Non-confidential Corporate Presentation

January 2022

UR1 Therapeutics, Inc.

Novel URAT1 Inhibitor with Established Long-term Efficacy and

Safety for the Treatment of Gout and Diabetic CKD

Forward Looking Statements

UR1 Therapeutics, Inc. is a subsidiary of Fortress Biotech, Inc.

Some statements in this presentation that are not descriptions of fact may be forward-looking statements, for which

we and our majority-owned parent company Fortress Biotech claim the protection of the safe harbor for forward-

looking statements contained in the Private Securities Litigation Reform Act of 1995. Such statements include, but

are not limited to, any statements relating to our growth strategy, products and product development programs.

Forward-looking statements are based on management’s current expectations and are subject to risks and

uncertainties that could negatively affect our business, operating results, and financial condition. Factors that could

cause actual results to differ materially from those currently anticipated include: risks related to our growth strategy;

risks relating to the results of research and development activities; our ability to obtain, perform under and maintain

financing and strategic agreements and relationships; uncertainties relating to preclinical and clinical testing; our

dependence on third party suppliers; our ability to attract, integrate, and retain key personnel; the early stage of

products under development; our need for and continued access to additional funds; government regulation; patent

and intellectual property matters; competition as well as other risks described in the Securities and Exchange

Commission filings of our parent, Fortress Biotech, Inc. We expressly disclaim any obligation or undertaking to

release publicly any updates or revisions to any forward looking statements contained herein to reflect any change in

our expectations or any changes in events, conditions or circumstances on which any such statement is based,

except as may be required by law. The information contained herein is intended to be reviewed in its totality, and any

stipulations, conditions or provisos that apply to a given piece of information in one part of this presentation should

be read as applying mutatis mutandis to every other instance of such information appearing herein.

Executive Summary

• There is significant unmet need in the management of gout

• URAT1 inhibition appears to be an underserved intervention path

• Existing URAT1 inhibitors have compound-specific safety issues

• Dotinurad appears to be the best-in-class URAT1 inhibitor

• Tested in >1000 Japanese subjects and approved in Japan

• Eisai licensed the rights for China and 5 Southeast Asian countries

• Dotinurad is materially de-risked

• Clinical data shows excellent safety profile and efficacy

• The clinical programs include treating gout, severe gout and CKD

• Strong IP position

Management and Advisory Board

Paul Brooke

Executive Chairman

• Chairman Emeritus of the Board of Caelum Biosciences, acquired by AstraZeneca in Oct 2021

• Founder and former Managing Partner of venBio, a pharmaceutical investment company

• Former global head of healthcare research and strategy at Morgan Stanley

Lindsay Rosenwald, MD

Director

• Currently also Chairman, President, and CEO at Fortress Biotech (NASDAQ: FBIO)

• Previously Founder/Board Member of multiple biotech companies: Cougar Biotechnology (acquired by JNJ), Chelsea

Therapeutics (acquired by Lundbeck), Indevus Pharma (acquired by Endo), Biocryst, Keryx, CorMedix, Ziopharm

Raymond Zheng, PhD

Chief Executive Officer

• Experienced Biotech Entrepreneur with combined 20+ years of experience in drug discovery and development

• Previously held multiple positions of business development at FortressBiotech, Agenus, Harvard Medical School

• Received PhD from University of California, Riverside, then completed research fellowship at Harvard Medical School

• Trained in clinical research, patent law, and expecting MBA of Pharmaceutical Management from Rutgers University

Scott Baumgartner, MD

Interim Chief Medical Officer

• Experienced clinical development and medical affairs expert

• Previously VP of Medical Affairs at AstraZeneca/Ardea Biosciences and Amgen

• Experience in the clinical development and post-launch activities of Lesinurad and Verinurad

• Received medical degree from University of Washington; has practiced rheumatology for ~20 years

Dr. Robert Terkeltaub, MD

University of California, San Diego

Chief of Rheumatology

• Professor of Medicine, UCSD, and Section Chief of Rheumatology at the VA Medical Center in San Diego

• Associate Editor of Arthritis and Rheumatism, and serves on numerous NIH Study Sections in arthritis

• Graduate of McGill University, where he completed his medicine residency and rheumatology fellowship

Dr. Michael Pillinger, MD

New York University

Chief of Rheumatology

• Chief of Rheumatology at VA NY Harbor Healthcare System

• Professor of Medicine at NYC Grossman School of Medicine

• Received the medical degree from NYU School of Medicine; has been in practice for more than 20 years

Dr. Lee Simon, MD

Consultant

• FDA's Division Director of Analgesic, Anti-inflammatory and Ophthalmologic Drug Products (2001-2003)

• Worked, for 12 years, as a NIH funded investigator and has served two terms on the Board of Directors of the

American College of Rheumatology (ACR)

• Served as Chair of Education for the ACR and the National Arthritis Foundation

Executive Management

Scientific Advisory Board

Gout Pathophysiology

o Elevated serum uric acid

• sUA > 6mg/dL

• Due to sUA over-production

and/or inadequate clearance

o A silent risk factor

• Often asymptomatic

• Associated with gout, gouty

nephropathy and nephrolithiasis

o Urate crystal deposition

• sUA solubility is limited ~ 7mg/dL

• sUA saturation may lead to crystal

deposition in tissue, especially in

the synovial fluid

o Gout flare (1-3 /yr)

• Urate crystals elicit inflammation,

which is amplified and resolved

over days to weeks

o Chronic inflammation

• Sustained high sUA levels cause

repeated flares

o Tophi formation

• Repeated flares/resolutions form

granulomatous mass, known as

Tophi

• Tophi damage bones, tendons

and deform the joints

1 in 5 asymptomatic

individuals will

progress to gout

1 in 3 patients on ULT

is inadequately treated

and may progress

Hyperuricemia

• US Prevalence ~45 million

• No treatment recommended

Gout

• US Prevalence ~10 million

• 6~7 million receive urate lowering drugs

• 2~3 million are inadequate controlled

Chronic Refractory Gout

• US Prevalence ~100,000

• Only a few thousand receive Krystexxa

• Most have chronically uncontrolled urate

Hyperuricemic/Diabetic CKD

• CKD is a prevalent condition of progressive renal function loss, and eventually renal failure

• Classified into Stage 1-5 by albuminuria and eGFR status

• According to CDC, 15% of US adults (37 million) have CKD

• Gout and Diabetic CKD frequently co-exist

Stage 1 Stage 2 Stage 3 Stage 4 Stage 5

Prevalence

3.4% 3.8% 7.4% 0.4% 0.1%

# US pts

8.3 million 9.3 million 18.2 million 1 million 250,000

eGFR mL/min

>90 60-90 30-60 15-30 <15

Albuminuria

Persistent

>3mo

Persistent

>3mo

Treatment

Lifestyle

change

ACE inhibitor, ARBs, SGLT2

inhibitors

Dialysis, Kidney transplant

Target market

Gout

A highly prevalent, often poorly managed, progressive inflammatory condition of the joints

• Excessive serum uric acid forms crystal around the joints

• Crystals elicit inflammation causing severe pain and disability

• Gout flares may become more frequent and become chronic

• Tophi can damage joints and limit movement

• Urate-lowering therapy (ULT) is disease-modifying

• Millions of gout patients could benefit from a novel ULT

Tophaceous Gout

Gout

Uric acid

deposits

Xanthine Oxidase Inhibitors Uricosuric Agents Uricases

Three Drug Classes are Approved to Lower Urate

o Oral drugs to reduce UA up

stream synthesis

o Inhibits liver xanthine oxidase

o Oral drugs to enhance UA renal

excretion

o Inhibits renal UA transporters,

such as URAT1 and others

o IV infused biologics that degrade

UA into allantoin

URAT1

Reabsorbs

Secreted UA

Glomerulus

Input

Allantoin

Allopurinol

Febuxostat

Dotinurad

Probenecid

Pegloticase

70%** via Renal

excretion

**Reduced in gout pts

30% via GI

excretion

Urate crystal

deposits

Tophi

Inflammation, Intense pain

Allantoin

(renally

secreted)

NSAID

Colchicine

IL-1 antibody

Dotinurad

URAT1

Intervention Points of the Gout Treatment

Sugar

Nucleotides

Metabolites

Hypoxanthine

Purines

Xanthine

Oxidase

Xanthine

Oxidase

Allopurinol

Febuxostat

Uricase

Uric acid

–

Current FDA-approved ULTs

Allopurinol

XOI approved in 1966

Once or twice daily

50-800 mg/day

Annual cost in low hundreds dollars

Febuxostat

XOI approved in 2009

Once daily

40-80 mg/day

Annual cost approximately $1000

Probenecid

Uricosuric approved in 1951

2-4 times a day

500-1000 mg/day

Annual cost in low hundreds dollars

Krystexxa

Uricase approved in 2010

I.v. infusion every 2 weeks

Annual cost >$300,000

Drug

Profile

Benefits

Risks

Utilization

Long history of use

Modest efficacy

Hypersensitivity reaction (HLA 58:1)

Dose limited in renal impaired pts

Titration burden & discontinuation

Slightly higher efficacy than Allo

Not limited by renal impairment

Higher CV death rate than Allo** Extensive drug-drug interaction

Rapid reduction of sUA

Tophi reduction

Extensive side effects

~40% response rate

Inconvenience due to i.v. infusion

Mild efficacy

Often used as add-on

Workhorse drug despite limitations

line use unless contraindicated

Low patient adherence***

Used by 80% of treated patients

/ 2

line use after allopurinol

Usage plummeted after CV warning

Used by 10% of treated patients

Extremely low utilization due to

limited efficacy, burdensome dosing

and drug interactions

Used by 1% of treated patients

Extremely low utilization (<2000

pts) due to high price and

reimbursement constrains

** Febuxostat Compared with Allopurinol in Patients with Hyperuricemia and Gout. N Engl J Med 2005; 353:2450-2461

***Allopurinol adherence, persistence and patterns of use in individuals with diabetes and gout. Semin Arthritis Rheum. 2021 Sep 16;51(6):1162-1169

Dotinurad Overview

• Dotinurad is a next generation, potent, selective, oral, once-daily URAT1 antagonist

• Approved as a monotherapy to treat first line gout and hyperuricemia in Japan in 2020

• Allowed to treat patients with CKD3 per Japanese label

• Japanese approval is based on Dotinurad treatment of 1072 subjects in 17 clinical trials

• >500 patients received Dotinurad in three Phase 3 trials up to 58 weeks

4-6

• 4mg Dotinurad achieved 97.5% and 100% treatment success (sUA <6mg/dL) at 34

and 58

week

• Very well-tolerated

• No significant cardiovascular, hepatic or renal adverse events

4-6

• We licensed the rights (US, EU, UK & Canada) from Fuji Yakuhin

• Eisai licensed the rights for China & Southeastern Asian countries

1. https://pubmed.ncbi.nlm.nih.gov/31754883/

2. https://www.fujiyakuhin.co.jp/medicine/m-fujiyakuhin/

3. 2mg Dotinurad resulted in 89.1% and 91.3% sUA under target at 34

and 58

week.

4. https://pubmed.ncbi.nlm.nih.gov/31980978/

5. https://pubmed.ncbi.nlm.nih.gov/31970593/

6. https://pubmed.ncbi.nlm.nih.gov/31875931/

Dotinurad Japanese Label

• Indication: Gout, hyperuricemia

• The percent reduction in serum uric acid level from baseline was 46.73% at 2 mg/day and

54.92% at 4 mg/day after 34 weeks of treatment, and 47.17% at 2 mg/day and 57.35% at 4

mg/day after 58 weeks of treatment.**

• The proportion of subjects achieving a serum uric acid level of ≤6.0 mg/dL was 89.11% (229/257

subjects) at 2 mg/day and 97.50% (39/40 subjects) at 4 mg/day after 34 weeks of treatment, and

91.30% (84/92 subjects) at 2 mg/day and 100.00% (13/13 subjects) at 4 mg/day after 58 weeks

of treatment.**

• The incidence of adverse reactions was 21.8% (72/330 subjects). Common adverse reactions

were gouty arthritis (12.7%, 42/330 subjects), arthritis (2.1%, 7/330 subjects), and limb

discomfort (2.1%, 7/330 subjects).**

**Section 17.1.3 of the Label

Dotinurad has Demonstrated High Efficacy

• In Japanese Phase3 trials, >500 pts were treated up to 4mg /d and 58 weeks in duration

• 100% response achieved sUA <6mg/dL after 58

week.

• Lesinurad, the first approved URAT1 (now discontinued) had ~55% response after 52

week.

• Dotinurad reduced sUA to 4.5 mg/dL.

6mg/dL

Dotinurad Phase3 (Japan), n=326 Lesinurad Phase3 (US)

6mg/dL

Dotinurad has Demonstrated Safety in Chronic Use

• Dotinurad 58wk treatment showed no increased liver, cardiovascular or renal adverse event

Dotinurad Japanese Label

Dotinurad is Potentially the Best-in-Class Uricosuric

• Dotinurad was safe at the therapeutic dose that achieved 100% sUA under target

• Dotinurad has a slow onset

• Excessive renal passage of UA may be one of the reasons of Lesinurad’s renal toxicity

• Slow onset may reduce the risks of acute renal tox and flare

• Combining Dotinurad with XOI may further reduce renal toxicity risk

• Dotinurad is highly URAT1-selective which may explain its superior safety profile

Renal tox Renal safety

Hyperuricemic Chronic Kidney Disease

A highly prevalent condition of progressive renal function loss, and eventually renal failure

• Hyperuricemia is independently associated with diabetes and CKD

• Gout and CKD frequently co-exist

• Diabetic CKD is characterized by albuminuria and reduced renal function

• Historical data suggest urate-lowering therapy has renoprotective effects

• URAT1 antagonist has shown promise to reduce albuminuria in recent trials

• Millions of CKD patients could benefit from a Dotinurad-based ULT

Hyperuricemia is an Independent Risk Factor for CKD

• The majority of published epidemiology studies showed that elevated serum uric

acid concentration is independently associated with metabolic syndrome, type 2

diabetes

1,2

, and there is a likely causal relation

• Serum uric acid concentration was reported to independently predict incident

CKD in people with or without diabetes

4,5

• 30-50% gout patients have CKD2/3, and 24% adult CKD3 patients have gout

1. Asymptomatic Hyperuricemia Without Comorbidities Predicts Cardiometabolic Diseases. Kuwabara M. et. al., Hypertension. 2017;69:1036–1044

2. Serum uric acid and the risk of cardiovascular and renal disease. Borghi C. et. al., Journal of Hypertension: September 2015 - Vol 33 - Issue 9 - p 1729-1741

3. Uric Acid and the Origins of Hypertension. Feig D. et. al. The Journal of Pediatrics. May 2013 Vol 162, Issue 5,, Pages 896-902

4. Increased Serum Sodium and Serum Osmolarity Are Independent Risk Factors for Developing Chronic Kidney Disease; 5 Year Cohort Study. Kuwabara M. et. al. PLOS ONE. 2017.

5. Uric acid and chronic kidney disease: which is chasing which? Nephrology Dialysis and Transplant. 2013. Vol. 28, Issue 9, Pg 2221–2228

6. Management of Gout and Hyperuricemia in CKD. Vargas-Santos A. and Neogi T. Am J Kidney Dis. 70(3):422-439

Product Positioning

Dotinurad is Designed to Fulfill Unmet Needs in US/EU Markets

• Potentially superior efficacy than existing options

• Benign monotherapy safety profile demonstrated in multiple Ph3 trials in Japan

• Convenient dosing

• Improving adherence

• Applicable to different disease segments

• Potential to transform the standard-of-care for gout and hyperuricemic CKD

Summary of Dotinurad Opportunity

• Millions of gout and CKD patients represent a significant potential unmet market need

• Dotinurad products are designed to offer safe, effective and convenient alternative treatments

• Approval in Japan informs regulatory pathway

• Strong IP position