March 2015

A drug development company focused on orphan diseases that have a uric acid imbalance.

Forward-Looking Statements

This document contains forward-looking information pursuant to applicable securities

law. All information that addresses activities or developments that we expect to occur

in the future are forward-looking statements. Forward-looking statements are based on

the estimates and opinions of management on the date the statements are made.

However, they should not be regarded as a representation that any of the plans or

objectives will be achieved. Actual results may differ materially from those expressed or

implied by the forward-looking information set forth in this document due to risks and

uncertainties affecting the Company, including access to capital, the successful

completion of clinical trials and receipt of all regulatory approvals. The forward-looking

statements in this document are based on a number of assumptions which may prove

to be incorrect, including assumptions concerning general business and economic

conditions, positive clinical trials and the availability of financing. XORTX assumes no

responsibility to update forward-looking statements in this document.

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Overview: XORTX Pharma Corp

• XORTX: focused on orphan diseases with uric acid imbalance.

• Strong clinical and scientific evidence shows that: Uric acid causes a ‘disease axis’ – vascular injury, high blood pressure, progressive kidney injury, and progression of diabetes.

• 7 Phase II studies…

2- Phase II studies show lowering uric acid can normalizes blood pressure;

3- Phase II studies show decreased progression of kidney injury.

2- Phase II studies showing uric acid lowering may benefit APDKD patients.

• Mfg and developing Oxypurinol: well established safety and efficacy profile - FDA previously allowed for treating gout on a compassionate basis.

• HIGHLY DE-RISKED: Manufacturing, Translated Clinical results, Established Safety & Efficacy, Experienced team who have already developed this drug through NDA submission (approvable letter).

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Strong Leadership Team -Directors

Allen Davidoff, Ph.D., CEO, President and Founding Board Member

• Former Co-Founder & CSO of Stem Cell Therapeutics• 12 Years Drug Development Experience- Bench to NDA• 8 yrs –C Level management experience-CSO, VP- Product Development• 2 IND’s – 9 Clinical trials – 1 NDA

Bob Rieder, President and CEO- EssaPharmaceuticals

• Current Chairman and Former Co-Founder & CEO Cardiome Pharma• Led successful development of antiarrythmic drug Vernakalant through European

Registration & Partnership• 25 yrs –C Level management experience-President, CEO, director

Alan Moore, Ph.D., Founding Board Member, Executive Consultant : Clinical and Regulatory Affairs

• 27 years pharmaceutical development experience with 23 years of senior management experience in pharmaceutical R&D with P&G

• Completed 11 investigational new drug ("IND") applications or supplemental IND's, 15 phase I studies, 12 phase II studies, 7 phase III studies and 2 new drug applications. Most recently CEO of BetaStem Inc.

Bruce Rowlands, Chairman & CEO - Eurocontrol Technics Group,

•Senior Vice President with Lorus Therapeutics- Biotechnology,•VP and Director of Dominick and Dominick Securities Canada: Investment banking firm

Alan Ezrin, Ph.D., join Board with Bradmer Merger 4

Strong Management Team (Cont’d)

Allen Davidoff, Ph.D., CEO, President and Director

• Former Co-Founder & CSO of Stem Cell Therapeutics

• 12 Years Drug Development Experience- Bench to NDA

• 8 yrs –C Level management experience-CSO, VP- Product Development

• 2 IND’s – 9 Clinical trials – 1 NDA

Grace Jung, Ph.D., Director Manufacturing and Synthetic Chemistry

• 21 years of experience in drug discovery and development

• Former Senior Director of Research (Chemistry) at Cardiome.

• Led the chemistry team in the discovery of antiarrhythmic vernakalant. Prior to

Cardiome, Grace spent 7 years at Boehringer Ingelheim - medicinal chemist- renin

inhibitors as antihypertensive drugs.

Brian Mangal, M.Sc., Director Business Development

• 12 years of clinical and regulatory development experience.

• Formerly Director Biostatistics at Cardiome.

• Extensive Clinical , Regulatory and Corporate development experience includes

design, analysis and reporting of over 50 clinical trials, three FDA submissions, one

TPD submission, a successful EMEA submission and numerous interactions with

regulatory authorities and large pharma partner accounts.

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Clinical Advisory Board

Dr. Richard J. Johnson:

Dr. Johnson is Chief of the Division of Renal Diseases and Hypertension at the

University of Colorado. Temple Hoyne Buell and NKF of Colorado Endowed Professor

of Medicine Chief, Division of Renal Diseases & Hypertension University of Colorado

Denver. Dr. Johnson is nationally and internationally renowned for his work on

mechanisms of renal injury and progression, including in glomerulonephritis, diabetes,

and hypertension.

Dr. Daniel Fieg:

Dr. Fieg is Director of the Pediatric Hypertension Program and Pediatric Renal

Transplant Program at the University of Alabama, Birmingham. He also serves on the

steering/planning committee for the hypertension studies being conducted by the

Pediatric Trials Network.

Dr. William Hiatt:

Dr. Hiatt has successfully led CPC as President since 1996. He is a past Chair of the

United States Food and Drug Administration (FDA) Cardiovascular and Renal

Advisory Committee (2003-08) and currently serves on the Endocrinologic and

Metabolic Drugs Advisory Committee. In addition, Dr. Hiatt is the Novartis Foundation

endowed professor for cardiovascular research in the Department of Medicine,

Division of Cardiology, University of Colorado School of Medicine.

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How is Uric Acid Managed?

Chronically increased Serum Uric Acid causes Progressive Kidney Injury Diabetes Diabetic Nephropathy

Uric Acid

XanthineOxidase

Food

Sugar, Protein,Yeast

Production

Excretion

Reuptake

Xanthine Oxidase Inhibitor

URAT-1 Inhibitor

Genetic Diseases = Orphan Indications (ADPKD, HH)

Allopurinol & Oxypurinol

Probenicid

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Chronically Increased Serum Uric Acid Causes Renal Injury and Worsens Health

Uric Acid: A Novel Mechanism of Action

1) Uric acid- Decreases Endothelial Nitric Oxide Production

2) Uric acid- Increases Renin-Angiotensin-Aldosterone Activation

3) Uric acid- Increases circulating Insulin concentration

4) Insulin in absence during Nitric Oxide

5) Uric Acid induces glomerular - kidney injury

VASOCONSTRICTION

Mazzali et al, Hypertension 38:1101-1106, 2001; JASN 2005; 16:35553-3562

Nakagawa et al, Am J Physiol 2006; 290:F625-631

Mazzali et al, AJP Renal Physiol 282:F991, 2002SALT SENSITIVEHYPERTENSION

Reaven GM, Lithell H, Landsberg L. N Engl J Med. 1996;334(6):374-381.

Conclusion: Increased Uric acid can cause

Progressive, Worsening Kidney Function

VASOCONSTRICTION

VASOCONSTRICTION

VASOCONSTRICTION

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Uric Acid: A Multi-Modal Cause of Kidney Injury

Uric Acid (UA) a Novel Mechanism of Action for Kidney Injury

Jalal et al. 2011 Semin. Nephrol 31(5): 459-465

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‘Normal’ Kidney

Autosomal Dominant Polycystic Kidney Disease

Kidney With ADPKD

Renal Complications

Hypertension 60-100%

Gross Hematuria 50%

Infection Common

Nephrolithiasis 20-25%

Renal Failure 50% By age 60 (PKD1)

Autosomal Dominant Polycystic Kidney Disease (ADPKD)- FDA approved orphan indication

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Clinical evidence:

1/ Hyperuricemia and early onset hypertension are independent risk factors for

accelerated deterioration of kidney function and end stage kidney disease (ESRD).

2/ Correction of Hyperuricemia may attenuate renal function decline in patients

with GFR between 70 and 30 mL/min.

Estimated ADPKD prevalence: ~400,000 individuals affected.

-85% have PKD1: ~350,625

-50% with Hypertens/Hypouricemic: ~175,000

-25% Stage 2-3: kidney dysfunction: ~42,000

-Market Potential: ~$1.6 B/yr

(Helal I, Nephrol Dial Transplant 28:380 ,2013)

Orphan Indication-1: ADPKD

(Han M, et al , BMC Nephrology 15:63; 2014)

After XOI

After XOI

Est. GFR

Est. GFR

(Han M, et al., Hyperuricemia and Deterioration of Renal function in ADPKD, BMC Nephrol 15:63-2014)

Hyperuricemic

Hyperuricemia and Deterioration of Renal Function in ADPKD

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(n=32;21)

*(p=0.001)

Oxypurinol - Well Established Safety Profile

Structure of

Oxypurinol

• Oxypurinol is a metabolic derivative of allopurinol, with a better safety profile.

• Oxypurinol has been used under an FDA compassionate protocol to lower uric acid

levels in 619 allopurinol intolerance gout patients (oral doses ranging from 100-800

mg/d)

• Oxypurinol is effective in reducing serum uric acid levels and has the advantage of

being safer than allopurinol in terms of overall hypersensitivity reactions.

• Data from allopurinol intolerant gout patients administered oxypurinol, showed

decreased dermal (skin) and hepatic (liver) adverse responses (~ 1/3% as often).

Suggesting oxypurinol has a superior safety profile compared to allopurinol.

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Orphan Drug Model

Orphan Drug Strategy

Premium Pricing

Shorter Development Timelines

Greater Regulatory Success

Longer Exclusivity Faster Uptake

Tax Credits/R&D Grants

Lower Hurdles to Approval

Favorable Reimbursement

Orphan drugs have market exclusivity for 7 years in the U.S. & 10 years in the EU (regardless of patent status)

Orphan Drug Pricing

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Orphan Drug Companies- Precedent for Being Acquired

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Year Target Buyer

Upfront

Payment

($MM)

Total

Deal

Value

($MM)

Clinical

StageIndication(s)

2014 Lumena Shire $260 $260+ 2Cholestatic liver diseases, non-

alcoholic steatohepatitis

2013 Onyx Amgen $9,700 $9,700 MarketMultiple myeloma,

hepatocellular carcinoma

2012 Enobia Alexion $610 $1,080 2 Hypophosphatasia

2011 Genzyme Sanofi $20,100 $20,100 Market Various

2010 ZyStor BioMarin $22 $115 0 Pompe disease

2010 Aton Valent $318 $318 Market Ophthalmology

2009Swedish Orphan

Biovitrum $493 $493 Market Various

2008 Zymenex Shire $135 $135 2 Metachromatic leukodystrophy

XORTX Program Milestones

2015 2016

XORLO – Orphan 1: ADPKD

Phase II Phase III a

XORLO –Orphan 2: Hereditary Hyporuicemia

2017 2018

NDA

XRx®-108 – Treatment of Diabetic Nephropathy

2019

MFG. & FDA

PhII approval

2020 2021

Phase II Phase III a NDA

1st licensing or acquisition opportunity

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Orphan Development Path

FDA pre-IND meeting H1 2015

Manufacture of Drug and Dog PK results H1 2015

FDA Phase II approval H2 2015

Initiation of Phase II clinical study H2 2015

Quarterly update Phase II trial & DSMB review Intermittent

Completion of Phase II trial H1 2017

Topline reporting Phase II trial H2 2017

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Use of Proceeds:

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Manufacturing/Formulation $1,200,000

Regulatory FDA $600,000

Phase II clinical trials $3,800,000

G&A $1,250,000

Legals, accounting & agent’s fees $700,000

Total $7,500,000

The XORTX Corporate Highlights

1. Strong Management Team - experience in early drug development

to market approval, tailored to developing Oxypurinol through

Orphan & New Drug Application (NDA).

2. Numerous phase II clinical trials validate orphan rationale: Clinical

data has demonstrated that lowering serum uric on early-stage

hypertension, progressive chronic kidney disease, ADPKD can

improve clinical outcome.

3. Oxypurinol has well established effectiveness and safety profile.

4. Orphan Drugs = Lower development costs and faster time to market.

Orphan drugs also have 7 years of market exclusivity.

5. Precedent for companies focused on orphan diseases have been

acquired demonstrates market appetite for this therapeutic space

and validates the return on investment opportunity.

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Contact Information:

A drug development company focused on orphan diseases that have a uric acid

imbalance.

Dr. Allen Davidoff, XORTX Pharma Corp.

www.xortx.com

adavidoff@xortx.com1-403-607-2621

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Appendix I – ADPKD Clinical Evidence

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Hyperuricemia is Common in High-Risk ADPKD

In the ADPKD population prevalence of hyperuricemia estimated to be

48% and prevalence of Gout is estimated to be 24%. Errasti P, Et al., Autosomal-dominant

polycystic kidney disease:… Transplant Proc, 2003, 35(5)1717 & Mejias E, et al, Hyperuricemia, Gout and Autosomal Polycystic Kidney Disease,

Am J Med Sci 1989 297(3) 399

Hyperuricemia is associated with Earlier Onset of Hypertension, larger

kidney volume and increase ESRD. (Helal I, Nephrol Dial Transplant 28:380 ,2013)

Hypertension is present in half of all patients aged 24-30 years and all

patients who reach kidney failure. (Torres VE, et al., Autosomal Dominant Polycystic Kidney Disease, The

Lancet 369: 1287-1301,2007)

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Hyperuricemia and endothelial dysfunction precede hypertension in

ADPKD. (Kocygit I, et al., SUA and endothelial dysfunction in Autosomal Dominant Polycystic Kidney Disease, Nephron Clin Practice,

123: 157-164,2012)

Hyperuricemia is Common in High-Risk ADPKD

In the healthy population prevalence of hyperuricemia estimated to be

3.2% and prevalence of Gout is estimated to be 1.2%. Zhu Y- Prevalence of Gout and

Hyperuricemia NHANES-III-Atrhritis Rheumatism-63-10-3136-2011

In the ADPKD population prevalence of hyperuricemia estimated to be

48% and prevalence of Gout is estimated to be 24%. Errasti P, Et al., Autosomal-dominant

polycystic kidney disease:… Transplant Proc, 2003, 35(5)1717 & Mejias E, et al, Hyperuricemia, Gout and Autosomal Polycystic Kidney Disease,

Am J Med Sci 1989 297(3) 399

Hyperuricemia is associated with Earlier Onset of Hypertension, larger

kidney volume and increase ESRD. (Helal I, Nephrol Dial Transplant 28:380 ,2013)

Hypertension is present in half of all patients aged 24-30 years and all

patients who reach kidney failure. (Torres VE, et al., Autosomal Dominant Polycystic Kidney Disease, The

Lancet 369: 1287-1301,2007)

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Hyperuricemia and endothelial dysfunction precede hypertension in

ADPKD. (Kocygit I, et al., SUA and endothelial dysfunction in Autosomal Dominant Polycystic Kidney Disease, Nephron Clin Practice,

123: 157-164,2012)

(Han, M, et al. Hyperuricemia & Deterioration of Renal Function in ADPKD,

BMC Nephrol 15:63-2014)(Goicoechea M, et al. Effect of Allopurinol in Chronic Kidney Disease Progression,

Clin j Am Nephrol 5:1388, 2014)

Effect of 100 mg/day -Allopurinol in Chronic Kidney Disease Progression

(Ritz E, et al. Uric Acid and Chronic Kidney Disease, Nephrol Dial Transplanation March 29, 2013)

ADPKD, Glomerular Filtration and Hyperuricemia

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ADPKD & Inflammation

Inflammation is evident in subjects at different stages of ADPKD and

more pronounced with severity of kidney disease. (Menon V, et al., Inflammation, Oxidative

Stress, and Insulin Resistance in Polycystic Kidney Disease, Clin J Am Soc Neprhol 6(1)7-13, 2011)

C-Reactive Protein, Il-6 were significantly higher in hypertensive ADPKD. (Menon V, et al., Inflammation, Oxidative Stress, and Insulin Resistance in Polycystic Kidney Disease, Clin J Am Soc Neprhol 6(1)7-13, 2011)

Urinary Monocyte Chemo-attractant Protein -1 excretion Is increased in

ADPKD. (Zheng D., et al Urinary excretion of MCP-1 in ADPKD., J Am Soc Nephrol, 14:2588, 2003)

TNF-a may mediate cyst growth and kidney volume expansion in

ADPKD. (Li X., et al., A TNF-a mediated pathway promoting autosomal dominant polycystic kidney disease., Nat Med 14:863, 2008 )

Uric acid stimulates the renin-angiotensin system, inhibits vascular nitric

oxide synthesis, and oxidative stress, which leads to up-regulation of

pro-inflammatory cytokines, renal interstitial inflammation and fibrosis. (Helal I,., SUA, kidney volume and progression in autosomal –dominant polycystic kidney disease, Nephrol Dial Transplant 28: 380, 2013 )

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Decreasing Uric Acid Normalizes Blood Pressure – A Second Phase II Trial Success

Randomized trial of 60 obese, pre-hypertensive adolescents, treated for 2

months to determine effect on blood pressure

Soletsky B. and Fieg D., Uric Acid Reduction Prehypertension in Obese Adolescents, Hypertension

60:1148: 2012

At 2 Months uric acid

lowering significantly

decreased:

Uric Acid: -2.4 mg/dL (p=0.0005)

SBP: -11.8 mmHg (p=0.0001)

DBP: - 9.6 mmHg (p=0.0002)

> 80% of individuals whose uric acid was

lowered blood pressure was also normalized.

Weight: -3.1 kg (p=0.039)(N.B. Placebo Corrected Differences Reported)

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(n=20;20;20)

Decreasing Uric Acid Improves Kidney Function(Proteinuria) Type 2 Diabetic Patients

Objective: Demonstrate the effect of uric acid lowering (low dose allopurinol – 100 mg/d for 4 months), on proteinuria in diabetic patients with nephropathy.

28Momeni A- Allopurinol on Protienuria Type 2 diabetes- 4- 128- 2010 Int J KidDis

Low Dose Allopurinol 100 mg/day for 4 months

(p=0.02)

(p=0.049)

Decreases Proteinuria significantly,compared to placebo control

(n=20;20)