Reata’s lead pivotal programs are aimed at the development and commercialization of therapies for Alport syndrome (AS), Friedreich’s ataxia (FA), connective tissue disease-associated pulmonary arterial hypertension (CTD-PAH), and autosomal dominant polycystic kidney disease (ADPKD). Ongoing inflammation, mitochondrial dysfunction, and oxidative stress are implicated in these diverse, chronic diseases for which there are few or no approved therapies.

Mitochondria play a critical role in balancing cellular energy production and the inflammatory response. Mitochondrial dysfunction occurs when cellular energy production is impaired in favor of production of proinflammatory reactive oxygen species (ROS). Therefore, mitochondrial dysfunction can lead to tissue fibrosis, organ remodeling, or other organ damage.

Alport Syndrome (AS)

  • Reata is conducting the pivotal, registrational, phase 2/3 CARDINAL study to evaluate the efficacy and safety of bardoxolone methyl in individuals with CKD caused by Alport syndrome. The CARDINAL trial is fully enrolled
  • Reata received orphan drug designation from the FDA and EU for bardoxolone methyl for the treatment of AS

Friedreich’s Ataxia (FA)

  • Reata is conducting the pivotal, registrational, MOXIe trial of omaveloxolone for the treatment of FA. The MOXIe trial is fully enrolled
  • Reata received orphan drug designation from the FDA and EU for omaveloxolone in the treatment of FA

Connective Tissue Disease-Associated Pulmonary Arterial Hypertension (CTD-PAH)

  • In October 2016, Reata began enrolling patients in the phase 3 CATALYST trial in CTD-PAH. CATALYST is an international, randomized, double-blind, placebo-controlled trial examining the safety, tolerability, and efficacy of bardoxolone methyl when added to standard therapy in patients with WHO Group I CTD-PAH
  • Reata received orphan drug designation from the FDA for bardoxolone methyl for the treatment of CTD-PAH

Autosomal Dominant Polycystic Kidney Disease (ADPKD) (coming soon)

References
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  2. Tecklenborg J, Clayton D, Siebert S, Coley SM. The role of the immune system in kidney disease. Clin Exp Immunol. 2018;192(2):142-150.
  3. Daenen K, Andries A, Mekahli D, Van Schepdael A, Jouret F, Bammens B. Oxidative stress in chronic kidney disease [published online August 13, 2018]. Pediatr Nephrol. doi:10.1007/s00467-018-4005-4.
  4. Flemming NB, Gallo LA, Forbes JM. Mitochondrial dysfunction and signaling in diabetic kidney disease: oxidative stress and beyond. Semin Nephrol. 2018;38(2):101-110.
  5. Bello-Klein A, Mancardi D, Araujo AS, Schenkel PC, Turck P, de Lima Seolin BG. Role of redox homeostasis and inflammation in the pathogenesis of pulmonary arterial hypertension. Curr Med Chem. 2018;25(11):1340-1351.
  6. Scott TE, Kemp-Harper BK, Hobbs AJ. Inflammasomes: a novel therapeutic target in pulmonary hypertension [published online May 30, 2018] Br J Pharmacol. doi:10.1111/bph.14375.
  7. Paupe V, Dassa EP, Goncalves S, et al. Impaired nuclear Nrf2 translocation undermines the oxidative stress response in Friedreich ataxia. PLoS One. 2009;4(1):e4253.
View References