Creating New Opportunities for Patients

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,” “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.

2

Company Overview

Developing small-molecule drugs for serious and life threatening orphan diseases

Lead programs: Nrf2 activators bardoxolone methyl (Bard) and omaveloxolone (Omav)– Nrf2 is a transcription factor that regulates over 200 genes that restore mitochondrial energy

production, downregulate inflammation, and reduce fibrosis– Mitochondrial dysfunction, chronic inflammation, and Nrf2 suppression are central to the

pathogenesis of the diseases we targetBard in Phase 3 for connective tissue disease-associated pulmonary arterial hypertension (CTD-PAH) with data expected 1H 2018Omav moving to pivotal Part 2 of MOXIe trial in Friedreich’s ataxia in 2H 2017

– Positive Part 1 data released in June 2017 – Potential to be first therapy approved for FA

Two additional orphan disease programs with potential to begin pivotal trials 2H 2017– Alport syndrome: Phase 2 data 2H 2017– Mitochondrial myopathy: Part 1 data 2H 2017

Additional expansion opportunities for Bard in interstial lung disease (ILD) and renal indications, and Omav in neurology and immuno-oncology

3

Nrf2 Activator Mechanism

Increased Energy Production• Increased ATP,NADH, FADH2,

production• Mitochondrial biogenesis• Anti-inflammatory metabolic shift

Antioxidant activity• Glutathione & NADPH • SOD, TRX, GRX, PRX, GPX• Redox homeostasis

Anti-inflammatory activity• IκBα/NF-κB & NLRP3 inhibition• Cytokine suppression: TNFα, IL-

1β, IL-6, MCP1, TGFβ• Resolution of inflammation

Disease TriggersAutoimmunity, Mutations, Cellular damage (DAMPs), Infection (PAMPs), Cytokines

• May acutely improve organ function

• May chronically reduce fibrosis and remodeling

Physiological• May improve 6MWD (PAH; PH-ILD)• May increase kidney function (Alport Syndrome)• May increase neurological function (FA)• May increase muscular function (MM)• May restore normal immune surveillance (Oncology)

Clinical

Disease DeficitsAcute

FatigueDecreased eGFR

Impaired Coordination

ChronicAbnormal

proliferationTissue remodeling

Fibrosis (TGFβ)

Potential Amelioration of Acute and Chronic Disease Deficits

4

Mitochondrial DysfunctionInsufficient energy (ATP)

High ROS levelsInflammatory metabolic shift

Oxidative StressCellular damage

Inflammatory signaling

InflammationNF-κB transcription activity

NLRP3 activation

Cytokine ProductionTNFα, IL-1β, IL-6

MCP1, TGFβ

Overview of CTD-PAH

CTD-PAH Pathophysiology– PAH that occurs in patients with connective tissue diseases such as scleroderma and

lupus erythematosus– Impaired mitochondrial function, inflammation, fibrosis, and tissue remodeling

implicated as prime drivers of PAH

Patient Statistics– 10% to 15% of scleroderma and lupus patients have CTD-PAH– CTD-PAH is the leading cause of death for scleroderma and lupus patients– 5-year survival of scleroderma patients with PAH is 10% versus 85% without PAH– Estimated prevalence: 12,000 in US; 50,000 worldwide; and 30% of all PAH

Disease Management– Vasodilators are the only current treatment options: PDE-5 inhibitors, endothelin

receptor antagonists (ERAs), and prostacyclins– Vasodilators have lower benefit in CTD-PAH versus idiopathic PAH (I-PAH)– Side effects include syncope, headache, flushing, and jaw pain– Poor risk-benefit for vasodilators in CTD-PAH given minimal treatment effect and

adverse events resulting from systemic vasodilation

5

CTD-PAH is Distinct from Idiopathic PAH

Survival in CTD vs Idiopathic PAH Patients

CTD-PAH is a more severe disease than I-PAH– Lower baseline six-minute walk distance (6MWD)– Median survival in U.S. is 4 years for CTD-PAH versus 7 years for I-PAH patients

Compared to I-PAH, CTD-PAH is driven more by fibrosis than by impaired hemodynamics, reducing the impact of vasodilators

– Fibrosis limits the ability of arteries to vasodilate, limiting vasodilator efficacy– Vasodilators produce one-third the impact on 6MWD in CTD-PAH versus I-PAH– Explains lower survival rate in CTD-PAH versus I-PAH

Rhee Meta-AnalysisHemodynamics and 6MWD Change for

CTD vs Idiopathic PAH PatientsCTD-PAH I-PAH

Baseline CharacteristicsRAP, mmHg 8 9.3

mPAP, mmHg 46 55

PVR, WU 10 136MWD (m) 351 365Response to Vasodilator Therapy6MWD (m) 9.6 30.1

6

LARIAT: Phase 2 Trial of Bard Combined with Approved Therapies

US-only, Phase 2, double-blind, randomized, placebo-controlled trial in I-PAH and CTD-PAH patients

– PAH patients required to be on 1 to 2 background therapies– Change in 6MWD from baseline through 16 weeks – Safety and tolerability through 16 weeks– Initially tested fixed doses of 2.5, 5, and 10 mg once daily (n=8 per dose group)

6-Minute Walk TestE EchocardiogramT Telephone Contact

Screening Part 1

W2Scr B W1 W8 W12Scr A

E

D1

E

D3

T

D10

T

W3

T

W4

E

W16

E

Bardoxolone Methyl

3:1

RPlacebo

Extension

Bardoxolone Methyl

7

Primary efficacy analysis of initial cohorts presented at CHEST 2015 showed a placebo-corrected 6MWD of 21 m (p=0.037) at doses of 2.5, 5, and 10 mg

Observed large treatment effect in subset of CTD-PAH patients (~ 30 m 6MWD)– Expanded LARIAT to enroll additional CTD-PAH patients– Tested titration design of 5 10 mg once daily

8

Phase 2 Data Suggest Robust Treatment Effect in CTD-PAH

Performed analysis of expanded dataset of all CTD-PAH patients dosed up to 10 mg that completed Week 16

– Included all patients and those who are CATALYST-eligible– Included analysis of time-averaged (Weeks 4, 8, 12, and 16) and Week 16 changes– Time-averaged change in Bard patients of ~ 27 m consistent with earlier data

Dataset Treatment NTime-Averaged Δ6MWD (m) Week 16 Δ6MWD (m)

Change from Baseline

Placebo-corrected

Change from Baseline

Placebo-corrected

AllPlacebo 7 0.6

p=0.96 - 9.8p=0.44 -

BARD 15 26.7p<0.001

26.1P=0.06

38.2p<0.001

28.4p=0.07

CATALYST Eligible

Placebo 5 -10.1p=0.39 - -5.8

p=0.68 -

BARD 14 30.2p<0.001

40.3p=0.009

42.7p<0.001

48.5p=0.005

Patients with moderate to severe anemia are excluded from CATALYST because anemia treatments can affect 6MWD independent of study drug– Noticed placebo responders received post-randomization anemia treatments– CATALYST-eligible patients showed change of 48.5 m (p=0.005) at Week 16– Pooled standard deviation was 37 m, lower than estimated for CATALYST (50 m)

CATALYST: Phase 3 Trial in CTD-PAH Underway

FDA concurred with proposed Phase 3 trial in CTD-PAH– International, double-blind, randomized, placebo-controlled trial– Will enroll 130 to 200 patients on 0-2 background therapies– Randomized 1:1 to receive Bard (5 10 mg) or placebo for 24 weeks– Primary endpoint: 6MWD at week 24

Screening Dose-Titration Period

W2W1 W8 W16Scr D1 D3

T

D10

T

W3

T

W4

Maintenance

W24

RPlacebo

1:1 Randomization

D31

T

W5

T

W6 W7

T

Bardoxolone Methyl (5 mg) Bardoxolone Methyl (10 mg)

6-Minute Walk TestT Telephone Contact

Data confirm that power calculations for CATALYST are appropriate– LARIAT end-of-treatment analysis shows placebo-corrected change in 6MWD of

48.5 m (p=0.005) at week 16– CATALYST powered to detect 12.5 m change at 24 weeks with p<0.05– Pre-specified adaptive component will assess baseline characteristics and

variability, as well as potentially modify the sample size to maintain power

Study enrolling, data expected 1H 2018

9

Friedreich’s Ataxia (FA): A Brief Summary

FA Pathophysiology– Caused by mutations that result in hypo-expression of frataxin– Frataxin is responsible for biosynthesis of iron-sulfur complexes in the mitochondria

used by OXPHOS complexes– Nrf2 is suppressed in FA due to frataxin deficiency, which leads to increased

oxidative stress and impaired energy production– Typically thought of as a neurodegenerative disease; however FA is a multi-system

disease that includes cardiomyopathy, diabetes, and fatigue

Patient Statistics– On average, patients are diagnosed in their early teens, wheelchair-bound in their

20s, and die in their 30s– Cardiomyopathy is the most common cause of death– Prevalence is approximately 6,000 in the U.S. and approximately 22,000 globally

Disease Management– No treatments are currently approved – Patients routinely take vitamin cocktails and antioxidants which have shown no

reproducible activity

10

Omav May Address Mitochondrial Dysfunction in FA

Shan Y et al., Antioxidant Redox Signal (2013); D’Oria V et al., Int J Mol Sci (2013); V Paupe et al, PLoS One (2009); Drinkard BE et al., Arch Phys Med Rehabil (2010)11

Nrf2 is suppressed in FA and contributes to mitochondrial dysfunction and reduced ATP production which inversely correlates with neurologic functionIn cultured muscle and FA cells, Omav induces Nrf2 target genes and increases mitochondrial ATP productionDose-response shows dose-dependent increases with plateau and then a decline

ATP Levels in Muscle Cells

Nrf2 Activation Status NQO1 Induction

Mitochondrial Function

12

MOXIe Study Design and Patient Disposition

MOXIe designed as a two-part study– Part 1 designed as first trial to test wide range of doses in humans– Part 2 designed to confirm efficacy and safety

Part 1: Phase 2, double-blind, randomized, placebo-controlled, dose-ranging, multi-center, international trial

– 69 total patients randomized 3:1 to Omav or placebo across 7 dose levels– 12 week treatment duration– Safety overseen by data safety monitoring board– Not powered for efficacy; assessing dose-dependent activity and separation from

placeboMultiple clinical assessments of muscular and neurological function assessed in Part I

– Muscular: peak work during exercise testing (primary endpoint)– Neurological: mFARS (key secondary endpoint) and timed 25 foot walk test

Omav was well-tolerated with one Omav and one placebo discontinuationBaseline characteristics were generally balanced across treatment groups

Omav Dose-Dependently Increases Nrf2 Targets and Markers of Mitochondrial Function

Robust changes in several Nrf2 targets, including ferritin and GGT at 80 – 300 mgAspartate transaminase (AST) and creatine kinase (CK) are regulated by Nrf2 and indicate improved metabolism and mitochondrial functionAST/CK changes maximal at 160 mg with reduced activity at 300 mg

13

Nrf2 Targets

GGT

AST

CK

a Change from baseline comparison to zero and LSMEAN estimates at Week 4 using mixed-model repeated measuresb Median change from baseline versus zero tested at Week 12 using a 1-way ANOVA

Ferritin

Bioenergetics

14

a Values are LS means from MMRM analysis b Change from baseline at Week 12 compared to zeroc Change from baseline at Week 12 in Omav patients compared to placebo patients

Pharmacodynamic Changes Associated with Efficacy Improvements

Omav significantly improved mFARS from baseline across all doses (p<0.0001)– mFARS changes mirrored AST induction– PD and efficacy responses more robust and maximal at doses of 80 – 160 mg

Placebo-corrected change at 160 mg (-2.3) neared statistical significance (p=0.06) and equivalent to ~1 year of progression

AST

mFARS

Mean mFARS Changea

N ΔWeek 12b PBO-Correctedc

All Placebo 17 -1.4p = 0.07 -

All Omav 52 -2.5p < 0.0001

-1.1p = 0.22

5 mg 6 -3.3p = 0.01

-1.8p = 0.23

10 mg 6 -2.0p = 0.13

-0.5p = 0.73

20 mg 6 -2.4p = 0.06

-1.0p = 0.51

40 mg 6 -2.4p = 0.06

-1.0p = 0.53

80 mg 6 -2.9p = 0.03

-1.4p = 0.35

160 mg 12 -3.8p = 0.0001

-2.3p = 0.06

300 mg 10 -0.9p = 0.38

0.6p = 0.65

15

mFARS Change More Robust in Patients without Musculoskeletal Foot Deformity

Patients who present with FA while growing can develop a musculoskeletal foot deformity that causes high arched feet and is called pes cavus

– Presence of foot deformity impairs patients’ ability to stand and coordinate their legs independent of neurological function

– Presence of foot deformity does not affect placebo change in mFARSPlacebo-corrected change in mFARS in patients without foot deformity is -4.4 points (p=0.01) at Omav 160 mg

Mean mFARS Changea

Without Foot Deformity

N ∆Week 12b PBO-Correctedc

All Placebo 7 -1.6p = 0.17 -

All Omav 30 -3.3p < 0.0001

-1.7p = 0.19

80 mg 4 -4.2p = 0.003

-2.7p = 0.11

160 mg 4 -6.0p < 0.0001

-4.4p = 0.01

mFARS

a Values are LS means from MMRM analysis b Change from baseline at Week 12 compared to zeroc Change from baseline at Week 12 in Omav patients compared to placebo patients

d Change from baseline comparison to zero and LSMEAN estimates at Week 12 using mixed-model repeated measures

MOXIe Part 2 Study Design

Assessing multiple efficacy endpointsMultiple design elements incorporated to limit variability and improve sensitivityConservatively powered to detect a smaller effect than observed in Part 1

16

Key Design Elements of Part 2

Endpoints • Primary: mFARS• Secondary: peak work• Exploratory: activities of daily living (ADL), 25-foot timed walk test, 9-hole

peg test, frequency of falls, SF-36

Dose • Patients randomized 1:1 (150 mg Omav : PBO)• Stratification by presence or absence of musculoskeletal foot deformity

Eligibility • mFARS 20-80 (Screening and Day 1 within ± 4.5)• Ability to complete exercise test

Duration • 24 week treatment duration

Size • 100 patients (80 patients without musculoskeletal foot deformity)

Stats • Study is powered to detect a placebo-corrected difference in mFARS of -1.2 (p<0.05) to -1.7 (p<0.01)

Overview of Alport Syndrome

Alport Syndrome Pathophysiology– Type IV collagen mutations cause defects in the glomerular basement membrane

(GBM)– Patients present with hematuria, and then develop proteinuria and deterioration of

kidney function, leading to end-stage renal disease (ESRD)– Deafness and ocular abnormalities are also common– Like diabetic chronic kidney disease (CKD), inflammation, fibrosis, and oxidative stress

are known to promote disease and drive progressive loss of kidney function

Patient Statistics– Prevalence of approximately 12,000 patients in the US and 40,000 globally– Median age at initiation of ESRD for males with most common form is 25– Median survival of approximately 55 years

Current Disease Management– No approved therapies– ACE inhibitors and ARBs are commonly used off-label– Dialysis or renal transplant is needed in most patients

17

Rationale for Bard in Alport Syndrome

Reata conducted comprehensive development program of Bard in diabetic CKDIn clinical trials of more than 2,800 patients, Bard improved markers of renal function such as estimated GFR (eGFR) and inulin and creatinine clearance

– Reata’s partner recently demonstrated that Bard improves renal function in humans using the gold standard inulin clearance method of measuring GFR

– Reata produced strong evidence that extended use of Bard is disease modifying in diabetic CKD by measuring eGFR after withdrawal of Bard

Reata terminated its diabetic CKD program in 2012 when it detected an increase in risk of fluid overload related heart failure hospitalizations

Reata identified the mechanism of increased fluid retention and implemented screening and monitoring procedures to mitigate fluid retention risk

The Alport development program leverages the large body of preclinical and clinical data for Bard in diabetic CKD

The pathophysiology underlying CKD caused by Alport syndrome is very similar to CKD caused by Type 2 diabetes

18

Bard has Consistently Improved Renal Function in Clinical Trials

Bard significantly increased markers of renal function such as eGFR, inulin clearance, and creatinine clearance across 10 clinical trials enrolling over 2,800 patients

StudyPhase/

CountryPatient

Population N∆eGFR

(mL/min/1.73m2)

402-C-0903 (BEACON) 3/Global CKD/Diabetes 2185 6.4 (p<0.001 vs PBO)

402-C-0804 (BEAM) 2/US CKD/Diabetes 227 8.6 (p<0.001 vs PBO)

RTA402-005 (TSUBAKI) 2/Japan CKD/Diabetes 40 Data not yet publicly disclosed

402-C-0902 2/US CKD/Diabetes 131 6.5 (p<0.001)

402-C-0801 (Stratum 1) 2a/US CKD/Diabetes 60 6.7 (p<0.001)

402-C-0801 (Stratum 2) 2b/US CKD/Diabetes 20 7.2 (p<0.001)

402-C-1102 1/US CKD/Diabetes 24 9.0 (p<0.05)

402-C-0501 1/US Cancer 47 18.2 (p<0.0001)

402-C-0702 1/2/US Cancer 34 32.2 (p=0.001)

402-C-1302 (LARIAT) 2/US Pulmonary Hypertension 54 14.7 (p<0.001 vs PBO)

19

Patients with CKD and Type 2 Diabetes Show Sustained Renal Function Improvement

Bard significantly increased eGFR (p<0.0001) in BEAM and BEACONChange was durable through one year, the longest duration testedChanges were associated with fewer renal SAEs and ESRD events

Pergola et al., NEJM (2011); De Zeeuw et al., NEJM (2013)

Number of PatientsPBO 1093 1023 885 726 547 402 281 125BARD 1092 958 795 628 461 345 241 103

20.0

24.0

28.0

32.0

0 8 16 24 32 40 48 56

Mea

n eG

FR ±

SE (m

l/min

/1.7

3 m

2)Treatment Week

PBO BARD-4

0

4

8

12

16

20

0 4 8 12 16 20 24 28 32 36 40 44 48 52

Mea

n eG

FR C

hang

e (m

l/min

/1.7

3 m

2 )

Week

150 mg (n = 14)

75 mg (n = 42)

25 mg (n = 69)

Placebo (n=51)

BEACONBEAM

20

Improvements in Renal Function are Partially Retained After Withdrawal of Bard

In BEAM and BEACON, a significant, placebo-corrected improvement in eGFR was retained after withdrawal of drug for four weeks– eGFR assessed after sub-therapeutic concentrations reached– End-of-treatment and withdrawal eGFR changes correlate– The larger the effect on-treatment, the larger the retained benefit– Data suggest Bard affects chronic remodeling and fibrosis

Withdrawal Analysis

Baseline eGFR

Placebo-Corrected

∆eGFR Post-Withdrawal

P-value

BEAM (n=172)

Low Dose 33 0.6 p>0.05

Mid Dose 32 4.7 p<0.05

High Dose 32 5.0 p<0.05

BEACON (n=498)

20 mg 23 1.8 p<0.001

21

Alport Syndrome Phase 2/3 Trial Design

Received guidance from FDA that retained eGFR after withdrawal of drug for four weeks would support approval

– Significant effect on retained eGFR after one year on drug could serve as the basis for accelerated approval

– Significant effect on retained eGFR after two years on drug could serve as the basis for full approval

Trial designed with input from international key opinion leaders and the AlportSyndrome Foundation

– Will enroll patients from 12 to 60 years old– Will enroll a broad range of kidney function (eGFR between 30-90 mL/min/1.73 m2)– Patients with stage 4 CKD, cardiovascular disease, or fluid retention will be excluded– Titration to be used to reach goal dose of 20 or 30 mg given orally, once daily

Phase 2 Cohort enrollment underway– Open-label cohort enrolling a total of 30 patients: 15 with microalbuminuria and 15 with

macroalbuminuria– Measuring change in eGFR following 12 weeks of treatment– Data not included in analysis of primary and secondary endpoints for Phase 3– Phase 3 will be initiated if pre-specified efficacy threshold met in Phase 2 cohort

22

Alport Syndrome Phase 2/3 Trial Design

Phase 3 Cohort– Placebo-controlled, double-blind trial with 1:1 randomization – Will enroll up to 180 patients with two years of follow-up– Primary endpoint of on-treatment eGFR change at Week 48– Key secondary endpoint of eGFR change after 4 weeks of drug withdrawal (Week 52)– Additional secondary endpoints of eGFR change at Week 100 and after 4 weeks of drug

withdrawal (Week 104)

Screening Dose-Titration Period

W2W1 W8 W12ScrA D1 D3

T

D10

T

W3

T

W4

Maintenance

W24

R

Placebo*

1:1 Randomization

D31

T

W5

T

W6 W7

T

BARD (5 mg)* BARD (20 mg)

W36 W48 W52

W/D

Off Study Drug

BARD (10 mg)

W64 W76 W88 W100

BARD (20 mg)

ScrB

Maintenance

Placebo

BARD (5 mg)* BARD (20 mg)BARD (10 mg) BARD (30 mg) BARD (30 mg)

Baseline ACR ≤ 300 mg/g

Baseline ACR > 300 mg/g

W104

F/U

Off Study Drug

Phase 3 Cohort

23

Design Implications From Previous Trials

Statistical design of Cardinal– Powered based on efficacy observed in BEAM (4.7 mL/min/1.73 m2 difference) – Enrolling twice as many patients– 99% and 90% power to achieve primary and secondary endpoints– Study could be successful with effect that is approximately 50% less than BEAM

NBL

eGFR

Placebo-Corrected ∆eGFR

Week 12 One Year Withdrawal

BEAM: Mid Dose 90 32.3 12 16 (p<0.001) 4.7 (p=0.02)

CARDINAL Modeling

Replicate BEAM with more patients 180 60 12 16 (p<0.001) 4.7 (p<0.001)

Minimal detectable difference 2.5 (p<0.05)

24

Data from Phase 2 study expected H2 2017

If Phase 2 positive, plan to initiate Phase 3 study during H2 2017

Upcoming Key Events and Timing

(1) Bard is currently being developed unilaterally by Reata, and AbbVie retains the right to opt back into development. Reata retains commercial rights in US market; KHK has rights in certain Asian markets; AbbVie has rights in non-KHK markets outside the US.

(2) Reata’s next milestone is data from the Phase 3 trial in CTD-PAH. Reata began enrolling patients in October 2016.(3) Reata retains US commercialization; Omaveloxolone is currently being developed unilaterally by Reata, and AbbVie retains

certain rights to opt back into development and commercialization.

25

Stage Disease Drug Event Timing

Lead Programs

Alport Syndrome(1) Bard P2 data 2H17

Mitochondrial Myopathies(3) Omav Part 1 data 2H17

CTD-PAH(1,2) Bard P3 data 1H18

Friedreich’s ataxia(3) Omav Part 2 initiation 2H17

Earlier StagePrograms

Pulmonary Hypertension (ILD)(1) Bard P2 data 2H17

Melanoma(3) Omav P1b data 2H17

Orphan Neurological Indications RTA 901 P1 data 2H17