OTCQB: RASP · 2019. 6. 21. · Rasna Therapeutics Inc. 6. RASNA LEADERSHIP TEAM. MANAGEMENT. Tiziano Lazzaretti. Chief Financial Officer • Previously Group Finance Director at

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OTC

QB:

RAS

P

NEW PARADIGMS FOR THE TREATMENT OF REFRACTORY BLOOD CANCERSINVESTOR PRESENTATION | 2019

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DISCLAIMERRasna Therapeutics (the “Company”)

The content of this presentation has been prepared for the purpose of providing general information about, and an overview of, the Company and its business. It is notintended to be a complete review of all matters concerning the Company. Whilst the Company has taken all reasonable care to ensure the information and facts contained inthis presentation are accurate and up-to-date, it does not make any representation or warranty, express or implied as to the accuracy or completeness of any informationincluded in this presentation. The Company does not accept liability for any loss arising directly or indirectly from the use of or reliance upon this presentation or information itcontains. The information in this presentation is subject to updating, completion, revision, further verification and amendment without notice.

This presentation does not constitute or form part of any offer for sale or solicitation of any offer to buy or subscribe for any securities including ordinary shares in theCompany nor does it constitute an invitation or inducement to engage in investment activity in the ordinary shares of the Company. It does not purport to contain informationthat shall form the basis of, or be relied upon in making such investment decisions. If you require any advice, please consult with a professional financial adviser. Allinvestments are subject to risk. The value of securities may go down as well as up. Past performance cannot be relied on as a guide for future performance.

This presentation may contain certain forward-looking statements concerning the financial condition, results of operations and businesses of the Company. All statementsother than statements of historical fact are, or may be deemed to be, forward-looking statements. Forward-looking statements are statements of future expectations that arebased on management’s current expectations and assumptions and involve known and unknown risks and uncertainties that could cause actual results, performance or eventsto differ materially from those expressed or implied in these statements. All forward-looking statements contained in this presentation are expressly qualified in their entiretyby the cautionary statements contained or referred to in this section. You should not place undue reliance on forward-looking statements. Each forward-looking statementspeaks only as of the date of this presentation. The Company does not undertake any obligation to publicly update or revise any forward-looking statement as a result of newinformation, future events or other information. In light of these risks, results could differ materially from those stated, implied or inferred from the forward-lookingstatements contained in this presentation.

This presentation should not be copied or distributed by recipients and, in particular, should not be distributed by any means including electronic transmission, to persons withaddresses in the United States of America, Canada, Australia, Republic of Ireland, South Africa, Japan or any other jurisdiction which prohibits the same except in compliancewith applicable securities laws. Any such distribution contrary to the above could result in a violation of the laws of such countries. This presentation is confidential and is beingsupplied to you solely for your information and may not be reproduced, re-distributed or passed to any other person or published in whole or in part for any purpose. Byaccepting receipt of this presentation, you agree to be bound by the limitations and restrictions set out above.

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CONTENTS

I. Introduction to Rasna

II. Clinical Strategy: Targeting Master Regulators of Leukemia

III. Development Pipeline

– RASP-101; Nanoparticle based actinomycin-D formulation

– RASP-201; Lysine-specific demethylase 1 (LSD1) inhibitor

– RASP-301; NPM1 inhibitor

IV. Contact Details

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I. INTRODUCTION TO RASNA

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INTRODUCTION

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• Formed in 2013, OTCQB:RASP in 2016 through reverse merger.

• Focused on novel targets to address the high unmet need that exists for AML and other life-threatening blood cancers.

• 5-year survival rate for AML is only 25%, with high risk of relapse and each round of treatment having serious side effects thatdrive long term survival in aged patients to almost zero - untreated AML may be fatal within weeks to months.

• Expert team including Professor Brunangelo Falini, a world-leading pioneer in NPM1 research

• Three druggable intervention points with potential to improve safety and efficacy of current AML combination therapies

1. Actinomycin-D (Act-D) -- established anticancer therapeutic, for which Rasna now has promising early clinical results showingcomplete remission in 40% of AML patients (N=10)

2. First in class NCE for NPM1 Currently at the pre-clinical stage, this small molecule has the potential to treat refractory AMLwith reduced toxicity.

3. Novel inhibitors of LSD-1, a pathway that blocks differentiation and confers a poor prognosis in AML. LSD-1 has beenidentified as a druggable target by GSK and Oryzon who are also developing their own compounds to inhibit this importanttarget.

• Lean and virtual R&D business model using highly experienced teams of experts for each business function to maximize valueaccretion and focus capital on the drug development and discovery processes.

• Robust protection and substantial freedom to operate in this space with extensive IP covering composition of matter, broadmethods of use across multiple clinical indications, specific manufacturing processes and biomarkers for patientstratification to provide

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RASNA LEADERSHIP TEAMM

ANAG

EMEN

T

Tiziano LazzarettiChief Financial Officer

• Previously Group Finance Director at Pharmentis –Teva Ratiopharm spin off

• Executive Director at Alliance Boots, Snia, Accenture and FIAT Group

• MBA, Bocconi University, Milan

• Corporate Finance, London Business School. BSc Accounting and Finance

• Co-founder , EVP & CSO Synergy Pharmaceuticals, NASDAQ listed biotech

• VP, Callisto Pharmaceuticals

• Group Leader, Monsanto Co.

• Ph.D. Biochemistry

• MBA, University of Missouri

Dr Kunwar ShailubhaiChief Executive Officer

SCIE

NTI

FIC

ADVI

SORS Professor

Roberto Pellicciari

• President and CEO of TES Pharma

• Co-founder and Head of Medicinal Chemistry at Intercept Pharmaceuticals,

• International reputation in molecular design, synthesis, mechanism of reaction, and modeling with over 300 publications in international journals and 40 patents

Professor Brunangelo Falini

• Director of the Hematology institute and the Bone Marrow Transplant unit at the University of Perugia

• World leading expert in lymphoma and acute leukemia and discoverer of the significance of the NPM1 gene lesion in AML

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RASNA BOARDBO

ARD

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• Senior executive, managerial and scientific roles in the pharmaceutical and biotechnology sector

• Peptide Therapeutics, Medivir UK, AstexTechnology, C4T S.C.ar.l., Siena Biotech and IRBM Science Park

Dr Alessandro PadovaChairman

• Retired CPA

• Former Chief Financial Officer of Accelerated Technologies, Inc.

• Member of the Board of Synergy Pharmaceuticals Inc., since July 2008 and ContraVir Pharmaceuticals, Inc. since Dec 2013

• Co-founder , EVP & CSO Synergy Pharmaceuticals, NASDAQ listed biotech

• VP, Callisto Pharmaceuticals

• Group Leader, Monsanto Co.

• Ph.D. Biochemistry

• MBA, University of Missouri

• CEO of Realm Therapeutics, since 2015

• Formerly Chief Operating Officer of Intercept Pharmaceuticals, Inc. and President of Moksha8 Pharmaceuticals, Inc.

John BrancaccioDirector

Dr Kunwar ShailubhaiCEODirector

John Alex MartinDirector

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“LEUKEMIA” DESCRIBES A BROAD GROUP OF CANCERS WHERE BLOOD CELLS PROLIFERATE ABNORMALLY

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Leukemia sub-types

Lymphocytic Myelogenous

Acute44% of cases worldwide

“ALL” “AML”

• Most common among children

• 70.1% five-year survival

• More common in adults, especially men

• 26% five-year survival

Chronic43% of cases worldwide

“CLL” “CML”

• Most common in adults above 55 years old, especially men

• 84.8% five-year survival

• Mainly in adults and rare in children

• 63.2% five-yearsurvival

What is leukemia?

• Fifth most common cause of cancer death in men and sixth most common cause of cancer death in women, with an estimated 62,130 new diagnoses and 24,500 deaths in 2017 (USA)*

• Caused DNA mutations in bone marrow stem cells leading to abnormal proliferation of white blood cells (leukocytes)

• Mutations may occur spontaneously or as a result of exposure to ionizing radiation or carcinogens which have been linked with an increased incidence of chronic lymphocytic leukemia (CLL)

• Leukemia cells overwhelm the bone marrow, enter the bloodstream and invade lymph nodes, spleen, liver, and CNS

• Immune system compromise and some virus infections, e.g. human T-cell leukemia virus I (HTLV-1), genetic predisposition, cigarette smoking, and some therapeutic drugs are also implicated in the etiology of leukemia

Source: Leukemia & Lymphoma Society, 2016, US data; an additional 17% of leukemias fall outside of this classification matrix

13%of cases

30%of cases

28%of cases

13%of cases

* American Cancer Society. Cancer Facts & Figures 2017

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BILLION DOLLAR ADDRESSABLE MARKET FOR AML

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Frequency of Leukemia (2014)

Type Total Male Female

ALL Acute Lymphoblastic Leukemia 6,020 3,140 2,880

CLL Chronic Lymphocytic Leukemia 15,720 9,100 6,620

AML Acute Myeloid Leukemia 18,860 11,530 7,330

CML Chronic Myeloid Leukemia 5,980 3,130 2,850

Other Leukemia 5,800 3,200 2,600

Total Estimated New Cases per Year 52,380 30,100 22,280

Cost of treatment in the USInduction of remission1 cycle $56,802

Consolidation2 cycles $113,176

Best supportive care (BSC) Chemotherapy Transplantation

Complete remissionoutpatient clinic

$14,8616 cycles

$14,8616 cycles

$2,477

Transplantation $154,739

Relapse $ 2,477 (BSC) $56,588 chemo 1 cycle

Total $187,315 $241,427 $327,194

USA62%

Rest of World38%

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Discovery Lead Optimisation Pre-Clinical IND Phase I Phase II Phase

III NDA

Actinomycin-DAML

RASP-101(NP-Act D)**

LSD-1 InhibitorAML

NPM1 InhibitorAML

Phase IIa study showed 44% clinical remission but dose-limiting toxicity was observedIP covering field of use for AML

Reversible inhibitor

ANTAGONIST

IND expected

2019

Lead candidate expected

2019

Formulation to be

improved*

Controlled-released formulation IP covering composition-of matter and use

IND expected

2019

FIRST-IN-CLASS

CANDIDATE FOR 505 (B)(2)

REGULATORYPATHWAY

* Rasna’s strategy is to reformulate actinomycin D for submission via the 505(b)(2) regulatory pathway for approval**Nanoparticle-based formulation of actinomycin D

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II. CLINICAL STRATEGY TARGETING MASTER REGULATORS OF LEUKEMIA

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• LSD1 is critically involved in stem cell phenotype

• Multiple action at stem cell and non-stem cell level

• Pre-clinical results suggest that LSD-1 is one of the most potent controllers of “stemness” in cancer cells

• NPM1 mutation common to a third of AML cases leads to dysregulated protein trafficking of key tumor associated proteins

• NPM1 dysfunction is also implicated in metastatic cancers of the breast, ovaries, prostate, thyroid, lung, liver, bladder and colorectal cancer

OUR STRATEGY: TARGET LEUKAEMIA MASTER REGULATORS

NPM1Nucleophosmin

Cell survival

Genomic stability

Ribosome biogenesis

Histone function

Key role in mitosis

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LSD1Lysine-specific

histone demethylase 1A

Histone acetylation

Cell differentiation

Cell proliferation

Cell survival

Cancer metastasis

Twin master regulator approaches

Associated roles

Associated roles

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NPM1 PLAYS A KEY ROLE IN THE STRESS RESPONSE CASCADE WITHIN THE NUCLEOLUS, TRIGGERING PROTEIN TRANSLOCATION

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Shown clearly as nucleolar stressors such as Actinomycin-D result in morphological changes of the nucleolus, imaged through staining

RibosomalDNA

RNA Polymerase I (Pol I)

TRANSCRIPTION

RibosomalRNA

Actinomycin-D‘nucleolar stressor’

NPM1 (Nucleophosmin) – GreenDAPI - Nuclear stain - Blue

NPM (green)Nucleolin (red)

Nucleoplasm

Nucleolus

NPM1

nucleolar stressresponse

Hdm2p53 p53 p53p53

p53 p53

Hdm2p53

NPM1

L5 L11

5S rRNA

apoptosisnucleoplasm p53 activation

Representation of human cell nucleolus

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RISING LEVELS OF MUTATED NPM1 PREDICT AML RELAPSE IN PATIENTS BEFORE PRESENTATION OF HEMATOLOGICAL CRISIS

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• 2016 New England Journal of Medicine study measured the status of mutated NPM1 versus AML relapse

• Mutated NPM1 preceded the onset of relapse. Rising expression levels in the bone marrow and peripheral blood is highly correlated with impending leukaemic relapse.

P.B. – Peripheral BloodB.M. – Bone marrow biopsy

Ivey er al. New England Journal of Medicine 2016; 374:422-433

Progression to AML relapse

NPM1 mutation is found in 35% of AML

• NPM1 mutations are never homozygous• NPM1 is essential for life – NPM1 knockout mice non-viable

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NPM1 MEDIATES SENSITIVITY TO DRUGS THAT ACT IN THE NUCLEOLUS: NEW THERAPEUTIC OPTIONS FOR AML

• Mutation of a single NPM allele results in translocatation of NPM1 to the cytoplasm and depletes the nucleolus of this key mediator

• Lack of nucleolar NPM1 affects response to therapy. NPM mutants fail to protect cells and render them more susceptible to chemotherapy-induced high-level genotoxicstress

• Actinomycin D, not normally used as an AML therapy is a nucleolar stressor with manageable side effects

• Our hypothesis is that in clinical cases where NPM1 is mutated and nucleolar NPM1 is depleted we would find greatly increased sensitivity to Actinomycin D

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Falini B, Martelli MP Blood 2011;118:2936-2938

Vulnerability of the nucleolus is NPM1 dependent

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III. DEVELOPMENT PIPELINE

i. Nanoparticle based actinomycin D formulationii. Lysine-specific demethylase 1 (LSD1) inhibitoriii. NPM1 inhibitor

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Actinomycin D

Existing antibiotic and anticancer agent (WHOEssential Medicine List) isolated from Streptomyces soil bacteria

Mechanism Indications Opportunity Competitive Edge IP/Ownership

• NPM1 mutants show more nucleolar instability and apoptosis

• Act D contributes to apoptosis through inhibition of repair.

• Interferes with DNA replication and RNA transcription through intercalation between adjacent G-C DNA base pairs

• AML

• NPM1 dysfunction is also implicated in metastatic cancers of the breast, ovaries, prostate,thyroid, lung, liver,bladder and colorectal cancer

• Act D is a potent and efficacious anti-cancer agent.

• Dose limiting toxicities lead to a narrow therapeutic index.

• Controlled release nanoparticle formulations may provide a more favorable drug exposure and dose regiment.

• Novel application to leukemias

• Nanoparticle formulation of Act D to control specific dose range withdefined range of Cmaxand AUC values. The controlled Cmax and AUC are anticipated to produce efficacy with reduced toxicities

• Two provisional patent applications filed1. Use of Act D for AML

treatment

2. Formulation patentcovers composition-of-matter and combination of Act D with other drugs. Formulation of Act D with PLA/PLGA nanoparticles is novel and patentable

ACTINOMYCIN D (DACTINOMYCIN)

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PROOF OF CONCEPT: CLINICAL THERAPY WITH ACTINOMYCIN D IS ASSOCIATED WITH REDUCED NPM1 EXPRESSION IN TISSUE BIOPSIES

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Source: Falini B, Brunetti L and Martelli MP. N Engl J Med 2015;373:1180-2

+ 27 months

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RECENT PRESS RELEASE

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Rasna Therapeutics, Inc. Announces Follow Up Phase II Clinical Data Confirming Efficacy of Actinomycin D in Patients with NPM1-mutated Acute Myeloid Leukemia

January 13, 2018

Treatment with Actinomycin D (Act D) as a single drug achieved complete remission in 4 out of 9 evaluable patients (44.4%)

Treatment with Act D at 15 µg/kg/day for 5 days every 28 days (which defines one cycle) was well tolerated with major toxicity limited only to oral mucositis

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STRATEGY FOR FORMULATION OF ACTINOMYCIN

PLA or PLGA

Act D

PEG or Lipids

• Stable PLA/PLGA/Polymeric NP. Composition-of-matter patent submitted

• Act D loading for once a week or once in two weeks IV

• Act D release controlled for Cmax range to minimize toxicity

• Act D release extended to achieve appropriate AUC value

• Loaded NP will be evaluated for in vitro release of Act D- Simulated buffer - Plasma

• PK study is rats with formulated Act D to ensure Cmax and AUC

• Toxicity study in rats for side by side comparison with free Act D and formulated NP-Act D (RASP-101)

• Efficacy study in AML model for side by side comparison with free Act D and formulated NP-Act D

• GMP manufacturing and FDA mandated stability

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III. DEVELOPMENT PIPELINE

i. Nanoparticle based actinomycin D formulationii. Lysine-specific demethylase 1 (LSD1) inhibitoriii. NPM1 inhibitor

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DDP-38003

Orally available small molecule that can restore sensitivity to all-trans retinoic acid (ATRA)

Mechanism Indications Opportunity Competitive Edge IP/Ownership

• Reverses the ‘stem cell’ phenotype in AML

• LSD1 demethylateshistone H3 and regulates chromatin/epigenomestructure

• High LSD1 expression blocks differentiation, a poor prognosis in AML

• Inhibition of LSD1 reactivates the retinoic acid receptor pathway in AML

• AML

• MLL-rearranged leukemias

• Small cell lung cancer

• Other solid tumors

• A first in class oral inhibitor of LSD-1

• All-trans retinoic acid (ATRA) is well tolerated but only efficacious in a small percentage of AML cases

• Pre-clinical data suggests LSD1 inhibition has the potential to render most AML responsive to retinoic acid

• Our inhibitor of LSD-1 is the only orally bioavailable inhibitor with fewer hematological side-effects than the Oryzon/Roche compound.

• Pre-clinical data suggests LSD-1 inhibitor is more efficacious vs. GSK or Oryzon/Roche compounds

• Primary patents filed

• Exclusive worldwide license from IOM to use the IPR and know-how arising out of the Research Agreement and LSD-1 patent to research, develop, manufacture, market, use and sell products

LSD-1 (KDM1A) INHIBITOR

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Perc

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urvi

val

Days after blast injection

VehiclesGSK 28799552 IVRASNA DDP38003 Oral

TREATMENT STARTED AT

+14 DAYS

28.5 41 79MEDIAN

SURVIVAL

SURVIVAL IN MURINE MLL-AF9 MODEL SIGNIFICANTLY IMPROVED VS. GSK COMPOUND

GSK TREATMENT PER PUBLISHED

PROTOCOL

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SURVIVAL IN MURINE MLL-AF9 MODEL SIGNIFICANTLY IMPROVED VS. STANDARD CHEMOTHERAPY OR ROCHE/ORYZON COMPOUND

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0 5 10 15 20 25 30 35 40 45 50 55 60 65

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Vehicle OralVehicle IVAraC Dox IVRoche/Oryzon IVRASNA DDP38003 Oral

TREATMENT STARTED AT +14

DAYS

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nc. i. Nanoparticle based actinomycin D formulation

ii. Lysine-specific demethylase 1 (LSD1) inhibitoriii. NPM1 inhibitor

III. DEVELOPMENT PIPELINE

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NPM1 Inhibitor

An orally available small molecule with the potential to treat refractory AML with reduced toxicity

Mechanism Indications Opportunity Competitive Edge IP/Ownership

• NPM1 mutation common to a third of AML cases leads to dysregulated protein trafficking of key tumor associated proteins

• Rising mutant NPM1 levels are associated with imminent relapse of AML

• Targeting NPM1 induces differentiation and loss of survival of human AML cells with mutant NPM1

• AML

• NPM1 dysfunction is also implicated in metastatic cancers of the breast, ovaries, prostate,thyroid, lung, liver,bladder and colorectal cancer

• Rasna Therapeutics has obtained a license to first in class compounds targeted to NPM1 developed by Professor Pellicciari and his group at TES Pharma (TES). Several compounds are being evaluated for selection as leads

• The Rasna team includes Professor Brunangelo Falini,recognized world expert in NPM1 and AML.

• Our NPM1 inhibitors are designed to be first in class drugs for this target that can be orally dosed with minimal side-effects with good solubility and PK

• Rasna has an exclusive worldwide license to use the IPR and know-how arising out of the Research Agreement with TES Pharma to research, develop, manufacture, market, use and sell products.

INHIBITOR OF NPM1

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NPM1 INHIBITOR ACTIVITY IS NPM1 EXPRESSION DEPENDENT

• No cytotoxic activity is observed on WI-38 cells, human diploid fibroblasts• WI-38 cells over-expressing NPM1, are sensitive to NPM1 inhibitors• Viability decreases with dose, in a dose-dependent manner• Conversely, the same cell lines are equally sensitive to the cytotoxic effects of tamoxifen

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0%10%20%30%40%50%60%70%80%90%

100%

0 2000 4000 6000 8000 10000

% v

iabi

lity

WI-38 control

WI-38 NPM-1 txf

0%10%20%30%40%50%60%70%80%90%

100%

0 1000 2000 3000

% v

iabi

lity

Tamoxifen cytotoxicityNPM1 inhibitor cytotoxicity

Increasing dose Increasing dose

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V. CONTACT DETAILS

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KEY CONTACT INFORMATION

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For more information please see: http://www.rasna.com/Investor_Relations.html

Stock Transfer Agent

Philadelphia Stock Transfer, Inc.2320 Haverford Rd.Suite 230Ardmore, PA 19003

Accounting/Auditing

Marcum, LLP750 Third AvenueNew YorkNY, 10017

Legal Counsel

Sheppard, Mullin, Richter & Hampton LLP30 Rockefeller PlazaNew YorkNY, 10112-0015

Additional InformationRASNA THERAPEUTICS

Rasna Therapeutics Inc.

US Office

420 Lexington Avenue, Suite 2525

New York, NY 10170

Tel.: +1 (646) 396-4080

E-mail: [email protected]

UK Office

55 Park Lane

London W1K 1NA

Tel.: +44 (0) 207 290 2472

Reporting Status U.S. Reporting: SEC Reporting

Audited Financials Audited

Latest Report March 31, 2018 10-Q

CIK 0001582249

Fiscal Year End 9/30

OTC Marketplace OTCQB

SIC - Industry Classification

2834 -Pharmaceutical preparations

Incorporated In: NV, USA

Year of Inc. 2012

Authorized Shares 200,000,000

Outstanding Shares 68,908,003

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THANK YOU

For more information please contact us

E-mail: [email protected] | Tel: +1 (646) 396-4080