Initial Results from a Phase 2 Trial of the Safety and Efficacy of Bardoxolone Methyl in Patients with Autosomal Dominant Polycystic Kidney Disease and IgA Nephropathy Common pathway of inflammation links diverse etiologies of chronic kidney diseases Chronic kidney diseases (CKD) develop due to multiple pathogenic processes that cause injury to cells, disruption of structure, and reduction in function, eventually leading to end-stage renal disease (ESRD)1-3 Despite diverse etiologies, CKDs share a common pathway for tissue damage via prolonged inflammation and oxidative stress, resulting in mesangial expansion, endothelial dysfunction, glomerulosclerosis, reduction in effective glomerular filtration surface area, tubular atrophy, and interstitial fibrosis1-3 Bardoxolone methyl (BARD) and close analogs improve kidney function and reduce fibrosis in multiple preclinical models Through induction of Nrf2 and suppression of NF-κB, BARD targets pro-inflammatory and fibrotic pathways that contribute to GFR loss in CKD4 BARD and close structural analogs improve kidney function and reduce remodeling and fibrosis in multiple models of CKD and AKI Markers of inflammation (eg, MCP-1) are higher in the WT 9-7 and WT 9-12 human ADPKD renal cyst cell lines than in the HK-2 normal human proximal tubule cell line and BARD increases Nrf2 activity (NQO1) and suppresses MCP-1 in ADPKD renal cyst cell lines (* P < 0.05; *** P < 0.001) BARD increases measured GFR and eGFR in Phase 2 & 3 studies In TSUBAKI, BARD treatment increased inulin clearance compared to placebo5 In the BEAM and BEACON trials, BARD treatment increased eGFR compared to placebo in patients with type 2 diabetes and CKD6,7 In initial data from Phase 2 open-label study CARDINAL, BARD significantly increased eGFR in patients with Alport syndrome through 36 weeks of treatment8,9 Increases in eGFR with BARD in patients with pulmonary arterial hypertension (PAH) in the LARIAT trial are durable for up to two years of treatment In BEAM and BEACON, eGFR change at 12 weeks significantly correlated with change at one year BARD may target the common pathways contributing to GFR loss in multiple forms of CKD Bardoxolone methyl was generally well-tolerated and significantly increased eGFR in patients with ADPKD and IgA nephropathy No treatment-related serious adverse events have been reported to date Bardoxolone methyl is currently being evaluated in other forms of chronic kidney disease PEP, GBA and GAB are consultants to Reata Pharmaceuticals AA, AR, GBA, LAI, DVR and ALS receive research funding from Reata Pharmaceuticals MC, AG and CJM are employees of Reata Pharmaceuticals BACKGROUND and Preclinical rationale BARDoxolone methyl – CLINICAL TRIALS EFFICACY: Change From Baseline in eGFR CONCLUSIONS DISCLOSURES REFERENCES BEAM (n=227) BEACON (n=2185) Presented at the European Renal Association – European Dialysis and Transplant Association May 25, 2018; Copenhagen, Denmark. Lopez-Hernandez and Lopez-Novoa. Cell Tissue Res. 2012, 347(1): 141-54. Fogo and Kon. Int J Biochem Cell Biol. 2010 42(9): 1388-97. Yamaguchi et al. F1000Res. 2015 4:1212. Ruiz et al. Kidney Int. 2013, 83:1029-1041. Nangaku et al., ASN Presentation, 2017. Pergola et al. N Engl J Med. 2011, 365(4):327-36. De Zeeuw et al. N Engl J Med. 2013, 369(26):2492-503. Block et al. J Am Soc Neph. 2017, 28: B3 (ASN Abstract). Press Release: http://investors.reatapharma.com/phoenix.zhtml?c=254306&p=irol-newsArticle&ID=2342167 FP806 Characteristic ADPKD (N=31) IgAN (N=26) Age, years (mean, SD) 47.4 ± 9.5 48.5 ± 9.5 Female (n,%) 21 (68%) 11 (42%) White/Caucasian (n,%) 25 (81%) 22 (85%) Baseline eGFR, mL/min/1.73 m2 (mean, SD) 47.7 ± 13.6 46.2 ± 12.6 Baseline ACR, mg/g (geometric mean) 44.4 104.0 Receiving ACEi or ARB (n,%) 25 (81%) 25 (96%) UACR Treatment with BARD leads to time-dependent increases in eGFR in patients with ADPKD and IgAN Vital Signs and BNP No significant changes in blood pressure No significant change from baseline in BNP Adverse Events No treatment-related serious adverse events to date No discontinuations to date AEs to date have generally been mild to moderate in intensity Most commonly reported AE is muscle spasms, which are associated with CK reductions SAFETY: Blood Pressure, BNP, and adverse events The PHOENIX Phase 2 trial (NCT03366337) was initiated to test the hypothesis that BARD will improve kidney function in patients with CKD due to ADPKD, IgA Nephropathy, Type 1 Diabetes, or FSGS Multicenter, open-label study, which is targeting enrollment of 25 patients per cohort Each cohort is enrolling and will be analyzed separately Patients receive once-daily, oral dosing of BARD for 12 weeks titrated from 5 mg to 20 or 30 mg goal dose Primary endpoint: change from baseline in eGFR at Week 12 BNP Diastolic BP Systolic BP DEMOGRAPHIC AND BASELINE DATA FROM PHOENIX CARDINAL (n=30) LARIAT (n=56) Baseline eGFR Change from Baseline in eGFR* WK1 WK4 WK8 WK12 ADPKD N 31 31 31 15 8 Mean ± SE 47.7 ± 2.4 3.5 ± 1.2 6.6 ± 0.9 9.3 ± 1.4 12.0 ± 1.4 p-value p<0.01 p<0.0001 p<0.0001 p<0.0001 IgAN N 26 24 16 9 - Mean ± SE 46.2 ± 2.5 4.0 ± 1.0 8.3 ± 1.1 8.4 ± 1.4 - p-value p<0.001 p<0.0001 p<0.0001 - UACR unchanged in ADPKD cohort, which generally enrolled patients with lower levels of albuminuria UACR increased in IgAN cohort, which enrolled patients with established proteinuria ULN Pablo E. Pergola, MD, PhD; Gerald B. Appel, MD; Ahmed Awad, MD; Geoffrey A. Block, MD; Melanie Chin, PhD; Angie Goldsberry, MS; Lesley A. Inker, MD; Colin J. Meyer, MD; Anjay Rastogi, MD, PhD; Dana V. Rizk, MD; Arnold L. Silva, MD, PhD BARD’s Renal Effects Characterized in Multiple Models Ang II-Induced GFR Decline; Ding, Kidney Int (2013) CKD-Induced Endothelial Dysfunction; Aminzadeh, Redox Biol (2013) 5/6 Nephrectomy; Aminzadeh, Xenobiotica (2014) Hypertensive CKD; Hisamichi, Hypertens Res (2017) Hypertensive CKD; Cuevas, Hypertension (2015) Diabetic CKD; Huang, J Med Chem (2017) Diabetic CKD and Atherosclerosis; Tan, Diabetes (2014) High Fat Diet-Induced CKD; Camer, Chem Biol Interact (2016) Lupus Nephritis; Wu, Arthritis Rheumatol (2014) Protein Overload; Zoja, ASN (2010) Ischemic-Reperfusion; Kocak, Clin Exp Pharm Physiol (2016) Ischemic-Reperfusion; Wu, AJP Renal Physiol (2011) Acute Kidney Injury; Wu, Toxicology (2014) FeNTA-Induced Acute Kidney Injury; Tanaka, Tox Appl Pharm (2008) Cisplatin-Induced Acute Kidney Injury; Aleksunes, JPET (2010) Cohort Adverse Event (Preferred Term) N (%) ADPKD (n=31) Muscle spasms 12 (39%) Upper respiratory tract infection 3 (10%) IgAN (n=26) Muscle spasms 3 (12%) Headache 3 (12%) AEs occurring in > 2 patients *Available data with > 25% of patients reporting data as of 15 May 2018 BARD Suppresses Inflammation in Renal Cyst Cell Lines We would like to thank Megan O’Grady and Rex Tungala for their help with data analysis and Isaac Trevino and Linda Hannigan for their work on pre-clinical data studies. Acknowledgements Exhibit 99.2
