Data from three clinical studies of bardoxolone methyl have demonstrated that the drug is:
Producing a significant increase in estimated glomerular filtration rate (eGFR), which is consistent in magnitude and in the high degree of patient response.
Improving CKD stage (ie: from Stage 4 to Stage 3) in the majority of patients.
Targeting Nrf2 pathway and supporting an anti-inflammatory mechanism.[13]
About Chronic Kidney Disease
Chronic Kidney Disease (CKD) is a common complication of diabetes and hypertension that affects over 26 million Americans.[14] It is a progressive condition that ultimately leads to End Stage Renal Disease (ESRD) and the need for dialysis or transplant, and is associated with dramatic increase in the risk of cardiovascular disease.[15] Current standard of care can slow the progression of the disease,[16] but no treatments are currently available to stop it. Due to the high prevalence of the condition, and absence of disease modifying therapy, CKD represents an area of significant unmet medical need.
Pipeline
Reata is developing a series of other Antioxidant Inflammation Modulators (AIMs) with activity against a variety of intractable diseases. These unique drugs help to restore the balance between pro-oxidant and antioxidant signaling molecules within the cell by mimicking the body's own natural regulators of inflammation.[17][18] By increasing the production of enzymes that maintain the antioxidant buffering system within the cell, they prevent harmful inflammation and the associated oxidative stress and organ/DNA damage caused by high concentrations of oxygen and nitrogen radicals. Also, by activating enzymes that maintain the antioxidant buffering system, they increase the body's ability to protect against tissue damage from toxic insults, chronic health problems, and aging.
Partnerships
January 7, 2010 - Reata announced that they entered into a licensing agreement with Kyowa Hakko Kirin Co., Ltd. The agreement provided Kyowa Hakko Kirin with the exclusive rights to develop and commercialize bardoxolone methyl for CKD and related indications in Japan, China, Taiwan, Korea, and other select Southeast Asian countries. In return, Reata is eligible to receive up to $272 million in up-front fees and milestone payments, in addition to escalating double-digit royalties from sales in the licensed territories.[19][20][21]
September 23, 2010 - Abbott and Reata announced that they entered into a collaboration agreement to develop and commercialize bardoxolone methyl. Under the agreement, Reata granted Abbott exclusive rights to develop and commercialize bardoxolone methyl outside the U.S., excluding Asian markets outlined in the January 7th agreement with Kyowa Hakko Kirin. In exchange, Reata received upfront and near-term cash payments of $450 million for the licensing rights and a minority equity stake in the company. Additionally, Reata will receive milestone payments upon completion of certain development and approval objectives for bardoxolone in the licensed territories.[22][23][24]
References
^Cachofeiro, Victoria; Goicochea, Marian; De Vinuesa, Soledad García; Oubiña, Pilar; Lahera, Vicente; Luño, José (2008). "Oxidative stress and inflammation, a link between chronic kidney disease and cardiovascular disease". Kidney International. 74: S4–9. doi:10.1038/ki.2008.516.
^Sela, S.; Shurtz-Swirski, R; Cohen-Mazor, M; Mazor, R; Chezar, J; Shapiro, G; Hassan, K; Shkolnik, G; Geron, R (2005). "Primed Peripheral Polymorphonuclear Leukocyte: A Culprit Underlying Chronic Low-Grade Inflammation and Systemic Oxidative Stress in Chronic Kidney Disease". Journal of the American Society of Nephrology. 16 (8): 2431–8. doi:10.1681/ASN.2004110929. PMID15987755.
^Vaziri, Nosratola D (2004). "Roles of oxidative stress and antioxidant therapy in chronic kidney disease and hypertension". Current Opinion in Nephrology and Hypertension. 13 (1): 93–9. doi:10.1097/00041552-200401000-00013. PMID15090865.
^Dhalla, Naranjan; Temsah, Rana; Netticadan, Thomas (2000). "Role of oxidative stress in cardiovascular diseases". Journal of Hypertension. 18 (6): 655–73. doi:10.1097/00004872-200018060-00002. PMID10872549.
^Madamanchi, N. R. (2004). "Oxidative Stress and Vascular Disease". Arteriosclerosis, Thrombosis, and Vascular Biology. doi:10.1161/01.ATV.0000150649.39934.13.
^Offen, Daniel; Gilgun-Sherki, Yossi; Melamed, Eldad (2004). "The role of oxidative stress in the pathogenesis of multiple sclerosis: the need for effective antioxidant therapy". Journal of Neurology. 251 (3): 261–8. doi:10.1007/s00415-004-0348-9. PMID15015004.
^Syburra, C; Passi, S (1999). "Oxidative stress in patients with multiple sclerosis". Ukrainskii biokhimicheskii zhurnal. 71 (3): 112–5. PMID10609336.
^Simpson, Ericka P.; Yen, Albert A.; Appel, Stanley H. (2003). "Oxidative Stress: a common denominator in the pathogenesis of amyotrophic lateral sclerosis". Current Opinion in Rheumatology. 15 (6): 730–6. doi:10.1097/00002281-200311000-00008. PMID14569202.
^Ferrante, Robert J.; Browne, Susan E.; Shinobu, Leslie A.; Bowling, Allen C.; Baik, M. Jay; MacGarvey, Usha; Kowall, Neil W.; Brown, Robert H.; Beal, M. Flint (2002). "Evidence of Increased Oxidative Damage in Both Sporadic and Familial Amyotrophic Lateral Sclerosis". Journal of Neurochemistry. 69 (5): 2064–74. doi:10.1046/j.1471-4159.1997.69052064.x. PMID9349552.
