Reata Pharmaceuticals, Inc. focuses on developing medicines for difficult-to-treat diseases. The company develops drugs with potent transcription-regulating activity called antioxidant inflammation modulators, which are potent activators of the biological transcription factor Nrf2 that controls the body's production of antioxidative and cytoprotective molecules, as well as protects against diseases involving inflammation and oxidative stress. Its product pipeline comprises drugs under development for treating immuno-oncology and ophthalmology problems, cancer supportive care, cardiovascular problems, bioenergetic diseases, and autoimmune and respiratory problems. Reata Pharmaceuticals, Inc. ...
2801 Gateway Drive
Irving, TX 75063
Founded in 2002
Reata Pharmaceuticals, Inc. Receives Clearance from the Division of Neurology Products of the FDA to Begin Two New Phase 2 Clinical Programs
Sep 30 14
Reata Pharmaceuticals, Inc. has received clearance from the Division of Neurology Products of the FDA to begin two new Phase 2 clinical programs in patients with Friedreich's Ataxia and Mitochondrial Myopathies. Both of these orphan diseases are associated with reduced energy production, fatigue, and impaired exercise capacity. There are no existing therapies specifically approved to treat patients with these diseases. Friedreich's ataxia is an inherited disorder caused by defects in the gene for frataxin, a protein that regulates iron levels in the mitochondria. Defects in frataxin result in mitochondrial iron overload, causing impaired metabolism, oxidative stress, and damage to mitochondrial DNA. Patients with FA suffer progressive degeneration of the central and peripheral nervous systems, impaired coordination and gait, and fatigue from energy deprivation and muscle loss. Mitochondrial Myopathies are a collection of individual orphan diseases that are associated with mitochondrial DNA mutations. These defects cause respiratory chain deficits and impaired energy production. Most of these patients share a similar phenotype characterized by skeletal muscle weakness and fatigue. These patients also may have other symptoms due to impaired energy production in other organ systems. RTA 408 works by inducing Nrf2, which regulates multiple genes that play both direct and indirect roles in the production of cellular energy within the mitochondria. Directly, activation of the Nrf2 pathway increases the efficient use of fuel (fatty acids and glucose) by mitochondria and increases mitochondrial biogenesis and basal oxygen consumption. Indirectly, activation of Nrf2, through its antioxidative effects, balances reducing equivalents and maintains mitochondrial homeostasis and efficiency. In addition to its positive effects on metabolic efficiency, Nrf2 activation has been shown in preclinical studies to promote muscle repair and recovery and reduce markers of oxidative stress and muscle injury. The two initial Phase 2 trials will both be multi-center, double-blind, randomized, dose-ranging, placebo-controlled studies. The primary efficacy endpoint in both studies will be peak work as assessed during exercise testing. The studies will also explore changes in other measures of physical activity, fatigue, and biomarkers associated with mitochondrial functioning.
Reata Enrolls First Patient in the PRIMROSE Study, a Phase 2 Study Examining RTA 408 in Breast Cancer Patients at Risk for Radiation Dermatitis
Jul 25 14
Reata announced the enrollment of the first patient in a Phase 2 dose-ranging study examining the safety, tolerability, and efficacy of RTA 408 Lotion (3% and 0.5%) versus vehicle for the prevention and treatment of radiation dermatitis in breast cancer patients for whom radiation therapy (RT) is recommended. PRIMROSE (A Randomized Double-Blind, Vehicle-Controlled, Parallel-Group Phase 2 Study of the Efficacy Safety, Pharmacokinetics, and Pharmacodynamics of RTA 408 Lotion in the Treatment of Patients at Risk for Radiation Dermatitis) is a multi-center study in approximately 180 patients. The primary efficacy endpoint is the time-averaged effect on radiation dermatitis severity. Radiation dermatitis is a complication experienced by a majority of patients receiving radiation therapy for cancer. RT can damage the cellular structures in the skin and cause pain, ulceration, necrosis, and fibrosis of exposed skin tissues. Radiation dermatitis usually manifests within one to four weeks after initiation of RT and can result in delays in or failure to complete RT, limiting the dose effect of RT, which can negatively affect treatment outcomes. There are currently no approved agents for the prevention of radiation-induced dermatitis.