Corporate PresentationMarch 2021

Jubilant Therapeutics: private biotech transitioning from preclinical to clinical stage

Business

Overview

• A patient-centric biopharmaceutical company advancing potent and selective small molecule modulators to address unmet medical needs in

oncology and autoimmune diseases

• Launched in 2019 in Bedminster, NJ with discovery labs in India

• Programs incubated in stealth mode for 3+ years prior to company launch

Key

Differentiators

• Advanced discovery engine integrates patient derived database, structure-based design and computational algorithms; technology platform

validated by Sanofi, Frazier Healthcare Partners and Janssen

• Novel, precision therapeutics against both first-in-class and validated but intractable targets in genetically-defined patient populations

• Primary programs address hematological malignancies and solid tumors, RA, lung fibrosis, select rare and orphan autoimmune disorders

• Leadership with large pharma and biotech pedigree, published in top journals, experience in taking drugs to clinic

• 25+ Dedicated team of drug hunters – biologists and chemists with decades of integrated drug discovery expertise

• KOLs and SAB from world class institutions such as Memorial Sloan, Francis Crick and Dana Farber

• Dedicated subsidiaries with IPs for lead programs

Pipeline

(advancing to

clinic in 12-18

months)

NON-CONFIDENTIAL 2

• Additional discovery programs PD-L1 (Head & Neck cancer), Intractable targets in Oncology

• Past programs partnered with Frazier Healthcare and Checkpoint Therapeutics

Applying an advanced, powerful discovery engine for novel target discovery and candidate selection

NON-CONFIDENTIAL 3

Proven technology platform and discovery team with exquisite chemistry capabilities to go after intractable targets• Jubilant’s technology platform built around structure based design approach with 550+ scientists has been successfully

validated through 75+ integrated discovery programs for big pharma, biotech and leading healthcare VCs that have successfully progressed to clinical trials or acquired

• Recent platform success: Discovery of Mavupharma’s first-in-class ENPP1 inhibitors (STING pathway) that lead to company being acquired by Abbvie in 2019

• 25-50 Dedicated scientific FTEs

• Discovery platform capable of generating future assets for intractable targets organically from hit stage and advancing to clinical candidate

• Advantageous business economics of having cutting edge ideas and experiments designed by Jubilant Therapeutics Inc. U.S, executed by high quality R&D team from world class labs in India (Bangalore and Noida)

NON-CONFIDENTIAL 4

Differentiated portfolio advancing toward Phase 1

NON-CONFIDENTIAL 5

Undisclosed

TargetOncology

BRD4Hematological cancers

Solid Tumors

Additional early-stage programs in intractable targets in oncology

Partnered

Partnered

LSD1/HDAC6

PROGRAMS TARGET TO LEAD LEAD OPTIMIZATION PRE-CLINICAL (IND)INDICATIONS

PAD4 inhibitors

PRMT5

Hematological cancers

Solid Tumors

Rheumatoid Arthritis,

Rare/orphan

autoimmune disorders

Glioblastoma

Lymphoma

Phase I

2H 2021

IND

2H 2021

NEXT

MILESTONE

IND

1H 2022

DEVELOPMENT STAGE

PD-L1-Small

MoleculeMultiple Cancers

IND

1H 2022

Strong scientific rationale for LSD1/HDAC6 inhibition inacute myeloid leukemia (AML) and select solid tumors

NON-CONFIDENTIAL 6

Scientific Rationale• LSD1 is essential for

cancer stem cell survival and

maintenance of AML blasts

Both LSD1 and HDAC6 lead to

immune suppression through distinct

mechanisms

• Both targets are over-expressed in

AML and multiple other cancers

• LSD1 and HDAC6 are part of

co-repressor complexes leading to

modulation of cancer-specific genes

Clinical Rationale• Current SoCs for AML have a low

response rate, limited single agent

activity and dose-limiting toxicities

• Novel therapies targeting multiple

pathways are beneficial

• LSD1 inhibitors alone has shown

limited single agent activity

• Selective inhibition of HDAC6 may

reduce the toxicity associated with

pan-HDAC inhibitors

Opportunity• Faster clearance, sustained target

engagement in malignant cells;

minimized systemic tox

• Patient stratification based on MLL

rearranged tumors, MDS and

erythroleukemia

• Synergy or overcome resistance

when combined with chemo/SoC

• Combine with checkpoint inhibitor

for solid tumors (sarcomas and

lymphomas)

Lead Indications of AML Sub-populations (MLL, Erythroleukemia)

and select solid tumors with specific gene signatures

LSD1/ HDAC6

Lead Indication-AML

Other Indications:

MDS, Lymphoma

SCLC, TNBC

Combination with

checkpoint inhibitors

JBI-802 - Novel mechanism of dual LSD1/HDAC6 inhibition to enter Phase 1 in 2H 2021• JBI-802 is orally available with novel dual mechanism of action of

Isoform selective HDAC6 inhibition and potent LSD1 inhibition

• Robust biomarker modulation of LSD1 (CD11b and CD86) and HDAC6 (tubulin acetylation) observed both in vitro and in vivo

• Superior in vivo efficacy as compared to LSD1 and HDAC6 inhibitors that are in clinic

• Efficacy demonstrated in multiple xenograft model

• Stronger efficacy in combination with immune checkpoint inhibitors

• No major adverse effects observed in the 14-day non-GLP repeat dose toxicity in mice

• Non-GMP material synthesized 1Kg ready for GLP tox

• PCT patent filed in major territories and expires in 2036

• IND enabling studies ongoing in the US; Filing 2H 2021

NON-CONFIDENTIAL 7

JBI-802

JBI-802

LSD1/

HDAC6i

Disease Focus

JBI-802: Anti tumor efficacy in Erythroleukemia model; significantly slows down tumor growth and prolongs survival

NON-CONFIDENTIAL 8

HEL 92.1.17 Erythroleukemia Xenograft Model

Kaplan Meier survival plot for HEL 92.1.7 Xenografts

0

200

400

600

800

1000

1200

1400

1600

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15

Avg

. T

um

or

Vo

lum

e,

mm

3±S

EM

Days

Vehicle control, PO, BID

Vehicle control, IP, QD

JBI-802, 25 mg/kg, PO, BID

JBI-802, 50 mg/kg, PO, BID

ORY-1001, 0.01 mg/kg, PO, QD

ACY-1215, 25 mg/kg, IP, QD

• Stronger tumor growth inhibition compared to single agents

• Excellent dose response with an ED50 of ~6.25 mpk (BID)

• Observed clear target engagement for both LSD1 and HDAC6

• Substantial increase in mean survival time

JBI-802

Disease Focus

JBI-802 shows superior activity with anti-PD1 mAb

NON-CONFIDENTIAL 9

CT-26 Syngeneic Model

0

500

1000

1500

2000

2500

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15

Avg

. T

um

or

Vo

lum

e,

mm

3±S

EM

Days

Vehicle control, PO, BID

Isotype Control (PD-1)

JBI-802. 50 mpk (po,BID)

anti-PD-1 mAb 100 ug/mouse

JBI-802+ PD-1 mAb

JBI-802 anti-PD1 mAb

Complete tumor growth regression in 3/8 animals (30 days dosing)

Combination of Dual inh.

and anti-PD1 mAb

JBI-802

Scientific and clinical rationale for PAD4 inhibitors in autoimmune disorders

NON-CONFIDENTIAL 10

Scientific Rationale• Next generation target in

autoimmune/inflammation beyond JAKs

and TNFs

• High anti-CCP (anti-cyclic citrullinated

peptide) levels are detected in RA patients

• Histone citrullination and associated NET

formation linked to pro-inflammation and

disease progression in several

autoimmune disorders including RA,

psoriasis, thrombosis, fibrosis, SLE etc.

• KO studies clearly prove the role of PAD4

in RA, SLE, DVT etc.

Clinical Rationale• Targeting PAD4 does not lead to

immune suppression nor risk of

thrombocytopenia and may offer

better therapeutic margin and safety

• Antibodies produced

against citrullinated proteins (anti-

CCP) are diagnostic, prognostic and

stratification markers of RA

• Potential to target inflammation

driven diseases

Opportunity• Differentiated first-in-class

mechanism to treat autoimmune

diseases

• Small molecule option for anti-TNF-

non-responders

• Broader application in various auto-

immune disorders such as lung

fibrosis (including Covid-19

ARDS), psoriasis, SLE, DVT

• Potential utility in niche indications

Lead Indications of RA and select orphan inflammatory

disease(s) for rapid PoC

PAD4

Disease Focus

PAD4 inhibitor JBI-1044 protects from disease progression inCIA-induced RA

NON-CONFIDENTIAL 11

Clinical score Body weight

JBI-1044

• JBI-1044 offers significant disease protection from CIA induced RA both in prophylactic and therapeutic treatment

• Well tolerated with no significant change in body weight

• Significant reduction in CitH3, IL-10 and IL-17 in arthritic paw samples

0

5

10

15

28 30 31 33 35 37 39 41 43 45

Avg. C

linic

al S

core

±S

E

Days

Clinical Score: CIA study

Normal Control Vehicle Control

JBI-1044 (50 mpk, BID, po) Dexamethasone (0.3mpk, QD, po)

0

5

10

15

20

25

30

0 3 6 9 12 15 18 21 24 27 30 33 36 39 42 45Avg. B

ody

Weig

ht,

gm

±S

E

Day

Body weight: CIA study

Normal Control Vehicle ControlJBI-1044 (50 mpk, BID, po) Dexamethasone (0.3mpk, QD, po)

CIA study: JBI-1044 reverses disease severity significantly at 3 mg/kg

NON-CONFIDENTIAL 12

JBI-1044

• JBI-1044 ED50 : 3mpk BID

Evaluation of JBI-1044 in Mouse model ofCollagen induced arthritis

Clin

ical S

co

re

(Me

an

SE

M)

Day 28 Day 30 Day 31 Day 33 Day 35 Day 37 Day 39 Day 41 Day 43 Day 450

3

6

9

12

*P<0.05 vs Vehicle Control, Two way ANOVA followed by Bonferroni multiple comparisons Test.

*****

**

Normal Control

JBI-1044 (3 mpk, BID, po)

JBI-1044 (6 mpk, BID, po)

JBI-1044 (12.5 mpk, QD, po)

Vehicle Control

Vehic

le c

ontrol

Dis

ease

contr

ol

3 m

pk, B

ID

6.25

mpk,

BID

12.5

mpk,

QD

0

5

10

15

Clinical score onday 45: JBI-1044

Clin

ica

l sc

ore

CIA study:% reversal of clinical score

% r

eve

rsal

of

cli

nic

al s

co

re

(Me

an

SE

M)

0

50

100

Vehicle Control

JBI-1044 (3 mpk, BID, po)

JBI-1044 (6 mpk, BID, po)

JBI-1044 (12.5 mpk, QD, po)

**

*

ED50: 3 mpk BID

% reversal of clinical score

RA subsets

JBI-1044

PAD4i

Lung

Fibrosis,

COVID19

pathologies

Select

orphan

inflammatory/

autoimmune

indications

JBI-1044 – PAD4 inhibitor targeting auto-immune disorder to complete IND filing in 2H 2021• Orally available novel, small molecule inhibitor complies with the rule of five

• Unique Mechanism of action: modulation of citrullination and NETosis

• Selective against PAD4 and does not inhibit other isoforms

• Excellent efficacy demonstrated in collagen induced arthritis model by oral

route of administration

• Efficacy demonstrated in lung fibrotic model and is comparable to

Nintedanib

• Efficacy has also been demonstrated in psoriasis, diabetic wound healing

and atopic dermatitis models

• Potential in select Rare Diseases and Orphan indications

• Good therapeutic margin based on 14-day tox study in rodent and non-

rodent - No signs of immune suppression as opposed to existing therapies

(TNF-α, JAK inhibitors)

• Clean in CEREP safety panel, cardiac profiler and AMES negative

• Two PCT patents filed in major territory and expires in 2038

NON-CONFIDENTIAL 13

JBI-1044

Scientific and clinical rationale for novel small molecule PRMT5 inhibitor

NON-CONFIDENTIAL 14

Scientific Rationale• Glioblastoma (GBM) is selectively

sensitive to inhibition of PRMT5 and has

been identified as a predictive biomarker

• PRMT5 inhibition disrupts the removal of

detained introns leading to modulation of

proliferation

• Represses expression of

several tumor suppressor genes, leading

to cancer progression

Clinical Rationale• Limited or no agents to treat GBM

• Poor response rate with SoC

• Potential for high ClNS1A/RIOK1

ratio to identify sensitive patients

• Brain penetrant

Opportunity• Mechanism is validated with a few

PRMT5 inhibitors in early clinical

trials

• Among few brain-penetrant PRMT5

inhibitors to address the

unmet medical need in

treating GBM

• Potential use in other cancers

where PRMT5 is over expressed

(Lymphoma)

Lead Indications of GBM and Lymphoma to address

high unmet need

PRMT5

Small molecule PRMT5 inhibitor – Key Features

NON-CONFIDENTIAL 15

JBI-778

Orthotopic Glioblastoma: Survival Data

Target Engagement in Brain

• Orally available novel small molecule inhibitor differentiated by:

- Binding to substrate/activating site as against SAM site

- Better brain exposure and target engagement in brain

• Inhibits the symmetrical dimethylation of Arginine

• Selective to PRMT5 in the arginine methyl transferase panel

• Superior efficacy has been demonstrated in xenograft model by oral route compared to the reference compound

• Efficacy has been demonstrated in the orthotopic GBM model by oral route

• Patent expires in 2038 and filed in all the major countries

Scientific and clinical rationale for novel small molecule PDL1 inhibitor

NON-CONFIDENTIAL 16

Scientific Rationale• PD1/PD-L1 pathway is a critical

component of T-cell immune checkpoint

• In the tumor microenvironment, PD-1 and

PD-L1 perform a vital role in tumor

progression

and survival by escaping tumor immune

surveillance

• Targeting PD-1 and PD-L1 simultaneously

could reactivate cytotoxic T cells to work

against cancer cells

Clinical Rationale• Anti-PD1/PD-L1 mAbs increase

overall survival compared to standard

of care in different tumors

• Since mAbs can activate a broad

range of immune cells, they can

trigger severe auto-immune reactions

• Potential to overcome immune

related adverse effects with a small

molecule

• Low patient compliance and high

cost of mAb therapies are potential

issues with SoC

Opportunity• Potential use after initial mAb

treatment as a lower-cost

maintenance therapy

• I/O combination in non-oncology

indications where small molecule

PD-1 oral modality is preferred

over IV mAbs

Oral alternative to mAbs for increased compliance and

long-term use in maintenance settings

PDL1

Small molecule PD-L1 inhibitor – Key Features

• Orally available novel, small molecule inhibitor

• Binds to PD-L1 protein and prevents interaction with PD-1

• Comparable tumor reduction to mAb in the humanized murine model

• Selectivity and Off target: Highly selective for PD-L1; Clean in Cerep 44 toxicity Panel; Negative in AMES test and no hERG or CYP liability

• MTD is >500 mg/kg in mice

• Well tolerated in the 14-day repeat dose toxicity study in mice at the highest dose

• Patent expires in 2038 and filed in all major countries

NON-CONFIDENTIAL 17

JBI-426 IO Selectivity Assays (Biochemical)

Tumor Growth Inhibition

JBI-426

0

500

1000

1500

2000

1 3 6 8 10 13Tu

mo

r vo

lum

e (

mm

3)

Days

RENCA Syngeneic Model (Balb/c)

Vehicle (IP)

Vehicle (PO)

PD-L1 mAb- 0.1 mg/mouse (IP)

JBI-426 – 50mpk, BID

0

20

40

60

80

100

120

AR

G1

AR

G2

BT

LA

:…

CB

L-B

CD

28:…

CD

38

CD

39

CD

40:…

CD

47:…

CD

47:…

CD

73

CO

X1

CO

X2

CD

13…

CS

F1…

CT

LA

…

GIT

R:…

IDO

1

IDO

2

OX

40:…

PD

-…

PD

-…

PD

-…

TD

O

TIG

IT:…

TP

H1

TP

H2

% I

nh

ibitio

n

JBI-426:IO selectivity panel

0.3µM 3µM

Select Key Advisors

NON-CONFIDENTIAL 18

Dr. Ron Christopher

Toxicology

• Senior entrepreneurial leader with extensive

experience in pharmaceutical research and

development

• Regulatory filing experience: >25 INDs, 4 NDAs, 3

MAAs

• PhD from Texas A&M University

Dr. Mary Celine Scott

Regulatory Affairs

• 30 years in the pharmaceutical/biotech industry

working to develop novel small molecules and

biotherapeutics.

• Worked in several pharma companies as regulatory

affairs person- Amgen, Pfizer, Schering Plough

• PhD in Purdue University

Dr. William (Bill) Lambert

CMC

• >30 years in the pharmaceutical/biotech industry in

supporting process development

• Worked in several pharma companies in CMC-

Upjohn, Pfizer, Eisai, AZ etc.

• PhD in University of Utah

Dr. Guy Gammon

Translation Medicine

• >25 years of Clinical experience

• Worked in Daichii, Receptor Biologix, Ambit

Bioscience, Prospect Therapeutics etc.

• MBBS University of London

Dr. Julian Downward

• Leads Lung Cancer Group within Division of

Molecular Pathology at the Institute of Cancer

research

• Associate Director of the Francis Crick Institute

• Heads research group working on oncogenic RAS

signaling in malignant transformation

Dr. Bill Hahn

• Expert in Functional genomics and human cell

transformation, Precision cancer medicine

• Accomplished researcher with numerous

discoveries that informed our current molecular

understanding of cancer and formed the foundation

of new translational studies

Dr. Ross Levine

• Physician-scientist focused on researching and

treating blood and bone marrow cancers, including

acute myeloid leukemia and the chronic

myeloproliferative neoplasms polycythemia vera,

essential thrombocytosis, and primary myelofibrosis

Contact Information

Partnering:

Rajiv Tyagi

Head – Business Development

rajiv.tyagi@jubilantTx.com

Investor Relations:

Shyam Pattabiraman

Chief Financial Officer

shyam.pattabiraman@jubilantTx.com

Location

1430 Route 206, Suite 110, Bedminster NJ 07921 www.JubilantTx.com

NON-CONFIDENTIAL 19