8-K

UNITED STATES

SECURITIES AND EXCHANGE COMMISSION

Washington, D.C. 20549

FORM 8-K

CURRENT REPORT

Pursuant to Section 13 or 15(d)

of the Securities Exchange Act of 1934

Date of Report (Date of earliest event reported): November 3, 2017 (November 3, 2017)

Reata Pharmaceuticals, Inc.

(Exact name of Registrant as Specified in Its Charter)

Delaware  (State or other jurisdiction of
incorporation or organization) 001-37785 (Commission File Number) 11-3651945
(I.R.S. Employer
Identification No.)

2801 Gateway Drive; Suite 150

Irving, TX 75063

(Address of Principal executive offices, including zip code)

(972) 865-2219

(Registrant’s telephone number, including area code)

Check the appropriate box below if the Form 8-K filing is intended to simultaneously satisfy the filing obligation of the registrant under any of the following provisions (see General Instruction A.2. below):

☐ Written communications pursuant to Rule 425 under the Securities Act (17 CFR 230.425)

☐ Soliciting material pursuant to Rule 14a-12 under the Exchange Act (17 CFR 240.14a-12)

☐ Pre-commencement communications pursuant to Rule 14d-2(b) under the Exchange Act (17 CFR 240.14d-2(b))

☐ Pre-commencement communications pursuant to Rule 13e-4(c) under the Exchange Act (17 CFR 240.13e-4(c))

Indicate by check mark whether the registrant is an emerging growth company as defined in as defined in Rule 405 of the Securities Act of 1933 (§230.405 of this chapter) or Rule 12b-2 of the Securities Exchange Act of 1934 (§240.12b-2 of this chapter).

Emerging growth company ☒

If an emerging growth company, indicate by check mark if the registrant has elected not to use the extended transition period for complying with any new or revised financial accounting standards provided pursuant to Section 13(a) of the Exchange Act. ☒

Item 8.01.Other Events.

On November 3, 2017, Reata Pharmaceuticals, Inc. (the “Company”) issued a press release announcing primary 12-week data from the Phase 2 portion of the CARDINAL trial studying bardoxolone methyl for the treatment of chronic kidney disease caused by Alport Syndrome. A copy of the press release is attached as Exhibit 99.1 and incorporated herein by reference. The complete data are being presented by Geoffrey A. Block, M.D., CCRI, director of clinical research at Denver Nephrology, on November 3, 2017, at 10 a.m. CT at the American Society of Nephrology Kidney Week 2017 Annual meeting. The results from the Phase 2 portion of the CARDINAL trial are attached as Exhibit 99.2 and incorporated herein by reference.

The Company plans to hold a conference call on November 6, 2017, at 8:30 a.m. ET to review the results of CARDINAL and discuss the Company’s PHOENIX program for studying bardoxolone methyl in other rare forms of chronic kidney disease. Management’s presentation will be accessible via webcast and via teleconference as set forth in the attached press release.

Cautionary Note Regarding Forward-Looking Statements

This Current Report on Form 8-K and oral statements made with respect to information contained in this report may contain forward looking information within the meaning of the Private Securities Litigation Reform Act of 1995.  You may identify forward-looking statements by the use of words such as “believe,” “expect,” “plan,” “intend,” “anticipate,” “estimate,” “predict,” “potential,” “may,” “should,” “will” or other words or expressions of similar meaning, although not all forward-looking statements contain such terms. These forward-looking statements include, but are not limited to, statements about the CARDINAL trial and the PHOENIX PROGRAM. 

Forward-looking statements are subject to risks and uncertainties, both known and unknown, that could cause actual results to differ materially from those expressed or implied in forward-looking statements. Such risks and uncertainties include, but are 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; 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; our expectations related to the use of our available cash; estimates of our expenses, future revenue, capital requirements, and our needs for additional financing; 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 scope of protection we are able to establish and maintain for intellectual property rights covering our product candidates; our ability to maintain and establish collaborations or obtain additional funding; our ability to maintain and establish relationships with third parties, such as contract research organizations, suppliers, and distributors; our expectations regarding the time during which we will be an emerging growth company under the JOBS Act; our ability to establish and maintain arrangements for manufacture of our product candidates; the impact of governmental laws and regulations; developments and projections relating to our competitors and our industry; and other risks and uncertainties included in our most recent report on Form 10-K and subsequent reports on Forms 10-Q and 8-K available on the Investor & News section of www.reatapharma.com. You should not place undue reliance on forward-looking statements, which speak only as of the date they are made, are not guarantees of future performance or results, and are subject to risks, uncertainties, and assumptions that are difficult to predict or quantify.  The Company undertakes no obligation to update or revise any forward-looking statement, whether as a result of new information, future events, or otherwise, except as may be required by law.

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Item 9.01.Financial Statements and Exhibits.

(d)Exhibits

Exhibit No.	Description
99.1	Press release dated November 3, 2017.
99.2	Results from the Phase 2 portion of the CARDINAL trial.

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SIGNATURES

Pursuant to the requirements of the Securities Exchange Act of 1934, the Registrant has duly caused this report to be signed on its behalf by the undersigned thereunto duly authorized.

	Reata Pharmaceuticals, Inc.
Date: November 3, 2017	By:	/s/ J. Warren Huff
		J. Warren Huff
		Chief Executive Officer

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EX-99.1

Exhibit 99.1

Reata announces PRIMARY results from the phase 2 cardinal study of bardoxolone in alport syndrome at the American Society of Nephrology Kidney Week 2017 Annual Meeting

met Primary endpoint of change in egfr at 12 weeks (p<0.000000001)

73% of patients had improvement in stage of CKD

bardoxolone was well tolerated without any safety concerns

Conference Call with management scheduled Monday, november 6^th at 8:30am ET

IRVING, Texas—November 3^rd, 2017—Reata Pharmaceuticals, Inc. (Nasdaq:RETA) (Reata or Company), a clinical-stage biopharmaceutical company, announces primary 12-week data from the Phase 2 portion of the CARDINAL trial studying bardoxolone methyl (bardoxolone) for the treatment of chronic kidney disease (CKD) caused by Alport syndrome.

Geoffrey A. Block, M.D., CCRI, director of clinical research at Denver Nephrology, is presenting, Initial Data Report from “CARDINAL”: A Phase 2/3 Study of Bardoxolone Methyl in Patients with Alport Syndrome, this morning at 10 a.m. CT at the American Society of Nephrology Kidney Week 2017 Annual Meeting in New Orleans, Louisiana.

The primary efficacy endpoint of the Phase 2 portion of CARDINAL was the change from baseline in estimated glomerular filtration rate (eGFR) for 30 patients with Alport syndrome who were administered bardoxolone orally, once-daily, for 12 weeks. All patients completed the treatment period without any discontinuations.  The mean baseline eGFR (± SD) was 54 ± 24 mL/min/1.73 m². Bardoxolone increased eGFR by 13.4 mL/min/1.73 m² (n=30, p<0.000000001, 95% CI 10.5 to 16.3) after 12 weeks of treatment, which was consistent with an interim release from CARDINAL in July 2017 that reported an increase of 12.7 mL/min/1.73 m² for the first eight patients that reached Week 12.  All patients had an increase from baseline, and 87% had an increase of at least 4 ml/min/1.73 m², which is the approximate annual rate of decline in kidney function in patients with Alport syndrome.  The increases in eGFR translated to an improvement in CKD stage for 22/30 (73%) patients.  No serious adverse events were reported, and adverse events were generally mild to moderate in intensity.

Reata management will host a call to review the results of CARDINAL and discuss the company’s PHOENIX program for studying bardoxolone in other rare forms of CKD on Monday, November 6^th, at 8:30 a.m. ET.

CONFERENCE CALL INFORMATION
Date:	Monday, November 6, 2017
Time:	8:30AM ET
Audience Dial-in (toll-free):	(844) 348-3946
Audience Dial-in (international):	(213) 358-0892
Passcode:	4588527
Webcast Link:	https://edge.media-server.com/m6/p/5s3pc9iz

About Alport Syndrome

Alport syndrome is a rare, genetic form of CKD caused by mutations in the genes encoding type IV collagen, which is a major structural component of the glomerular basement membrane (GBM) in the kidney.  The abnormal expression of type IV collagen causes loss of GBM integrity, abnormal leakage of proteins through the GBM, and excessive reabsorption of protein in the proximal tubules of the kidney.  Like other forms of CKD, excessive reabsorption of protein in the tubules induces oxidative stress, chronic inflammation, and renal interstitial inflammation and fibrosis.

Alport syndrome affects approximately 12,000 people in the United States and approximately 40,000 people globally.  Almost all patients with Alport syndrome develop end-stage renal disease, and approximately 50% of male patients require dialysis or a kidney transplant by the age of 25.  There are currently no approved therapies to treat Alport syndrome.

About Bardoxolone

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.  Bardoxolone is also currently being studied in CATALYST, a Phase 3 study for the treatment of connective tissue disease associated pulmonary arterial hypertension.

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 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, 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

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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.

Contact:
Reata Pharmaceuticals, Inc.

(972) 865-2219

info@reatapharma.com

http://news.reatapharma.com

Investor Relations:

Vinny Jindal

Vice President, Strategy & Analytics

(469) 374-8721

ir@reatapharma.com

Media:

Matt Middleman, M.D.

LifeSci Public Relations

(646 627-8384

matt.middleman@lifescipublicrelations.com

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EX-99.2

Primary phase 2 analyses from CARDINAL: a Phase 2/3 Study of Bardoxolone Methyl in Patients with Alport Syndrome 2017 American Society of Nephrology Meeting Geoffrey A. Block1, Pablo E. Pergola2, Lesley Inker3, Peter A. McCullough4, Melanie Chin5, Colin J. Meyer5, Michelle N. Rheault6, Clifford E. Kashtan6, David G. Warnock7 1 Denver Nephrology, Denver, CO; 2 Renal Associates, San Antonio, TX; 3 Tufts Medical Center, Boston, MA; 4 Baylor University Medical Center, Dallas, TX; 5 Reata Pharmaceuticals, Irving, TX; 6 University of Minnesota, Minneapolis, MN; 7 UAB, Birmingham, AL Exhibit 99.2

Rationale for Study Bardoxolone methyl (Bard) is an investigational drug that activates Nrf2 and suppresses inflammation, which contributes to GFR loss in chronic kidney diseases, including Alport syndrome Mechanisms of eGFR increases with Bard in preclinical models: Dynamic increases in glomerular surface area for filtration (↑ Kf) Chronic suppression of remodeling and fibrosis Bard and analogs have been shown to improve renal function and have protective effects in multiple preclinical models of renal disease: 5/6 nephrectomy model of hyperfiltration Protein overload-induced secondary nephropathy Diabetic nephropathy Hypertensive CKD Lupus nephritis Previous clinical studies that enrolled over 2,600 patients with type 2 diabetes and CKD demonstrate that Bard significantly increases eGFR, inulin clearance, creatinine clearance, and other renal function parameters Post-hoc analyses of the BEACON study identified a specific subset of at-risk patients for fluid overload, who can be excluded from future trials CARDINAL study conducted to evaluate safety and efficacy of Bard in patients with Alport syndrome, who have progressive loss of kidney function and no approved therapies

CARDINAL Phase 2 Open-Label Study Design Enrolled 30 patients with genetic or histologic confirmation of Alport syndrome Dose-titration scheme used to reach goal dose of 20 or 30 mg given orally, once daily Primary efficacy endpoint: change from baseline in eGFR at Week 12 Key eligibility criteria: O eGFR determination T Telephone Contact Primary efficacy analysis * Patients under the age of 18 will receive study drug (BARD or placebo) every other day during Week 1 Inclusion Exclusion Age: 12 to 60 years old BNP > 200 pg/mL eGFR: 30 to 90 mL/min/1.73 m2 Serum albumin < 3 g/dL Stable dosage of RAAS blockade for 6 weeks, unless medically contraindicated ACR > 3500 mg/g Additional follow-up through 2 yrs Data presented in this presentation include all efficacy and safety data through the primary endpoint, Week 12

Phase 2 Patient Demographics and Baseline Characteristics Characteristic Total (N=30) Age, years Mean ± SD 44 ± 13 Median (range) 49 (14, 59) Age < 18 years (n,%) 2 (7%) Female (n,%) 18 (60%) White/Caucasian (n,%) 26 (87%) Baseline eGFR, mL/min/1.73 m2 Mean ± SD 54 ± 24 Median (range) 42 (28, 94) Baseline ACR, mg/g (geometric mean) 148 ACR ≤ 300 mg/g (n,%) 18 (60%) ACR > 300 to ≤ 1000 mg/g (n,%) 7 (23%) ACR > 1000 to ≤ 3500 mg/g (n,%) 5 (17%) Histologic Confirmation 2 (7%) Genetic Confirmation 28 (93%) X-linked (n,%) 22 (73%) Autosomal (n,%) 5 (17%) Unknown (n,%) 1 (3%) Receiving ACEi or ARB (n,%) 25 (83%)

Phase 2 Primary Efficacy Analysis All patients completed treatment through Week 12 eGFR data show time-dependent increases through Week 12 Changes consistent with Bard treatment in prior diabetic CKD studies Change from Baseline in eGFR Week 1 Week 4 Week 8 Week 12 N 30 30 30 30 Mean ± SE 3.0 ± 0.7 6.7 ± 1.3 8.9 ± 1.3 13.4 ± 1.4 95% CI (1.6, 4.4) (4.1, 9.3) (6.2, 11.6) (10.5, 16.3) p-value 0.0001 <0.0001 <0.000001 <0.000000001 LS mean eGFR change from baseline at each visit is compared to zero using a mixed-model repeated measures analysis using baseline eGFR and log-transformed ACR as continuous covariates.

Distribution of eGFR Changes All patients demonstrated eGFR increases from baseline 87% of patients demonstrated increases of at least 4 ml/min/1.73 m2 63% of patients demonstrated increases of at least 10 ml/min/1.73 m2 22/30 (73%) of patients had an improvement in CKD stage and none worsened Baseline CKD Stage Week 12 CKD Stage N Stage 4 Stage 3b Stage 3a Stage 2 Stage 1 Stage 4 (eGFR <30) 5 1 4 - - - Stage 3b (eGFR 30 to 44) 11 - 4 7 - - Stage 3a (eGFR 45 to 59) 2 - - 0 2 - Stage 2 (eGFR 60 to 89) 10 - - - 1 9 Stage 1 (eGFR >90) 2 - - - - 2 Improved CKD Stage eGFR Changes for All Patients

eGFR Changes by Subgroups Clinically meaningful increases in eGFR across multiple subgroups Activity in earlier and later stages of disease Baseline Characteristic Subgroup N Baseline Week 12 Mean ΔeGFR Change ± SD % Change eGFR ≥ 60 12 81.3 ± 7.5 18.4 ± 7.7 23% < 60 18 36.1 ± 9.3 10.0 ± 6.6 30% UACR Non-macro 18 62.5 ± 22.2 16.0 ± 8.6 29% Macro 12 41.7 ± 22.0 9.4 ± 5.5 24% Gender Male 12 50.5 ± 25.1 14.0 ± 8.3 30% Female 18 56.6 ± 23.8 12.9 ± 8.1 25% Age < 18 2 86.1 ± 9.1 26.1 ± 10.8 31% ≤ 45 11 48.4 ± 24.8 10.1 ± 9.5 20% > 45 19 57.5 ± 23.7 15.3 ± 6.7 31%

Blood Pressure and BNP Patients with poorly controlled hypertension or BNP > 200 pg/mL were ineligible Blood pressure and volume status under control upon study entry and maintained post-initiation of treatment Average BNP upon entry was 1/10th allowable limit and 1/5th ULN Median BNP levels maintained well below ULN threshold No evidence of overt fluid overload SBP DBP 2x ULN BNP ULN

Weight Weight decreases with Bard, possibly due to improved mitochondrial function and metabolism as shown in preclinical models Mean decrease in weight (~1 kg / month) consistent with prior clinical trials with Bard Patients with higher baseline BMI demonstrated larger weight loss Mean decreases in weight not observed in patients < 18 years of age Weight Change by Age Weight Over Time

Urine Albumin to Creatinine Ratio Increases in UACR with Bard consistent with increases in filtration (↑ GFR) Normalization of UACR with eGFR show UACR/eGFR ratios are unchanged from baseline UACR (Log UACR) / eGFR Ratio

Summary of Safety No discontinuations No serious adverse events AEs to date have generally been mild to moderate in intensity No reports of fluid overload No consistent AEs yet, except muscle spasms Also observed in prior diabetic CKD trials Present as contraction, usually in the lower extremity, and similar to exercise-induced cramps Usually transient; occur in first month and resolve a few weeks after titration is completed Not associated with evidence of muscle toxicity as assessed by CK Number of Patients Reporting AEs 27 (90%) Number of AEs 87 Preferred Term Number (%) of Patients* Muscle spasms 15 (50%) Nausea 4 (13%) Fatigue 4 (13%) Headache 4 (13%) Hyperkalemia 3 (10%) *AEs reported in >2 patients Creatine Kinase

Conclusions Phase 2 CARDINAL study demonstrates bardoxolone methyl significantly increases eGFR in patients with Alport syndrome after 12 weeks of treatment eGFR increases in CARDINAL were observed over full range of baseline eGFR values (range: 28 to 94 mL/min/1.73 m2) and across multiple subgroups Most patients demonstrated improvements in CKD stage Increases are similar in magnitude to those previously observed in patients with type 2 diabetes and Stage 3b-4 CKD Bard was well tolerated in patients with Alport syndrome No discontinuations from study No serious adverse events No effect on blood pressure When normalized by change in eGFR, urinary protein was unchanged from baseline AEs to date have been mild to moderate in intensity Muscle spasms were most commonly reported AE and not associated with evidence of muscle toxicity Phase 3 portion of CARDINAL study is actively enrolling Site activations in Phase 2 PHOENIX trial studying Bard in ADPKD, type 1 diabetic CKD, IgA nephropathy, and FSGS are underway KHK, Reata’s Japanese partner, is planning to initiate a Phase 3 trial of Bard in diabetic CKD in Japan in 2018