Vittarthaa Life Sciences

Registered office:No. 66, 8th ‘A’ main, BTM layout 1st stage,Bangalore – 560029Karnataka, IndiaPhone: +91 80 26781424

Research Facility:Plot No. 29, 1st floor

Bommasandra Industrial Area,KIADB, Anekal Tq., Bangalore – 560099

Karnataka, IndiaPhone: +91 80 48527566

Contact:Dr. Yogananda Moolemath,

Mobile: +91 9740516025Skype: moolemath

Email: yogananda@vittarthaa.comwww.vittarthaa.com

Non-confidential Document In private circulation only

About us

Vittarthaa Life Sciences is a Drug Discovery and Development company focused onidentifying unmet clinical needs to develop pharmaceuticals molecules.

All Research program are based on integrated approach towards target-based discoverystrategies and phenotypic screening for end point evaluation. Focused on innovativeDiscovery and Development approaches for progressing molecules into market.

Dr. Moolemath received his PhD from Madras University, India with over 20 years ofResearch experience. Last assignment was in Preclinical Biology, Heading the preclinicalBiology at Connexios Life Sciences, Drug Discovery company for small molecule (NCEs). Hadbeen the part of 4 programs - Diabetes Type II, Liver Fibrosis, Obesity and Cardiovasculardiseases. Co-authored more than 10 research publications in peer-reviewed Journals.LinkedIn: www.linkedin.com/in/yogananda-moolemath-72ab4a22

Dr. Yogananda Moolemath,Director,

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Vittarthaa Life Sciences is developing Pharmaceutical Compound for the treatment ofUrea Cycle Disorder (UCD) and Gout.

Pharmaceutical compounds are designed, patented and ready for assessment inpreclinical development (DMPK*, POC** and safety).

We are open for discussion on Drug Development strategies and Business Models fordevelopment of Patented Pharmaceuticals Compounds for Urea Cycle Disorder (UCD) andGout.

Proposal

* Drug Metabolism and Pharmacokinetics; ** proof-of-concept

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Patent No.: US 9,475,747 B1

Date of Patent: Oct. 25, 2016

Proposed Pharmaceutical Compounds are patent protected

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Urea Cycle Disorder (UCD)

Overview

• Genetic deficiency in 1 of 8 enzymes/ transporters that constitute the urea cycle

• Liver is unable to properly convert ammonia to urea to be eliminated from the body as urine

− Elevated levels of ammoniain the blood can be toxic

• Severity varies greatly depending on subtype, full or partial deficiency and other factors

•Wide range of symptoms− Results in frequent

misdiagnoses

• Excessively high levels of ammonia can result in a hyperammonemic crises

− May result in irreversible brain damage, coma or death

• Symptoms typically first appear in infants, but can also present later in life

• Blood ammonia level and other tests utilized

• New born screening detects 3 of the 8 subtypes

Symptoms and Diagnosis

• Dietary protein restriction

• Dietary supplements− Amino acids− Sodium benzoate

• Phenylbutyric acid (PBA)medications, also known asammonia scavengers− RAVICTI: oral liquid form forchronic use− BUPHENYL: tablet or powderform for chronic use− AMMONUL®: IV form foracute hospital use

Management

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Other Drugs for Urea Cycle Disorder

• Ammonul

• Buphenyl

• calcium acetate

• Calphron

• Carbaglu

• Carglumic acid

• Eliphos

• Glycerol phenylbutyrate

• phenylbutyrate sodium

• PhosLo

• Phoslyra

• Ravicti

• Sodium benzoate/sodium

phenylacetate

• Sodium phenylbutyrate

Drugs Marketing

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Epidemiology of UCD in general population

Reference: Mol Genet Metab. 2013 ; 110(0): 179–180. doi:10.1016/j.ymgme.2013.07.008.

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Proposed Pharmaceutical Compounds for UCD

Compound code Pharmaceutical Compound

V-UCD-003

2 moles of Phenylbutyrate

+ 1 mole of EPA

V-UCD-006

1 mole of phenylbutyrate

+ 2 moles of EPA

Phenylbutyrate

Eicosapentaenoic acid (EPA)

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Overview

• Similar to arthritis caused by deposition of uric acid crystals in the joints tendons, and surrounding tissues

• Overproduction of uric acid or produce a normal amount, but kidneys can’t process it efficiently and an excess of uric acid builds up.

• Uric acid form needle-like crystals in a joint and cause sudden, severe episodes of pain, tenderness, redness, warmth and swelling

• Asymptomatic hyperuricemia- rate crystals are being deposited in tissue and causing slight damage

• Acute gout- urate crystals that have been deposited suddenly cause acute inflammation and intense pain

• Chronic tophaceous gout- final stage is the most debilitating form of the disease, where permanent damage may have occurred in the joints and the kidneys

Symptoms and Diagnosis

Gout

• Lifestyle and dietary guidelines

• To avoid foods that are high in purines

- Reducing Uric Acid Levels• Febuxostat decreases the amount

of uric acid made in the body

• Allopurinol reduces the production of uric acid

• Probenecid acts on the kidneys to help the body eliminate uric acid

• Lesinurad is an oral drug that helps the body eliminate uric acid

• Nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine or corticosteroids

Management

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Epidemiology of gout in general population

Reference: Cea Soriano et al. Arthritis Research & Therapy 2011, 13:R39http://arthritis-research.com/content/13/2/R39

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Proposed Pharmaceutical Compounds for Gout

Compound code Pharmaceutical Compound

V-GOU-005

2 moles of Febuxostat

+ 1 mole of EPA

Eicosapentaenoic acid (EPA)

Febuxostat

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Strong Revenue Base for Future Growth

Historical Net Revenues* ($ in millions)

0

20

40

60

80

100

120

Q1 2013 Q1 2014 Q1 2015 Q1 2016

1

14

24

66

BUPHENYL RAVICTI

Number of cases

• Patients born with genetic defect of urea synthesis 1 in every 8,500 to 25,000 new borns.

• The incidence of gout per 1,000 person-years was 2.68 (4.42 in men and 1.32 in women) and increases with average age of 50-60 years of age.

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* Data for Buphenyl and Ravicti sales from Horizon Pharma plc

Attractive Fit with Orphan Disease Business

• Patients born with genetic defect of urea synthesis

• Contemporary incidence of gout globally remains substantial due to lifestyle and dietary habits

• Ultra‐orphan disease with an estimated U.S. prevalence of about 2,000 cases and incidence of about 1 in every 8,500 to 25,000 new borns

• Europe and Japan prevalence of about 2,000 cases total

• Variable age of diagnosis(new born to adulthood),with neurological deficits ranging from mild mental retardation to coma and death

• In general, with prompt diagnosis and careful management involving dietary restriction, alternative pathway therapy can lead to good clinical outcomes

• Outcomes are poor for untreated, severely affected individuals

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Thanks…

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Contact:Dr. Yogananda Moolemath,

Mobile: +91 9740516025Skype: moolemath

Email: yogananda@vittarthaa.comwww.vittarthaa.com