels of VEGF, are not perfect. Therefore, it is imperative to identify more targetable candidates to develop alternative therapies," Wang said. "We are hopeful that our study will pave the way for the development of new treatments, ultimately reducing the burden of neovascular-related illnesses."