Exhibit 99.1

bardoxolone methyl improveD kidney function in patients with autosomal dominant polycystic kidney disease and iga nephropathy in the ongoing phase 2 phoenix Study

interim data DEMONSTRATE significant improvement in kidney function in both diseases

Conference Call with management scheduled today, May 25, 2018 at 8:00am ET

IRVING, Texas, May 25, 2018 – Reata Pharmaceuticals, Inc. (NASDAQ:RETA), a clinical-stage biopharmaceutical company, today announced that positive interim data from the autosomal dominant polycystic kidney disease (ADPKD) and IgA nephropathy cohorts of the ongoing, open-label, Phase 2 PHOENIX trial are being presented by Pablo E. Pergola, M.D., Ph.D., Research Director, Renal Associates, PA, San Antonio, at the European Renal Association and European Dialysis and Transplant Association (ERA-EDTA) meeting in Copenhagen.

The ADPKD cohort of PHOENIX enrolled 31 patients, and available data demonstrate that bardoxolone methyl (bardoxolone) significantly improved kidney function in ADPKD patients as measured by their estimated glomerular filtration rate (eGFR).  Bardoxolone-treated patients showed a mean improvement of 6.6 mL/min/1.73 m ² at Week 4 (n=31; p<0.0001), increasing to 12.0 mL/min/1.73 m ² at Week 12 (n=8; p<0.0001) from a mean baseline eGFR of 47.7 mL/min/1.73 m ² .  The IgA nephropathy cohort enrolled 26 patients, and data were reported through Week 8.  Bardoxolone-treated patients showed a mean improvement of 8.4 mL/min/1.73 m ² at Week 8 (n=9; p<0.0001) from a mean baseline eGFR of 46.2 mL/min/1.73 m ² .  No drug-related serious adverse events have been reported, and reported adverse events have generally been mild to moderate in intensity.  Full data for the primary endpoint of change in eGFR at Week 12 for the ADPKD, IgA nephropathy, and type 1 diabetic chronic kidney disease (CKD) cohorts of PHOENIX will be available in the third quarter of 2018.

“Bardoxolone has now produced large improvements in kidney function in a high percentage of patients spanning 11 trials and five different forms of chronic kidney disease,” said Dr. Pergola.  “These observations suggest that bardoxolone is addressing pathogenic pathways of inflammation and fibrosis that contribute to the loss of kidney function in patients with chronic kidney disease.”

Additionally, Dr. Christoph Wanner, M.D., Chief of the Division of Nephrology and Hypertension at the University Hospital of Würzburg, Germany, gave an oral presentation at ERA-EDTA entitled “Bardoxolone Methyl Prevents eGFR Decline in Patients with Chronic Kidney Disease Stage 4 and Type 2 Diabetes ─ Post-hoc Analyses from BEACON.”  The analysis demonstrated that patients randomized to bardoxolone were more than 50 percent less likely than patients receiving placebo to experience events that predict kidney failure.  The authors of the abstract concluded that bardoxolone preserves kidney function and may delay the onset of kidney failure in patients with type 2 diabetes and stage 4 CKD.  The abstract was named a Ten Best Abstract by the Paper Selection Committee of ERA-EDTA.

“Bardoxolone’s improvements in kidney function in patients with ADPKD and IgA nephropathy are consistent with improvements observed in other forms of CKD, which have been durable and predictive of retained eGFR benefit after

withdrawal of drug in prior trials,” said Colin Meyer, M.D., Reata’s Chief Medical Officer.  “Additionally, selection of the BEACON outcomes analysis for oral presentation at one the world’s top nephr ology meetings, six years after BEACON concluded, reinforces the importance of the study’s results.  The durable increases in eGFR associated with a 50 percent reduction in outcomes inspire optimism for bardoxolone’s potential to delay or prevent dialysis in CKD.”

Reata management will host a call at 8:00 a.m. ET today to review these data and the development program for bardoxolone in chronic kidney disease.

About Autosomal Dominant Polycystic Kidney Disease

ADPKD is a genetic form of CKD caused by mutations in PKD1 and PKD2 genes leading to inflammation that stimulates the formation of fluid-filled cysts in the kidneys that cause pain and progressive loss of kidney function.  ADPKD is the leading inheritable cause of kidney failure with an estimated 116,000 diagnosed patients in the United States.

About IgA Nephropathy

IgA nephropathy, also known as Berger’s Disease, is a rare form of CKD that is characterized by deposits of IgA immune complexes in the glomeruli leading to persistent inflammation, oxidative stress, and loss of kidney function.  IgA nephropathy is one of the most prevalent primary chronic glomerular diseases with an estimated 120,000 patients in the United States.  There are currently no FDA-approved therapies for IgA nephropathy.

About the PHOENIX Study

The Phase 2 PHOENIX program is studying bardoxolone in patients with ADPKD, IgA nephropathy, focal segmental glomerulosclerosis, and CKD associated with type 1 diabetes.  Patients receive bardoxolone open-label, orally, once-daily for 12 weeks, and the primary efficacy endpoint is change from baseline in eGFR after 12 weeks of treatment.  Endpoints will be assessed for each cohort separately.

About Bardoxolone Methyl

Bardoxolone is an experimental, oral, once-daily activator of Nrf2, a transcription factor that induces molecular pathways that promote the resolution of inflammation by restoring mitochondrial function, reducing oxidative stress, and inhibiting pro-inflammatory signaling.  The FDA has granted orphan designation to bardoxolone for the treatment of Alport syndrome and for the treatment of connective tissue disease associated pulmonary arterial hypertension.

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About Reata Pharmaceuticals, Inc.

Reata is a clinical-stage biopharmaceutical company that develops novel therapeutics for patients with serious or life-threatening diseases by targeting molecular pathways involved in the regulation of cellular metabolism and inflammation.  Reata’s two most advanced clinical candidates, bardoxolone methyl and omaveloxolone, target the important transcription factor Nrf2 that promotes the resolution of inflammation by restoring mitochondrial function, reducing oxidative stress, and inhibiting pro-inflammatory signaling.

Forward-Looking Statements

This press release includes certain disclosures which contain “forward-looking statements,” including, without limitation, statements regarding the success, cost and timing of our product development activities and clinical trials, our plans to research, develop and commercialize our product candidates, and our ability to obtain and retain regulatory approval of our product candidates.  You can identify forward-looking statements because they contain words such as “believes,” “will,” “may,” “aims,” “plans,” and “expects.”  Forward-looking statements are based on Reata’s current expectations and assumptions.  Because forward-looking statements relate to the future, they are subject to inherent uncertainties, risks, and changes in circumstances that may differ materially from those contemplated by the forward-looking statements, which are neither statements of historical fact nor guarantees or assurances of future performance.  Important factors that could cause actual results to differ materially from those in the forward-looking statements include, but are not limited to (i) the timing, costs, conduct, and outcome of our clinical trials and future preclinical studies and clinical trials, including the timing of the initiation and availability of data from such trials; (ii) the timing and likelihood of regulatory filings and approvals for our product candidates; (iii) the potential market size and the size of the patient populations for our product candidates, if approved for commercial use, and the market opportunities for our product candidates; and (iv) other factors set forth in Reata’s filings with the U.S. Securities and Exchange Commission, including its Annual Report on Form 10-K, under the caption “Risk Factors.”  The forward-looking statements speak only as of the date made and, other than as required by law, we undertake no obligation to publicly update or revise any forward-looking statements, whether as a result of new information, future events, or otherwise.

Corporate:
Reata Pharmaceuticals, Inc.

(972) 865-2219

info@reatapharma.com

http://news.reatapharma.com

Investor:

Vinny Jindal

Vice President, Strategy

(855) 55-REATA

ir@reatapharma.com

Media:

Matt Middleman, M.D.

LifeSci Public Relations

(646) 627-8384

matt.middleman@lifescipublicrelations.com

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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

Management call to discuss interim phoenix data Exhibit 99.3

Forward-Looking Statements This presentation contains certain “forward-looking” statements that are made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. All statements, other than statements of historical or present facts, are forward-looking statements, including statements regarding our future financial condition, business strategy, and plans and objectives of management for future operations. In some cases, you can identify forward-looking statements by terminology such as “believe,” “will,” “may,” “estimate,” “continue,” “aim,” “assume,” “anticipate,” “contemplate,” “model,” “intend,” “target,” “project,” “should,” “plan,” “expect,” “predict,” “could,” “possible,” “seek,” “goal”, “potential,” “hypothesize,” “likely” or the negative of these terms or other similar terms or expressions that concern our expectations, strategy, plans, or intentions. These statements are based on our intentions, beliefs, projections, outlook, analyses, or current expectations using currently available information, are not guarantees of future performance, and involve certain risks and uncertainties. Although we believe that the expectations reflected in these forward-looking statements are reasonable, we cannot assure you that our expectations will prove to be correct. Therefore, actual outcomes and results could materially differ from what is expressed, implied, or forecast in these statements. Any differences could be caused by a number of factors including but not limited to: the success, cost, and timing of our product development activities and clinical trials; our ability to advance our NRF2 activators and other technologies; our ability to obtain and maintain regulatory approval of our product candidates, and limitations and warnings in the label of an approved product candidate; our ability to obtain funding for our operations, including funding necessary to complete further development and commercialization of our product candidates; our plans to research, develop, and commercialize our product candidates; the commercialization of our product candidates, if approved; the rate and degree of market acceptance of our product candidates; the size and growth potential of the markets for our product candidates, and our ability to identify target patient populations and serve those markets, especially for diseases with small patient populations; the success of competing therapies that are or may become available; our expectations regarding our ability to obtain and maintain intellectual property protection for our product candidates; the ability to license additional intellectual property relating to our product candidates and to comply with our existing license agreements; our ability to contract with third-party suppliers and manufacturers and their ability to perform adequately; our ability to attract collaborators with development, regulatory, and commercialization expertise; our ability to attract and retain key scientific or management personnel; our ability to grow our organization and increase the size of our facilities to meet our anticipated growth; the accuracy of our estimates regarding expenses, future revenue, capital requirements, and needs for additional financing; and regulatory developments in the United States and foreign countries. Additional factors that could cause actual results to differ materially from our expectations can be found in our Securities and Exchange Commission filings. Moreover, we operate in a very competitive and rapidly changing environment. New risk factors emerge from time to time, and it is not possible for our management to predict all risk factors, nor can we assess the effects of all factors on our business or the extent to which any factor, or combination of factors, may cause actual results to differ materially from those contained in, or implied by, any forward-looking statements. All forward-looking statements included in this presentation are expressly qualified in their entirety by these cautionary statements. The forward-looking statements speak only as of the date made and, other than as required by law, we undertake no obligation to publicly update or revise any forward-looking statements, whether as a result of new information, future events, or otherwise.

Bowman’s Capsule (Parietal Epithelium) Tubule Filtrate Urine Blood Blood Normalized Glomerular Basement Membrane Normalized Endothelial Layer Bardoxolone Improved Fenestrations More Filtrate Urine Bowman’s Capsule (Parietal Epithelium) Tubule Filtrate Blood Blood Thickened Glomerular Basement Membrane Dysfunctional Endothelial Layer Inflamed Reduced Fenestrations Less Filtrate Bardoxolone Consistently Improved Kidney Function Through Unique MOA 3 In 11 clinical trials, bardoxolone increased estimated GFR (eGFR) compared to placebo Bardoxolone increases GFR by reducing inflammatory signaling and restoring glomerular function as demonstrated in animal models eGFR increases verified as true improvement by “gold standard” inulin clearance method Kidney function improvements have been durable for up to two years and are partially retained following drug withdrawal Bardoxolone reduced the risk of kidney failure in diabetic CKD

CARDINAL Phase 2 Results Through Week 36 Large, significant increases in eGFR observed through Week 36 High patient retention rate with 90% of patients on study after 9 months No discontinuations due to bardoxolone-related adverse events Patients followed for 2 years, retained benefit analysis at week 52 will occur in 3Q18 eGFR Changes for All Patients Change From Baseline in eGFR Week 12 Week 36 N 30 27 Mean ± SE 13.4 ± 1.4 11.3 ± 1.6 95% CI (10.5, 16.3) (7.9, 14.6) p-value <0.000000001 <0.000001

Disease Baseline eGFR Interim eGFR Increase Time point Long-term eGFR Increase Time point BEAM T2D CKD 32 12 Week 12 11 1 year CARDINAL Alport 54 13 Week 12 11 9 months LARIAT PAH 77 11 Week 16 11 2 years Bardoxolone Previously Improved Kidney Function in Three Forms of CKD 5 Alport Syndrome Glomerular Defects FSGS Podocytopathies ADPKD Cyst Formation IgAN Activated IgA Diabetic CKD Hyperglycemia PAH Cardio-renal Syndrome Inflammation and Fibrosis Loss of Kidney Function (eGFR) ESRD Dialysis Transplant

PHOENIX Study Design Overview Design Open-label, multi-center Phase 2 Study Enrollment size Approximately 100 patients; 25-30 patients in each of 4 cohorts Treatment Titration from 5 mg up to 20 mg or 30 mg daily for 12 weeks Key Eligibility Criteria Inclusion Exclusion Age ≥ 18 – 65 years old ADPKD: PKD1 mutation by genetic testing IgAN: biopsy confirmation Baseline eGFR: 30 to 90 mL/min/1.73 m2 Significant cardiovascular history BNP > 200 ng/mL Endpoints eGFR change at week 12 Safety Screening Dose-Titration Period W2 W1 W8 ScrA D1 D3 T D10 T W3 T W4 Maintenance D31 T W5 T W6 W7 T BARD (5 mg) BARD (20 mg) W12 BARD (10 mg) Primary efficacy analysis O eGFR determination T Telephone Contact ScrB BARD (5 mg) BARD (20 mg) BARD (10 mg) BARD (30 mg) Baseline ACR ≤ 300 mg/g Baseline ACR > 300 mg/g Off Study Drug

PHOENIX Baseline Characteristics 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) 44.3 104.0 Receiving ACEi or ARB (n,%) 25 (81%) 25 (96%)

Bard Significantly Improved eGFR in ADPKD Patients BL eGFR Change from Baseline in eGFR WK1 WK4 WK8 WK12 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 95% CI (1.2 , 5.9) (4.8, 8.5 ) (6.5, 12.1 ) (9.2, 14.9 ) p-value - p=0.005 p<0.0001 p<0.0001 p<0.0001

Bard Significantly Improved eGFR in IgAN Patients BL eGFR Change from Baseline in eGFR WK1 WK4 WK8 N 26 24 16 9 Mean ± SE 46.2 ± 2.5 4.0 ± 1.0 8.3 ± 1.1 8.4 ± 1.4 95% CI (2.0 , 5.9) (6.1, 10.6 ) (5.7, 11.1 ) p-value - p=0.0001 p<0.0001 p<0.0001 Data not shown beyond Week 8 since <25% of final data are available

Summary of Albuminuria Data Urinary albumin excretion, measured as ACR, unchanged in ADPKD cohort because PKD patients have an intact filtration barrier Patients had normal to near-normal levels of albuminuria at baseline and after treatment Increases in eGFR not expected to increase ACR because healthy filtration barrier blocks it Upon study entry, ACR is abnormally high in IgA nephropathy cohort because protein filtration is impaired due to the disease process Patients had elevated albuminuria at baseline and after treatment Increases in GFR increase flow of protein through the impaired filtration barrier Log ACR/eGFR ratio is unchanged from baseline, demonstrating that increases in eGFR observed in the IgA nephropathy cohort are accounted for by increases in GFR ACR Log ACR/eGFR Ratio

Summary Blood Pressure and BNP Blood pressure and BNP stable and within normal limits upon study entry No significant changes from baseline during treatment No evidence of overt fluid retention BNP Diastolic BP Systolic BP

Summary of Safety No treatment-related serious adverse events to date AEs to date have been mild to moderate in intensity Most commonly reported AE is muscle spasms, which is associated with reductions in CK *AEs reported in >2 patients Preferred Term ADPKD (N=31) Muscle spasms 12 (39%) Upper respiratory tract infection 3 (10%) *AEs reported in >2 patients Preferred Term IgAN (N=26) Muscle spasms 3 (12%) Headache 3 (12%)

Increases in eGFR Translated to Reduced Risk of Kidney Failure Outcomes in BEACON Post-hoc analyses from the BEACON study in T2D CKD showed bardoxolone methyl significantly reduced likelihood of kidney failure outcomes Composite of adjudicated ESRD, 30% decline, or eGFR < 15: HR=0.48, p<0.001 Selected as a Top 10 Abstract at ERA-EDTA and presented by Christoph Wanner, one of the top European and global KOLs ESRD, ≥ 30% Decline or eGFR < 15 mL/min/1.73 m2 Number of Patients PBO 1097 1041 850 734 570 429 317 216 92 13 BARD 1088 991 823 687 538 390 304 185 91 11 HR: 0.48 p<0.0001

Future Development and Commercialization Large unmet medical need exists in ADPKD and IgA nephropathy In the U.S., ADPKD is the leading inheritable cause of CKD and the 4th leading cause of ESRD U.S. prevalence of ADPKD is approximately 400,000 people; 116,000 patients are diagnosed 50% of patients progress to ESRD; ADPKD is responsible for 5% of all ESRD IgA nephropathy is the most prevalent primary chronic glomerular disease worldwide U.S. prevalence of IgA nephropathy is approximately 120,000 people 50% of patients progress to ESRD; Leading cause of ESRD in young Caucasian adults Bardoxolone may substantially impact the cost burden of ADPKD and IgAN Bardoxolone significantly reduced the likelihood of kidney failure outcomes in BEACON The average per-patient cost burden for ADPKD at ESRD is 3x the cost burden at stage 3 U.S. Medicare spending alone totaled $64B for CKD and $34B for ESRD in 2015 Significant upcoming news flow for bardoxolone in CKD Full week 12 data for ADPKD, IgAN and T1D CKD in 3Q18 52-week retained benefit data from Phase 2 of CARDINAL in 3Q18 KHK commences pivotal T2D CKD trial in Japan in 2018 Full week 12 data for FSGS in 1H19 Pivotal CARDINAL data in 2H19

Q&A