corporate presentation august 2020

Corporate Presentation – August 2020

(NASDAQ: LMNL)

© 2020 Liminal BioSciences Inc.

This presentation contains forward-looking statements about Liminal BioSciences’ objectives, strategies and businesses that involve risks and uncertainties.

Forward‐looking information includes statements concerning, among other things, statements with respect to the timing of any planned Biologics License Application

resubmission for Ryplazim® plasminogen (human) or Ryplazim®, the development of R&D programs, the timing of initiation of clinical trials, the exploration of potential

alternatives for the future commercialization of Ryplazim®, if approved, including through a third-party marketing collaboration, and the potential commercial launch of

Ryplazim®, if approved, and the impact of COVID-19 on our business.

These statements are "forward-looking" because they are based on our current expectations about the markets we operate in and on various estimates and assumptions.

Actual events or results may differ materially from those anticipated in these forward-looking statements if known or unknown risks affect our business, or if our

estimates or assumptions turn out to be inaccurate. Such risks and assumptions include, but are not limited to, Liminal BioSciences’ ability to develop, manufacture, and

successfully commercialize value-added pharmaceutical products, the availability of funds and resources to pursue R&D projects, the successful and timely completion of

clinical studies, the ability of Liminal BioSciences’ to take advantage of business opportunities in the pharmaceutical industry, uncertainties related to the regulatory

process and general changes in economic conditions.

You will find a more detailed assessment of these risks, uncertainties and other risks that could cause actual events or results to materially differ from our current

expectations in the Company’s U.S. Securities and Exchange Commission and Canadian Securities Commission filings and reports, including in the Annual Report on Form

20-F for the year ended December 31, 2019, the 6-K containing our results for the quarter ended March 31 and June 30, 2020 and future filings and reports by the

Company, from time to time. As a result, we cannot guarantee that any forward-looking statement will materialize. We assume no obligation to update any forward-

looking statement even if new information becomes available, as a result of future events or for any other reason, unless required by applicable securities laws and

regulations.

Copyright notice

The information contained in this presentation (including names, images, logos and descriptions portraying Liminal BioSciences’ products and/or services) is the property

of Liminal BioSciences Inc., of its divisions and / or of its subsidiaries (“Liminal”) and is protected by copyright, patent and trademark law and / or other intellectual

property rights. Neither this presentation nor any part may be reproduced or transmitted in any form or by any means, electronic or mechanical, including printing and

photocopying, or by any information storage or retrieval system without prior permission in writing from Liminal.

Disclaimer

Liminal BioSciences’ reserves the right to make improvements, corrections and/or changes to this presentation at any time

Safe Harbour


• Management team and key advisors with a track record of successful development and business strategies assumed control in 2019 after a shareholder re-organization

• Following an extensive review and investment cycle, clinical candidates are ready to move forward

• Committed shareholder backing from Thomvest and Consonance Capital

New management and scientific teams

set the stage for long term value creation

• Deep domain expertise in small molecule drug development, biology of fibrosis and GPCRs

• Lead small molecule candidate, fezagepras, with an intriguing pre-clinical activity and tolerability profile

• Broadening pre-clinical R&D pipeline focused on novel biologic pathways

• Filing of BLA anticipated in Q3-2020 with US commercial launch to follow if approved by FDA

• Foreign market access strategy under development

• Initial patient population addressable with a targeted commercial infrastructure and potential for broadening commercial opportunity with new indications

• BLA approval to potentially trigger a priority review voucher (PRV)

Liminal BioSciences at a Glance

3

Development pipeline led by

fezagepras

BLA-ready plasminogen deficiency

therapy, Ryplazim®


Product Pipeline

4

Selective OXER1 Antagonist

Selective GPR84 Antagonist

Fezagepras (PBI-4050)

Plasma Segment:

Therapeutic Indication Preclinical Phase I Phase II Phase IIIProgram Status

BLA resubmission Q3-2020Expected PDUFA in Q1-2021

In H2-2020 higher dose in healthy volunteers followed by high triglyceride patients

Phase 2 clinical trials for fezagepras in selected fibrosis indications expected to be initiated after multiple ascending dose study (MAD) study

NDA/BLA

Congenital Deficiency

Additional MAD

Liver:

NASH

Lung:

IPF

Kidney:

Alström Syndrome

Respiratory / GI

Fibrosis Lead candidate nomination H2-2020

Expected nomination of preclinical product candidate for OXER 1 antagonist program in H2-2021

Ryplazim®

Small Molecule Segment:

CKD


Most fibrotic diseases are progressive and fatal with few treatment options available

Pulmonary fibrosis, renal fibrosis and NASH are well known examples of fibrotic diseases

Fibrosis can occur in many organs as a result of formation of excess fibrous connective tissue due to chronic disease

Our novel biology focused on targeting PPARs, FFARs and related GPCRs to halt the progression of, or reverse, fibrosis

Fibrosis: Significant Unmet Needs in Multiple Therapeutic Areas

Fibrosis

5

*Fezagepras, previously referred to as PBI-4050

Fibrosis is an aberrant response of the body

to tissue injury, but its causes aren’t fully

understood

Fibrotic disease is driven by both metabolic and inflammatory processes and is very complex. We believe this complexity will likely lead to the need for multi-targeted therapy


Fezagepras(formerly PBI-4050)


Pre-clinical and preliminary, open-

label human data suggestive of

anti-fibrotic activity in multiple

organs provides future development

rationale

Dosed daily for up to 12 weeks up to

1,200mg

Orphan drug designation for two

indications (IPF and Alström

Syndrome)

Evaluated in over 250 individuals

(166 patients) in 8 clinical studies

Fezagepras

Anti-inflammatory and

anti-fibrotic small

molecule

Reduces fibrosis via regulation of

macrophages, fibroblasts/

myofibroblasts and epithelial cells

Fezagepras Profile: A Well-Tolerated, Novel, Oral Anti-Fibrotic Agent

7


Both play a role in

the pathogenesis of

NAFLD and NASH

PPARa appears to

modulate lipids;

FFAR1 appears to

modulate glucose

To date, empirical

evidence consistent

with presumed

mechanism

Both have a well

understood impact on

metabolic control, but

act through distinct

pathways

Presumed Mechanism of Action for Fezagepras

Activates both PPARa

and FFAR1 (GPR40)

8


FFAR1 (GPR40) Agonists: An Emerging Class for T2DM

9

• FFAR1 (GPR40) is a well-validated target for the treatment of Type 2 Diabetes

• Strong clinical evidence that GPR40 agonists can improve glucose control, without the risk of hypoglycemia

• Liver toxicity led to the discontinuation the most advanced clinical-stage product (TAK-875)

• Recent studies confirmed toxicity related to unique structure of TAK-875 not GPR40 MOA

• Numerous programs are underway to optimize drug design and reduce the risk of toxicity

• Eli Lilly, BMS, Amgen, J&J and Merck are among the companies working on next-generation GPR40 agonists

• At least 10 programs are in the pre-clinical phase or Phase 1 safety studies

• Below are two GPR40 agonists as disclosed currently in clinical development:

Stage of Development

Company Drug Indication Target

Phase 1 Hyundai Pharma HOB-047 T2D Dual GPR40 & GPR119 agonist

Phase 1Scohia Pharma

(Takeda)SCO-267 T2D / Obesity GPR40 full agonist

© 2020 Liminal BioSciences Inc.10

PPAR Alpha as an Anti-fibrosis Target

• PPARa is a ligand-activated nuclear receptor

• Enriched in tissues with high fatty acid oxidation (FAO) rates such as liver, heart, skeletal muscle and brown adipose tissue

• Expressed in intestine, vascular endothelium, smooth muscle and immune cells such as monocytes, macrophages and lymphocytes

• Transcriptional regulator of genes involved in peroxisomal and mitochondrial B-oxidation and FA transport

• Negatively regulates pro-inflammatory and acute phase response signalling pathways


PPAR Agonists and Fibrosis: An Evolving Landscape

PPAR agonism has long been a well-validated target for the treatment of metabolic disease with a strong rationale in fibrotic disease, however, clinical success has proven elusive

• Traditional PPARa agonists do not appear to create a therapeutic effect on fibrosis

• Traditional PPARg agonists have shown some efficacy, but with a troublesome toxicity profile

• Finding the correct dose is paramount to drug activity

Updated research has improved the understanding of the class and newer modalities of PPAR activation which appear to have a differentiated impact on the target and have shown more promise in early stage development for fibrotic disease

PPARa PPARd PPARg

Pemafibrate (Kowa Pharma) x

Lanifibranor (Inventiva Pharma) x x x

Elafibranor (Genfit) x x

Seladelpar (CymaBay) x

Bezafibrate (Intercept) x


• Bleomycin-induced lung fibrosis (Liminal)

• Comparison with pirfenidone

• Comparison with nintedanib

• TGFβ-induced lung fibrosis (Kolb / McMaster U.)

• Acute Lung Injury post pancreatitis (Liminal)

• IPF patients fibroblasts (McMaster – Liminal)

Lung models

• CCL4 induced liver fibrosis (Liminal)

• CCL4 induced hepatocarcinoma (Liminal)

• High-fat diet mice (Liminal)

• Liver steatosis in db/db eNOS-/- mice

(Vanderbilt)

• Upper Bile duct ligation Rat (Liminal)

Liver models

• 5/6 nephrectomised rats – CKD ESRD (Liminal)

• db/db uninephrectomized mice (Liminal)

• db/db eNOS-/- mice (Vanderbilt)

• Doxorubicin-induced nephrotoxicity mice (Liminal)

• Adenine model in -/- animals (U of Ottawa)

• UUO – ischemia models (Liminal)

Kidney models

• FBN-1 mice scleroderma model (Vanderbilt)

Skin models

• Suprarenal banding of aorta (MHI)

• Myocardial infarction rat model (MHI)

Heart models

• Type-1 Non-Obese diabetic mice (NOD)

(Liminal)

• db/db eNOS-/- mice (Vanderbilt)

Pancreas models:

Fezagepras: Anti-fibrotic Activity in Six Different Organ Systems

12

PBI-4050 has been tested in >30 animal models and in vitro experiments on human / patient cells; it has shown pre-clinical activity in all of the key models listed below:

*MHI = Montreal Heart Institute


Effect on Liver Stiffness in Patients with Alström Syndrome

13

Results shown are from an open-label, single-centre study; FibroScan® is a measure of liver stiffness, a surrogate for liver fibrosis


Effect on IPF from Open-label Study

Pulmonary

Function Test

FEZAGEPRAS(N = 9)

FEZAGEPRAS +NINTEDANIB

(N = 16)

FEZAGEPRAS +PIRFENIDONE

(N = 15)

TOTAL(N = 40)

FVC (mL)

Mean change (±

SD) at Week 12

-12.2

(137.09)

1.875

(127.6)

-102

(137.80)

-40.3

(138.96)

95% confidence

interval

-117.60,

93.157

-66.121,

69.871

-178.31,

-25.69

-84.692,

4.192

• Though a small sample size (N=9) Fezagepras monotherapy showed an effect at 12 weeks.

• Combination results were mixed, but Fezagepras + Nintedanib did show improved lung function over baseline at 12 weeks.

• Tolerability acceptable.


We plan to initiate a Phase 1 clinical trial

in 2H 2020 to evaluate multiple ascending

doses of fezagepras in normal healthy

volunteers and in Q1 2021 in patients (T2DM

with high TG's)

Long-term repeat dose toxicity animal studies of

fezagepras suggests maximum daily dosing of 2,400

mg in humans; BID dosing also to be studied

Dose dependent responses in our preclinical studies

suggest higher doses than previously studied to date

could lead to increased efficacy in human trials

The optimal dose and dosing regimen of fezagepras

is expected to be further evaluated in Phase 2

clinical trials in selected fibrosis indications to be

initiated in 2021

Finding the optimal dose of fezagepras will be a

large factor in clinical success due to the

complexity of fibrosis. Recent clinical experience of

competing compounds has reinforced this point.

Data and biomarkers (TG's, fgf21, HbA1c, etc.)

will help define dose levels and regimen for any

future clinical trials evaluating fezagepras

Determining the Optimal Dose for Fezagepras

15


• Reduced steatosis, ballooning and

total NAFLD score in High Fat Diet

models of metabolic syndrome

• Reduced liver stiffness scores in 10

out of 11 human subjects, as

measured by FibroScan® in an

open label Phase 2 study in Alström

Syndrome

Liver Fibrosis

• Improved Lung Function in

Bleomycin and TGF-b induced

models of Pulmonary Fibrosis

• Held lung function as measured by

FVC to a small decline at 12 weeks

(=12.2 ml) in 9 patients

monotherapy arm of Phase 2 open

label study in IPF

Respiratory Fibrosis

• Reduced tubulointerstitial fibrosis

levels and Increased renal function

and reduced anemia in adenine

induced model of kidney fibrosis

• Drug concentration levels quickly

returned to normal in both single

and multiple dose administrations

in patients with stable renal

impairment

Renal Fibrosis

Fezagepras: One Candidate, Many Possibilities

16

Phase 1 multiple ascending dose ranging study to determine next steps in 3 key areas with phase 2 well-controlled, randomized clinical studies in selected fibrosis indications expected in 2021. Existing pre-clinical and/or clinical data have shown:


Ryplazim®

(plasminogen)


Plasminogen Overview

18

A naturally occurring enzyme, plasminogen plays a role in many complex biological processes regarding the regulation of plasma proteins

Amongst the areas where plasminogen plays a role are the lysis of blood clots and the wound healing process (fibrinolysis)

Our primary focus has been on Type 1 congenital plasminogen deficiency (C-PLGD) with the development of Ryplazim®, however, we believe plasminogen’s broad role could create additional therapeutic opportunities in the future

Other potential therapeutic applications based on both fundamental biology and our pre-clinical findings are:

• Hereditary angioedema with a plasminogen gene mutation• Complex wound healing, including in a post-radiation therapy setting• Idiopathic pulmonary fibrosis, including acute exacerbations


Potentially eligible for Priority Review

Voucher (PRV) if approved

Attractive initial launch

opportunity either for Liminal

or a collaboration partner

Potential for growth through

additional clinical indications and

foreign markets

Potentially first FDA-approved

treatment for plasminogen deficiency, a

rare congenital disorder

BLA to be re-submitted in Q3-2020

following efforts to address CMC

issues raised in initial CRL in 2018

Achieved both co-primary

endpoints in pivotal Phase

2/3 trial

Ryplazim® Plasminogen Replacement Therapy

19


Type 1 Congenital Plasminogen Deficiency (C-PLGD): A Rare Genetic Disease with Potentially Devastating Effects

Inadequate plasminogen activity levels result in fibrinous lesions on mucous membranes.

• These lesions vary from patient to patient in terms of size, location, and clinical consequences.

• They may initially develop and/or recur at any age.

Potential life-altering consequences of C-PLGD include

• Vision loss

• Airway obstruction

• Hydrocephalus

• Infertility

• Impaired postsurgical wound healing

20


Current Treatment Options are not FDA Approved

21

• No FDA-approved treatments or standardized treatment guidelines

• No current options treat the underlying systemic plasminogen deficiency

• Fresh frozen plasma may be used, but durability of relief is uncertain

• Surgical removal of growths is also an option but comes with associated risks

and offers only temporary relief

• Topical eyedrops for ligneous conjunctivitis have no confirmed efficacy

• Teams of specialists (paediatricians, ophthalmologists, hematologists, dental

specialists, pulmonologists) may be necessary to manage C-PLGD


Patients in the US remained on

treatment beyond 48 weeks and were

moved to a compassionate access

program

Dosing of 6.6 mg/kg via IV infusion for

10 to 30 minutes every 2 to 4 days for

48 weeks of treatment

Primary endpoints:

(1) increase of individual trough

plasminogen activity by at least

an absolute 10% from baseline

through 12 weeks of therapy; and

(2) 50% resolution of lesions in 50%

of patients after 48 weeks of

therapy

Two clinical sites: Indiana Hemophilia

and Thrombosis Center and Oslo

University Hospital

Evaluate PK, efficacy and safety of

Ryplazim® in 15 pediatric and adult

subjects with hypoplasminogenemia

Ryplazim® Pivotal Phase 2/3 Study Design

22

Safety

• Most AE’s were characterized as mild

• Most frequent AE’s were nasopharyngitis, headache and GI related

• No deaths or SAE’s

• No drug-related AE’s that caused study discontinuation

Ryplazim® Pivotal Phase 2/3 Study Summary Results

Efficacy

• Achieved primary endpoint to improve trough plasminogen by greater than 10%

• All patients achieved this level of trough plasminogen improvement

• Ryplazim® treatment resolved all lesions in all 15 patients treated for 48 weeks.

• 73% of patients had a significant resolution of lesions after 12 weeks of treatment

• US patients have remained on Ryplazim® compassionate use study since 2018

23


U.S. launch initially where

literature suggests

prevalence of between 500-

1000 patients1

Traditional orphan indication sized

salesforce to target universe of

treating haematologists and

ophthalmologists

Work with payors to secure

reimbursement consistent with

patient benefit as an orphan

disease

Initial group of patients well

identified via clinical trial and

compassionate use conversion

along with IMS code

Efforts to support patient

registry and patient advocacy

groups ongoing

Potential for future growth from

additional indications (HAE, IPF and

wound care) and ex-U.S. launches (10

to 15X > US market)

Ryplazim®(plasminogen) Commercial Plans

24

1Literature indicates 1.6 birth/million incidence rate or 500 in the US. Proprietary internal Liminal estimates suggest 1000 patients


Early-stage R&D Pipeline: GPR84 and OXER1


GPR84 is a pro-inflammatory target primarily expressed on cells associated with the immune system and its expression levels increase significantly during periods of inflammatory stress

Developing a selective GPR84 antagonist would build on Liminal’s in-house expertise in novel biology targets

GPR84 antagonist could be used in combination therapy with either internal or external agents

GPR84 Antagonist Discovery Program

GLPG1205, currently in Phase 2 for IPF, is the only other GPR84 antagonist in development to our knowledge

26


GPR84: Role in Fibrosis and Metabolic Diseases

• GPR84 expression is not restricted to cells in the immune system

• Also expressed in brain, heart, muscle, colon, thymus, spleen, kidney, liver,

intestine, placenta and lung

• Liminal has shown that GPR84-deficient mice develop reduced fibrosis in a model of

kidney fibrosis (adenine-induced chronic kidney disease)

• GPR84 may also be a mediator of the relationship between inflammation, obesity

and diabetes

• Rodent models have shown that GPR84 expression is up-regulated in adipocytes in

response to TNF-α released from infiltrating macrophages

• In the presence of TNF-α, medium chain fatty acids down-regulate adiponectin

mRNA expression in 3T3-L1 adipocytes

• Adiponectin is a key adipokine that has insulin sensitizing effects and directly

enhances fatty acid oxidation


Liminal: Key GPR84 Preclinical Studies

Liminal’s research has shown that:

• GPR84-deficient mice develop reduced fibrosis in a model of kidney fibrosis

(adenine-induced chronic kidney disease)

• GPR84 mRNA is overexpressed in various acute and chronic kidney models such as:

• 5/6-nephrectomy (Nx)-induced chronic kidney disease

• Doxorubicin (DOX)-induced nephropathy

• Adenine-induced tubulointerstitial injury

• GPR84 expression is increased in murine macrophages following inflammatory

stimuli

Eosinophils are major effector cells in the immune system

• Part of the innate immune system

• When activated, they release a cocktail of cytotoxic proteins and cytokines from the eosinophilic granules

Eosinophils have a key role in Type 2 inflammation-driven diseases

• May help to regulate the type of immune response generated

• Cytokines such as IL-4, IL-13 and IL-25 are found within eosinophilic granules

• Direct the response to be Th2–polarised

• Th2-polarised responses are linked with asthma and other allergic and inflammatory diseases

• Activated eosinophils also release lipid mediators that can cause airway smooth muscle contraction and contribute to airway hyper-responsiveness

• Aberrantly-activated eosinophils are known to be present in patients with severe asthma and other eosinophil-related diseases

Summary of Opportunity in Eosinophilic-Driven Diseases

29

Potential Indications in Eosinophilic-Driven Diseases:

Respiratory and Inflammatory Disease:

• Severe eosinophilic asthma

• COPD

• Hypereosinophilic syndrome (HES)

• Nasal polyposis

• Atopic dermatitis

• Chronic spontaneous urticaria

Gastrointestinal Disease:

• Eosinophilic gastritis

• Eosinophilic esophagitis (EoE)

• Eosinophilic gastroenteritis


Novel Pathway: OXER1 for 5-oxo-ETE

• 5-oxo-ETE is one of the metabolites generated via 5-LO metabolism of AA

• 5-oxo-ETE is a potent pro-inflammatory mediator; a powerful eosinophil chemoattractant

• Also aids eosinophil migration out of blood vessels and into the surrounding tissues

• Produced by several activated immune cell types and by damaged structural cells

• Also produced by activated eosinophils; acts in an autocrine fashion to sustain their own activation

• Its receptor is known as the OXE receptor (OXER1)

• OXER1 is also expressed on neutrophils, macrophages & basophils, but to a lesser extent

• Series of highly potent synthetic antagonists for the OXER1 with activity in non-human primates

• Multiple potential clinical indications to explore, including orphan diseases

*Blattermann et al


Corporate Overview


Kenneth Galbraith, Chief Executive Officer

Murielle Lortie, Chief Financial Officer

Moira Daniels, Head of Regulatory Affairs and Quality Assurance

Management Team and Key Advisors

32

Dr. Gary Bridger, Board Member and Strategic Scientific Adviser

Dr. Jeffrey Smith, Strategic Medical Adviser

Mr. Galbraith well-known member of the life sciences community with over 30 years of experience acting as an executive, director, investor and advisor to companies in the biotechnology, medical device, pharmaceutical and healthcare sectors. Mr. Galbraith has served at the leadership and board level for many organisations within the healthcare industry including Macrogenics (MGNX), Profound (PROF), AnorMED, QLT Inc., Zymeworks, Angiotech Pharmaceuticals (ANPI), Aquinox (AQXP), Alder Pharmaceuticals (ALDR), Tekmira (TKMR) and Celator Pharma (CPXX).

Dr. Bridger has extensive experience in leading research and development through to commercialisation. Dr. Bridger previously served as Executive Vice President of Research and Development at Xenon Pharmaceuticals Inc., Senior Vice President of Research and Development of Genzyme Corporation and co-founded AnorMED Inc., eventually acquired by Genzyme.

Moira brings significant experience in product development and regulatory affairs as well as change management within the industry. Prior to joining Liminal, Moira was VP at UCB Pharma, PAREXEL and AstraZeneca holding senior positions in Regulatory Affairs and leading trade association teams on key policy topics at an international level. Moira has worked successfully in different therapeutic areas securing regulatory approvals globally.

Dr. Smith has held many senior positions within the pharmaceutical industry, most recently, Managing Director of Alder Biopharmaceuticals Inc. Dublin, Ireland and before that Senior Vice President, Translational Medicine at Alder Biopharmaceuticals Inc, Seattle. Dr. Smith was responsible for the clinical development (phase I - III) of eptinezumab (anti-CGRP antibody for migraine) and clazakizumab (anti -IL-6 antibody for rheumatoid arthritis and cancer cachexia). Dr. Smith was also a founder of Alder Biopharmaceutcials Inc.

Murielle brings a vast amount of experience in finance and corporate strategy. Prior to joining Liminal Murielle was employedas Vice President & Chief Financial Officer at Pharmascience Inc. Previous to this, Murielle has held senior positions in finance at Bristol Myers Squibb including Vice-President of Finance and Global Director of Finance.


As of June 30th, 2020 (in Canadian $):

• Cash balances of $26.0M

• $10M in debt (due 2024) and unutilized $29M line of credit with Thomvest

• Potential proceeds from sale of Priority Review Voucher (PRV) if Ryplazim® is

approved and PRV is granted

• Potential collaborations being explored for both Ryplazim®, if approved, and

fezagepras

• Common shares of 23.4M with additional 2.4M options and warrants outstanding

• Thomvest currently owns 72% (65.5% fully-diluted) of common shares

Financial Position

33


• Joined with other leading plasma companies to form the CoVIg-19 Plasma Alliance

• Utilizing our plasma collection network to collect plasma from convalescent donors who have

recovered from COVID-19 for use in clinical studies by third parties

• Evaluating internal and external research regarding the use of plasminogen replacement therapy to

treat serious COVID-19 infected patients

• Evaluating other products, assets and infrastructure that may be useful in fight against COVID-19

• Protective measures in place for our employees, patients, donors and our communities

Liminal Response to COVID-19 Pandemic

34


Anticipated Key Milestones

• Expected resubmission of BLA for Ryplazim® in Q3-2020

• Anticipated initiation of Phase 1 multiple ascending dose study (MAD) for fezagepras in H2-2020

• Expected nomination of preclinical product candidate for GPR84 antagonist program in H2-2020

• Pending FDA approval, expected PDUFA date for Ryplazim® in Q1-2021

• Potential monetization of PRV, if granted by FDA on successful Ryplazim® BLA approval, in 2021

• Phase 2 clinical trials for fezagepras in selected fibrosis indications expected to be initiated after MAD study

• US launch of Ryplazim®, if approved, in 2021

• Expected nomination of preclinical product candidate for OXER1 antagonist program in H2-2021

• Anticipated initiation of additional clinical studies for Ryplazim® in H2-2021

• Potential marketing collaborations and patient access for Ryplazim® in selected ex-US markets in 2021 and 2022 pending FDA approval

35


Liminal BioSciences Summary

• Corporate re-organization and investment cycle has set the stage for maximizing the value of the

clinical portfolio

• Novel, oral small-molecule, fezagepras has pre-clinical and early open-label clinical data

potentially indicative of anti-fibrotic activity in multiple organ systems

• Fezagepras tolerability profile allowing for the exploration of increased dosage levels and

alternate dosing regimens in dose ranging study planned

• Broadening R&D portfolio focused on novel biologic pathways

• BLA filing expected in Q3-2020 for plasma-based therapeutic, Ryplazim® for treatment of

congenital plasminogen deficiency; a rare genetic disorder

• Potential collaborations being explored for both Ryplazim® and fezagepras

36


Selected Preclinical Data for Fezagepras


Effect on Bleomycin Mouse Models of Lung Fibrosis

• Fezagepras reduced histological lesions of lung fibrosis in a dose-dependent manner

• Fezagepras (200 mg/kg) significantlydecreased (p ≤ 0.05) the mRNA expression of CTGF, collagen 1 and IL-23p19

38


Effect on TGF-binduced model of Pulmonary Fibrosis

39


Effect on High Fat Diet Models of MetabolicDisease

Liver Histology

40


Effect on Adenine-fed Models of Kidney Disease

Ad

en

ine +

Veh

icle

Ad

en

ine +

PB

I

0

2

4

6

8

T u b u lo in te rs titia l fib ro s is %

Fib

ro

tic

are

a

(%)

<0.0001

41


Selected Clinical Data for Fezagepras


Clinical Data: Effect on Cardiac Fibrosis in Patients with Alström Syndrome

43

Measured by cardiac MRI T1-Mapping

Intervention group results are from an open-label, single-centre study, ‘control’ group is an untreated cohort of patients followed over time, not a placebo-treated group


Treatment with PBI-4050 led to a reduction in the level of 5 different biomarkers, all related to kidney injury

Kidney Injury Biomarkers% Change

Week 24 / Baseline

P value

N=12

KIM-1 ↓ 33% 0.02

Clusterin ↓ 34% 0.03

Cystatin C ↓ 25% 0.01

MCP-1 ↓ 15% 0.03

Osteopontin ↓ 18% 0.03

Biomarkers tested in urine samples

Alström Syndrome: Reduction in Biomarkers of Kidney Injury


Selected Clinical Data for Ryplazim®


Ryplazim® Pivotal Phase 2/3 Efficacy Results

Subject

Population

Overall Clinical Success a

(%) Based on All Lesions

(Number of Subjects)

Overall Clinical Successa (%)

Based on Visible Lesions


Overall Clinical Success a (%)

Based on Measurable Lesions


Pediatric b 100% (3/3) 100% (2/2) 100% (2/2)

Adult 100% (8/8) 86% (6/7) 100% (4/4)

Combined 100% (11/11) 89% (8/9) 100% (6/6)

aOverall clinical success is defined as 50% of subjects with visible or other measurable lesions achieving at least 50% improvement in lesion number/size orfunctionality impact from baseline.bPediatric is defined as subjects < 18 years of age at baseline.

Subject

Population

Time to Lesion Resolution

Based on All Lesions

Resolved


Based on Visible Lesions

Resolved


Based on Measurable Lesions

Resolved

Pediatric a 12 weeks 8 weeks 8 weeks

Adult 8 weeks 6 weeks 6 weeks

Combined 8 weeks 8 weeks 8 weeks

a Pediatric is defined as subjects < 18 years of age at baseline.

Overall Clinical Success at Week 48


Ryplazim® Impact on Plasminogen Trough Activity Levels and Safety Profile

47

Safety

• Plasminogen (Human) Intravenous at a dose of 6.6 mg/kg administered E2D to E5D for 48 weeks and E1D to E7D for up to 124 weeks was well tolerated in pediatric and adult subjects with congenital plasminogen deficiency.

• Most AE’s were characterized as mild

• Most frequent AE’s were nasopharyngitis, headache and GI related

• No Deaths or SAE’s

• No drug related AE’s that caused study discontinuation

• No Immunogenicity

corporate presentation august 2020

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