Exhibit 99.1

Reata announces positive Topline results from the moxie Registrational trial of omaveloxolone in patients with friedreich’s ataxia

Achieved primary endpoint of Statistically significant improvement in mfars compared to Placebo after 48 weeks of treatment

Conference call with Management scheduled for October 15, 2019, at 8:00 aM ET

IRVING, Texas—October 14, 2019—Reata Pharmaceuticals, Inc. (Nasdaq: RETA), a clinical-stage biopharmaceutical company, announced today that the registrational Part 2 portion of the MOXIe Phase 2 trial of omaveloxolone in patients with Friedreich’s ataxia (FA) met its primary endpoint of change in the modified Friedreich’s Ataxia Rating Scale (mFARS) relative to placebo after 48 weeks of treatment.  Patients treated with omaveloxolone (150 mg/day) demonstrated a statistically significant, placebo-corrected 2.40 point improvement in mFARS after 48 weeks of treatment (p=0.014).  Omaveloxolone treatment was generally reported to be well-tolerated.  Based on these positive results, and subject to discussions with regulatory authorities, the company plans to proceed with the submission of regulatory filings for marketing approval in the United States and internationally.

“The results of MOXIe represent a truly historic moment for the patients, families, and caregivers that comprise the Friedreich’s ataxia community,” said Ronald Bartek, President of the Friedreich’s Ataxia Research Alliance (FARA).  “Based on the results reported today for omaveloxolone, we are hopeful that our community will finally have its first approved therapy that can slow this relentlessly progressive disease.  We are extremely proud of, and grateful for, the FA community including all those who have participated in this clinical trial and in the natural history study important in designing the trial.  We are also grateful to the clinical teams who conducted the trial and to our Reata colleagues.  We look forward to continuing the Reata-FARA partnership as we work in pursuit of approval of the first FA therapy.”

“Patients living with Friedreich’s ataxia experience a devastating and progressive loss of neurological function.  The MOXIe trial with omaveloxolone is the first study to demonstrate a significant improvement in neurological function in patients with FA.  We believe that the MOXIe findings announced today bring us closer to our goal of providing an urgently needed therapy to patients with FA,” said Warren Huff, President and Chief Executive Officer of Reata.  “On behalf of everyone at Reata, I would like to express my sincere appreciation to all of the patients, families, and investigators who participated in the MOXIe study.”

Full MOXIe study results will be presented at a future medical meeting.

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Trial Overview and Results

Part 2 of MOXIe, an international, multi-center, double-blind, placebo-controlled, randomized registrational Phase 2 trial, enrolled 103 patients with FA at 11 study sites in the United States, Europe, and Australia and is the largest global, interventional study ever conducted in FA.  Patients were randomized 1:1 to 150 mg of omaveloxolone or placebo.  The primary analysis population included patients without pes cavus (n=82), a musculoskeletal foot deformity that may interfere with the patient’s ability to perform some components of the mFARS exam.  Safety analyses were evaluated in the all randomized population (n=103).

The primary endpoint for the study was change in the mFARS score relative to placebo after 48 weeks of treatment.  The mFARS is a physician-assessed neurological rating scale used to measure FA disease progression.  It includes four sections that measure the patient’s performance of activities such as speaking and swallowing, upper limb coordination, lower limb coordination, and standing and walking.  The United States Food and Drug Administration (FDA) has indicated that mFARS is an acceptable primary endpoint to evaluate the effect of omaveloxolone for the treatment of patients with FA.

Omaveloxolone treatment met the primary endpoint of the study producing a statistically significant, placebo-corrected 2.40 point improvement (decrease) in mFARS (n=82; p=0.014).  Patients treated with omaveloxolone experienced a mean improvement in mFARS of -1.55 points from baseline, while patients treated with placebo experienced a mean worsening in mFARS of +0.85 points from baseline.  The observed placebo-corrected improvements in mFARS were time-dependent, increasing over the course of treatment with the largest improvement observed after 48 weeks of treatment.  

Omaveloxolone treatment also improved the mFARS scores of patients with pes cavus.  When the pes cavus patients are included in the analysis of the mFARS scores at Week 48 (the all randomized population), omaveloxolone treatment produced a mean statistically significant, placebo-corrected 1.93 point improvement in mFARS (n=103; p=0.034). Omaveloxolone treatment also improved several secondary endpoints included in the study.  

Omaveloxolone was generally reported to be well tolerated in this study.  Four (8%) omaveloxolone patients and two (4%) placebo patients discontinued study drug due to an adverse event (AE).  The reported AEs were generally mild to moderate in intensity, and the most common AEs (> 20%) observed more frequently compared to placebo were headache, nausea, increased aminotransferases, fatigue, and abdominal pain.  Increases in aminotransferases are a pharmacological effect of omaveloxolone, which increases production of aminotransferases in vitro, and we believe are related to restoration of mitochondrial function.  In MOXIe, the aminotransferase increases were associated with improvements (reductions) in total bilirubin and were not associated with liver injury.  The overall rate of serious adverse events (SAEs) was low, with three patients in each group reporting SAEs while receiving study drug.  Two additional omaveloxolone-treated patients reported SAEs approximately two weeks after receiving their final dose.

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Reata management will host a call to discuss these results tomorrow, October, 15, 2019 at 8:00 a.m. ET.

This press release and the management slide presentation for the call will be available on Reata’s website shortly before the call at http://reatapharma.com/investors/ and will be available for 12 months after the call. The audio recording and webcast of the call will be accessible for at least 90 days after the call at http://reatapharma.com/investors/.

About Friedreich's Ataxia

FA is an inherited, debilitating, and degenerative neuromuscular disorder that is typically diagnosed during adolescence and can ultimately lead to premature death.  Patients with FA experience progressive loss of coordination, muscle weakness, and fatigue, which commonly progresses to motor incapacitation and wheelchair reliance.  Symptoms generally occur in children, with patients requiring a wheelchair by their teens or early ’20s.  FA affects approximately 5,000 children and adults in the United States and 22,000 globally.  Currently, there are no treatments approved by the FDA for FA.

About Omaveloxolone

Omaveloxolone is an experimental, oral, once-daily activator of Nrf2, a transcription factor that induces molecular pathways that promote restoration of mitochondrial function, reduction of oxidative stress, and inhibition of pro-inflammatory signaling.  The FDA and the European Commission have granted orphan drug designation to omaveloxolone for the treatment of Friedreich’s ataxia.

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 (bardoxolone) and omaveloxolone, target the important transcription factor Nrf2 that promotes restoration of mitochondrial function, reduction of oxidative stress, and inhibition of pro-inflammatory signaling.  Bardoxolone and omaveloxolone are investigational drugs, and their safety and efficacy have not been established by any agency.

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Forward-Looking Statements

This press release includes certain disclosures that 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, our plans to submit regulatory filings, 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,” “model,” 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) whether regulatory authorities determine that additional trials or data are necessary in order to obtain approval; (iv) 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 (v) 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.

Contact:

Reata Pharmaceuticals, Inc.

(972) 865-2219

http://reatapharma.com

Investor Relations:

Vinny Jindal

Vice President, Strategy

(469) 374-8721

ir@reatapharma.com

http://reatapharma.com/contact-us/

Media:

Matt Middleman, M.D.

LifeSci Public Relations

(646) 627-8384

matt.middleman@lifescipublicrelations.com

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Management call to discuss Positive topline pivotal MOXIE Data Exhibit 99.2

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, future revenues, projected costs, prospects, business strategy, and plans and objectives of management for future operations, including our plans to submit for regulatory filings. In some cases, you can identify forward-looking statements by terminology such as “believe,” “will,” “may,” “might,” “estimate,” “continue,” “anticipate,” “intend,” “target,” “project,” “model,” “should,” “would,” “plan,” “expect,” “predict,” “could,” “seek,” “goal”, “potential,” 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: our expectations regarding the timing, costs, conduct, and outcome of our clinical trials, including statements regarding the timing of the initiation and availability of data from such trials; the timing and likelihood of regulatory filings and approvals for our product candidates; whether regulatory authorities determine that additional trials or data are necessary in order to obtain approval; 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; our expectations regarding the potential market size and the size of the patient populations for our product candidates, if approved for commercial use, and the potential market opportunities for commercializing our product candidates; 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 maintain and establish relationships with third parties, such as contract research organizations, suppliers, and distributors; our ability to maintain and establish 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; our expectations related to the use of our available cash; our ability to develop, acquire, and advance product candidates into, and successfully complete, clinical trials; the initiation, timing, progress, and results of future preclinical studies and clinical trials, and our research and development programs; the impact of governmental laws and regulations and regulatory developments in the United States and foreign countries; and developments and projections relating to our competitors and our industry. 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. Bardoxolone methyl and omaveloxolone are investigational drugs, and their safety and efficacy have not been established by any agency.

Friedreich’s Ataxia Overview 1 Parkinson MH, et al., J Neurochem. 2013; 52Santos R, et al., Antioxid Redox Signal. 2010; 3Klockgether T, et al., Brain. 1998 Estimated Prevalence ~5,000 in US ~22,000 Globally Friedreich’s ataxia (FA) is a rare, debilitating, life-shortening, neuromuscular disorder Patients typically become wheelchair-dependent 10 to 15 years after diagnosis and eventually lose independence Numerous failed trials and no approved therapies Most patients diagnosed as children and survive into their mid-30s1-3

Mitochondrial Dysfunction Leads to Impaired Neurological Function in FA FA is caused by mutations in the frataxin gene, resulting in impaired mitochondrial function, Nrf2 suppression, neuroinflammation, and neurodegeneration Drinkard, et al., Arch Phys Med Rehabil (2010) Mitochondrial Function (Peak VO2) Worsening Neurological Function (FARS) p=0.002

Study Rationale: Omaveloxolone (Omav) Improves Mitochondrial Function Omav restored mitochondrial function in FA patient samples in vitro Omav improved neurological function in patients with FA in MOXIe Part 1 Omav Restored Mitochondrial Function in FA Patient Samples MOXIe Part 1: Omav Improved Neurological Function * As assessed by mitochondrial transmembrane potential IMPROVED Neurological Function Omav (vs Pbo) -2.35pt

MOXIe Part 2: Pivotal Study Design International, double-blind, placebo-controlled, randomized, registrational trial Largest global interventional study in patients with FA Enrolled a wide and representative range of patients with FA Baseline mFARS: 20 to 80 Age: 16 to 40 years Patients randomized 1:1 to receive 150 mg Omav or placebo for 48 weeks Primary analysis population: no pes cavus (n=82) All randomized population: includes pes cavus (n=103) Primary endpoint: change from baseline in mFARS at Week 48

mFARS: Physician-Assessed Neurological Exam that Tracks Progression of FA mFARS has four sections that are considered clinically meaningful In FA patients, mFARS worsens (increases) on average one to two points annually FDA provided guidance that mFARS is an approvable endpoint in FA Patel et al., Annals of Clinical and Translational Neurology (2016) 0 Diagnosis 10-15 years old Non-Ambulatory Mid-20’s Death Mid-30’s 99 90 55 - 60 25-35 mFARS Scores Associated with Progression mFARS Sections Bulbar Upper Limb Lower Limb Upright Stability

Omav Treatment Met Primary Endpoint of Study Omav treatment significantly improved mFARS by 2.40 points relative to placebo in the primary analysis population (n=82; p=0.014) In the all randomized population, with inclusion of pes cavus patients, Omav treatment improved mFARS by 1.93 points relative to placebo (n=103; p=0.034) IMPROVED Neurological Function WORSENED Neurological Function Placebo Omav Difference=2.40 (p=0.014) Primary Endpoint: Change in mFARS at Week 48 -1.55pt +0.85pt

mFARS Improved Over Time Worsened Improved -1.55 pts +0.85 pts

Omav Improved Several Secondary Endpoints Improvements observed in Patient Global Impression of Change (PGIC) Primary analysis population (n=82; p=0.125) All randomized population (n=103; p=0.028) Patient-reported PGIC correlated with physician-assessed changes in mFARS (p<0.001) Activities of Daily Living score achieved nominal significance versus placebo (n=82; p=0.042) 65% reduction in frequency of falls Activities of Daily Living Section Improved with Omav1 Speech ü Swallowing ü Cutting Food and Handling Utensils ü Dressing ü Personal Hygiene ü Falling ü Walking ü Quality of Sitting Position ü Bladder Function ü Total ü (p=0.042) 1 All sections demonstrated numerical improvements relative to placebo

Summary of Discontinuations and Adverse Events AEs generally mild to moderate in intensity 4 (8%) Omav patients and 2 (4%) placebo patients discontinued study due to AEs Three additional Omav patients discontinued by withdrawal of consent 98% of eligible patients elected to enroll in MOXIe Part 3 extension study ALT and AST increases are a pharmacological effect of Omav1 ALT increases at Week 4 significantly correlated with improvements in mFARS at Week 48 Not associated with liver injury Coincided with decreases in total bilirubin May reflect improvements in mitochondrial metabolism Overall low rate of cardiac and vascular AEs that was reduced in the Omav group 1Miller et al., ASN 2010 Summary of Adverse Events* *AEs reported in >20% of patients in either group Preferred Term Placebo (n=52) Omav (n=51) Contusion 19 (37%) 17 (33%) Headache 13 (25%) 19 (37%) Upper respiratory tract infection 15 (29%) 14 (28%) Excoriation 12 (23%) 13 (26%) Nausea 7 (14%) 17 (33%) ALT increased 1 (2%) 19 (37%) Fatigue 7 (14%) 11 (22%) Abdominal pain 3 (6%) 11 (22%) AST increased 1 (2%) 11 (22%)

Summary of Serious Adverse Events Low rate of serious AEs (SAEs) SAEs reported in 3 (6%) Omav patients and 3 (6%) placebo patients while receiving study drug Two additional Omav patients reported SAEs approximately 2 weeks after receiving final dose No safety signals and SAEs were sporadic and generally expected for FA patients In three patients who reported SAEs while receiving Omav, none led to discontinuation Atrial fibrillation was balanced and reported in one Omav and one placebo patient One Omav patient reported anemia that was due to a complication of a procedure and was considered unrelated to Omav One Omav patient reported multiple SAEs, including viral upper respiratory tract infection and laryngitis, along with palpitations, non-cardiac chest pain, and sinus tachycardia Several of these SAEs were considered possibly related to Omav No imbalances in infection or arrhythmia adverse events

Summary and Next Steps Reata believes that the MOXIe data provide evidence that Omav provides a clinically meaningful benefit to patients with FA Potential for Omav to be first approved treatment for FA Working closely with the Friedreich’s Ataxia Research Alliance (FARA) to communicate with the patient community Planning to meet with FDA and other regulatory agencies to discuss marketing application submission plans Determining feasibility of launching an early access program in the US Beginning to plan for ex-US launch as a result of recent reacquisition of global rights

Omav Pharmacology May Be Applicable to Broad Set of Neurodegenerative Diseases MOXIe results provide proof of concept for use of Omav in other neurodegenerative diseases Mitochondrial dysfunction and neuroinflammation are common features of FA and other neurodegenerative diseases Omav and analogs have demonstrated broad activity in neurodegenerative models Huntington’s Disease ALS Parkinson’s Disease Alzheimer’s Disease Epilepsy Yang et al., PLoS One (2009); Neymotin et al., Free Rad Bio (2011); Dinkova-Kostova et al., (2015) Stack et al., Free Rad Biol Med 49 (2010); Dumont et al., J Neurochem (2009); Kim et al., Cells (2019); Shekh-Ahmad, et al., Brain (2018); Wei et al., Sci Rep (2017)

Q&A