CARDINAL PHASE 2 RESULTS AND UPDATE Exhibit 99.2

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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 CKD, oxidative stress, inflammation, and fibrosis are known to promote disease and drive progressive loss of kidney function Patient Statistics Prevalence of approximately 12,000 patients in the U.S. 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 3

CARDINAL Phase 2 Trial Design Open-label trial designed with input from international key opinion leaders and the Alport Syndrome Foundation Key eligibility criteria include: Genetically-confirmed diagnosis Age range from 12 to 60 years old Broad range of kidney function (eGFR between 30-90 mL/min/1.73 m2) Patients with stage 4 CKD, cardiovascular disease, or fluid retention are excluded Titration is used to reach goal dose of 20 or 30 mg given orally, once daily Week 12 treatment effect from ongoing Phase 2 trial used to guide decision making 4 Week 12 eGFR Change (ml/min/1.73 m2) Decision < 3 Do not proceed to Phase 3 3 to < 5.5 Proceed to Phase 3 and increase sample size ≥ 5.5 Proceed to Phase 3 without increasing sample size

Interim Results from CARDINAL Phase 2 Demonstrate Significant, Time-Dependent Effect on eGFR Change from Baseline in eGFR (mL/min/1.73 m2) in All Patients   Week 1 Week 4 Week 8 Week 12 N* 23 19 13 8 Mean 4.0 6.9 8.5 12.7 95% Confidence Interval 2.5 – 5.6 3.7 – 10.2 4.4 – 12.5 7.9 – 17.5 p-value < 0.0005    < 0.0005 < 0.0005 < 0.00005 *Trial is ongoing; N represents the number of patients who have reached the applicable week Fully enrolled 30 total patients with all patients still on study From a mean baseline eGFR of 54.7 mL/min/1.73 m2, patients experienced a mean improvement of 12.7 mL/min/1.73 m2 at Week 12 Over 80% of patients demonstrated a clinically meaningful improvement in eGFR of at least 3.0 mL/min/1.73 m2 by Week 8 Lower bound of the 95% confidence interval exceeds the on-treatment eGFR improvement that we anticipate will be indicative of success in Phase 3 Observed treatment surpasses the threshold of 3.0 mL/min/1.73 m2 that was the minimum effect size necessary to proceed to the Phase 3 portion of the trial

CARDINAL Results Consistent with Previous Trials in Diabetic CKD CARDINAL Phase 2 efficacy data to date are consistent with results from trials in diabetic CKD that enrolled over 2,600 patients Efficacy data to date is similar to BEAM (primarily Stage 3 diabetic CKD) and better than BEACON (Stage 4 diabetic CKD) Both prior trials were placebo-controlled and at least one year in duration Note: The above chart is a post-hoc comparison of eGFR data from the referenced trials, all of which enrolled different patient populations and had different trial designs. 6

Summary of Available Phase 2 CARDINAL Safety Data No premature discontinuations No serious adverse events No consistent AEs, except muscle spasms, which were observed in diabetic CKD patients and not associated with muscle injury AEs to date have generally been mild to moderate in intensity No safety concerns identified by independent Data Monitoring Committee Data Monitoring Committee reviewed all available safety data and voted to recommend opening the Phase 3 portion of the trial Adverse Events Reported in > 1 Patient Preferred Term N (%) Muscle spasms 9 (30%) Headache 2 (7%) Fatigue 2 (7%) Back pain 2 (7%) Diarrhea 2 (7%) Hypotension 2 (7%) Hypertension 2 (7%)

CARDINAL Phase 3 Trial Phase 3 portion of the trial is designed to support regulatory approval for Alport syndrome Design incorporates insights from all prior CKD studies including dose-response, predictors of response, and other design elements Double-blind, placebo-controlled with 1:1 randomization at up to 100 sites worldwide Enrolling up to 150 patients with two years of follow-up All key endpoints are eGFR-based and objective Primary endpoint: Change in on-treatment eGFR relative to placebo at Week 48 Key secondary endpoint: Retained eGFR relative to placebo at Week 52 following a 4-week withdrawal period Patients will be re-started on study drug and treated for additional year to measure on treatment and retained eGFR at year two FDA guidance: Retained eGFR after one year may support accelerated approval and retained eGFR after two years may support full approval

Statistical Design Leverages Phase 2 and Prior Diabetic CKD Data Primary and key secondary endpoints are powered as follows: Primary endpoint has at least 80% power to detect eGFR change of 3.1 mL/min/1.73 m2 Key secondary endpoint powered to detect eGFR change of 2.2 mL/min/1.73 m2 BEAM and BEACON demonstrated strong, positive correlations (p<0.0001) between Week 12 changes in eGFR and one year on-treatment and retained eGFR changes These studies suggest that the observed eGFR change at Week 12 in CARDINAL would be sustained through Week 48 in the Phase 3 portion of CARDINAL These studies suggest the retained eGFR benefit in the Phase 3 portion of CARDINAL would be 40% of the eGFR improvement at Week 12 Based on the available Phase 2 Week 12 data and the observed BEAM and BEACON correlations, the Phase 3: Week 48 on-treatment eGFR change is modeled to be 7.9 to 17.5 mL/min/1.73 m2 Week 52 retained eGFR benefit is modeled to be 3.2 to 7.0 mL/min/1.73 m2 Phase 2 Observed and Phase 3 Modeled eGFR Changes (mL/min/1.73 m2) Phase 2 Week 12 (on-treatment) Phase 3 Week 48 (on-treatment) Phase 3 Week 52 (retained) Minimum Detectable Week 52 (retained) Mean: 12.7 95% CI: 7.9 – 17.5 Mean: 12.7 Range: 7.9 – 17.5 Mean: 5.1 Range: 3.2 – 7.0 2.2 Note: Modeled changes are not intended as a forecast of probable results. No assurance is given about the results that will be obtained.

CARDINAL is Optimized Phase 3 has multiple layers of conservatism CARDINAL sample size is anticipated to be 66% greater than BEAM Baseline eGFR expected to be higher than BEAM Modeling assumes no placebo decline, which is unlikely Study could be successful with effect size 60% less than CARDINAL Phase 2 results available to date N Placebo-Corrected ∆eGFR (ml/min/1.73 m2) Week 12 Retained BEAM: Mid Dose 90 12.0 4.7 (p=0.02) CARDINAL Phase 3 Modeling Replicate BEAM with more patients 150 12.0 4.7 (p<0.001) Phase 3 replicates Phase 2 150 12.7 5.1 (p<0.001) Minimum detectable difference 150 5.5* 2.2 (p<0.05) *Estimated Week 12 eGFR change that would correspond to the minimum detectable withdrawal effect Phase 3 sample size reduced from 180 to 150 patients due to observed on-treatment eGFR effect, standard deviation, and intra-patient eGFR correlations in the ongoing Phase 2 portion of the study Note: Modeled changes are not intended as a forecast of probable results. No assurance is given about the results that will be obtained.

Potential Bard Alport Syndrome Target Product Profile Bard has potential to become the first treatment approved for Alport syndrome No therapies are approved for this deadly, chronic, orphan disease Off-label use of RAAS agents has minimal impact of slowing disease progression Bard has a novel, potent mechanism that affects inflammation, fibrosis, and GFR Bard targets the underlying renal pathophysiology driving disease Bard inhibits the acute and chronic inflammation-mediated pathways, and exerts anti-proliferative and anti-fibrotic effects that affect tissue remodeling and GFR loss Bard is an easy-to-administer, oral, once-daily capsule Bard has the potential to be combined with any of class of RAAS compounds We believe that meeting approval endpoint of retained benefit is strong evidence of disease-modifying activity and can drive adoption and reimbursement Approximately 12,000 patients in the U.S. and 40,000 globally Bard pricing expected to be consistent with other disease modifying therapies for orphan indications 11

Bard Targets Common Phenotype Shared by Many Types of Chronic Kidney Disease Bard targets inflammatory processes that degrade renal function in many forms of CKD CARDINAL results to date and existing body of data encourage study of bard in additional, rare renal diseases Potential additional target indications include: IgA nephropathy Fabry disease Type 1 diabetic CKD Polycystic kidney disease FSGS Other inflammatory conditions Mezzano, Nephrol Dial Transplant 2004; Schmid, Diabetes 2006; Fornoni, Curr Diabetes Rev 2008; Ha, Diabetes Res Clin Pract 2008; Navarro-Gonzalez, J Am Soc Nephrol 2008; Zoccali, H Am Soc Nephrol 2006; Zoccali, Nephrol Dial Transplant 2008; Perticone, Circulation 2004; Motohashi, Trends Mol Med 2004; Hirayama, Free Radic Biol Med 2003; Li, Physiol Genomics 2004; Yoh, Kidney Intl 2001; Ma, Cancer Res 2006; Raptis, Exp Clin Endocrinol Diagetes 2001; Hayashi, Kidney Intl 1992; Jennette JC, Heptinstall RH. Heptinstall's pathology of the kidney. 6th ed ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2007 12