Corporate PresentationQ3, 2017

This presentation may contain forward-looking statements, which reflect Trillium's current expectation regarding future

events. These forward-looking statements involve risks and uncertainties that may cause actual results, events or

developments to be materially different from any future results, events or developments expressed or implied by such

forward-looking statements. Such factors include, but are not limited to, Trillium's ability to obtain financing to advance

the products in its development portfolio; changing market conditions; the successful and timely completion of pre-

clinical and clinical studies; the establishment of corporate alliances; the impact of competitive products and pricing;

new product development risks; uncertainties related to the regulatory approval process or the ability to obtain drug

product in sufficient quantity or at standards acceptable to health regulatory authorities to complete clinical trials or to

meet commercial demand; and other risks detailed from time to time in Trillium's ongoing quarterly and annual

reporting. Forward-looking statements are made only as of the date of this presentation and except as required by

applicable securities laws, Trillium undertakes no obligation to publicly update or revise any forward-looking statements,

whether as a result of new information, future events or otherwise.

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Investment Highlights

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Immuno-oncology company developing a next generation checkpoint inhibitor, engaging multiple arms of the immune system

Lead programs targets CD47, a “do not eat” signal tumor cells exploit to escape destruction by the immune system

Phase 1b enrolling 13 cohorts of advanced hematologic malignancies and select solid tumors; Second trial in solid tumors and mycosis fungoides is currently recruiting

Multiple anti-tumor responses observed across both myeloid and lymphoid malignancies

Proprietary fluorine-based medicinal chemistry platform generating a pipeline of pre-clinical oncology assets

Trillium Pipeline: A Clinical Focus on CD47 Blockade with a Platform for Generating New Oncology Assets

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Discovery Preclinical Phase 1 Phase 2

TTI-621 (Systemic)

TTI-621 (Intratumoral)

Bromodomain Inhibitor

EGFR Inhibitor

Hematologicmalignancies + selectsolid tumors

Solid tumors +mycosis fungoides

High brain penetrationfor glioblastoma & brain mets

TBD

SIRPαFc (CD47 Blockade)

Fluorine Med Chem Platform

Undisclosed IO Targets

TTI-622 Combination therapy

Many Tumor Cells Use the CD47 “Do Not Eat” Signal to Inhibit Macrophage Phagocytosis

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High CD47 expression often correlates with aggressive disease and poor clinical outcomes

Many hematologic and solid tumors express high levels of CD47

CD47 delivers an inhibitory “do not eat” signal to macrophages through SIRPα

TTI-621: A Dual Function SIRPαFc Decoy Receptor that is Differentiated from Other CD47 Blocking Agents

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Blocks the DO NOT EAT signal from CD47but does not bind CD47+ red blood cells

Delivers an EAT signal to macrophages through FcγRs; differentiated from IgG4 antibodies

CD47 binding domain of

human SIRPα

Human IgG1 Fc

TTI-621 is a dual function decoy receptor that blocks the suppressive CD47 signal while engaging activating Fc receptors

SIRPaFc (TTI-621): Inducing Anti-Tumor Responses Through Blockade of the CD47 “Do Not Eat” Signal

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TTI-621 Activates Both the Innate and Adaptive Immune Systems

©Audra Geras

TTI-621 Enables Macrophages to Phagocytose A Broad Array of Human Tumor Cells In Vitro

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Control Fc (1 mM) TTI-621 (1 mM)

TTI-621 In Vitro Activity: Dose-dependent increase in phagocytosis Mean EC50 = 10 nM (767 ng/mL) Active against a broad range of hematologic

and solid tumors Activates phagocytosis by M1 and M2

macrophagesRepresentative phagocytosis data (AML target)

TTI-621 is Highly Potent in Vivo

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TTI-621 dosed at 0.2 mg/kg IP 3x/wk (0.05 mg/kg/wk HED) for 4 wks starting 14d after engraftment

Intrafemoral injection of AML patient tumor cells

TTI-621 In Vivo Activity: Active across a range of xenograft models Activity in the AML xenograft model at 0.05

mg/kg/wk HED* Similar potency observed with a mouse

surrogate SIRPaFc (in presence of antigen sink) In non-human primate studies, no severe

toxicity occurs up to an HED of 0.3 mg/kg/week

Results suggest a potent effect at 0.05 mg/kg HED and the presence of a therapeutic window for efficacy

*Human Equivalent Dose

CD47 Blockade by TTI-621 Activates Both the Innate and Adaptive Immune Systems

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Increased tumor cell phagocytosis by TTI-621 leads to enhanced antigen presentation and T cell proliferation using a model (CMV) antigen system

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Standard 3+3 dose escalation in lymphoma patients completed

Expansion across a range of hematological malignancies and small cell lung cancer

10 North American sites:

City of Hope, Duarte CA Cleveland Clinic, Cleveland OH Colorado Blood Cancer Institute, Denver CO Tennessee Oncology, Nashville TN Columbia University, New York NY Mayo Clinic, Rochester MN Memorial Sloan Kettering Cancer Center, New York NY Princess Margaret Cancer Centre, Toronto ON Seattle Cancer Care Alliance, Seattle WA BC Cancer Agency, Vancouver BC

Clinicaltrials.gov: NCT02663518

TTI-621-01: Phase 1 Study in Patients with Advanced Hematologic Malignancies and Selected Solid Tumors

Phase 1b Expansion Cohorts

MonotherapyMyeloid Malignancies

Acute Myeloid LeukemiaMyelodysplastic Syndrome

Myeloproliferative NeoplasmsLymphoid Malignancies

Acute Lymphoblastic LeukemiaChronic Lymphocytic Leukemia

Hodgkin LymphomaIndolent B Cell Lymphoma

Aggressive B Cell LymphomaT Cell Lymphoma

Multiple MyelomaSolid Tumors

Small Cell Lung Cancer

Combination TherapyCD20+ Lymphoma with rituximab

Hodgkin Lymphoma with nivolumab

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First dose is associated with manageable infusion reactions (similar to rituximab)

No induced anemia, consistent with lack of appreciable drug binding to human erythrocytes

Transient, dose-dependent thrombocytopenia observed

Attenuated after the first infusion

Pre-dose platelet levels remain relatively constant as circulating drug levels increase

MTD cautiously defined at 0.2 mg/kg; case by case dose intensification underway to determine if patients tolerate and benefit from higher exposure

TTI-621-01 Safety: TTI-621 is Well-Tolerated in an Outpatient Setting

Platelet Nadirs after Multiple Infusions

Trough Drug Levels and Pre-Dose Platelet Counts

MIP-1α MIP-1β TNF-α

IFN-γ CXCL10 GM-CSF

IL-6 IL-8 IL-10

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After 6 infusions the half-life is ~ 4 days, consistent with other Fc fusion proteins

Receptor occupancy approaching 50% observed on circulating leukemic cells; levels correlate with preclinical activity

Increases in serum cytokines/chemokines associated with macrophage activation observed:

Several chemokines (e.g., MIP-1α) are associated with TTI-621 activity in preclinical models

Profile suggests rapid engagement of the innate immune system

TTI-621-01 PK/PD: Target Binding Leads to Rapid Engagement of the Innate Immune System

Receptor Occupancy on Circulating Leukemic Blasts

Serum Cytokines Post-Infusion

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B cell lymphoma: one Hodgkin lymphoma patient with a transient partial response; several lymphoma patients with prolonged progression-free intervals characterized by decreasing volume disease and decreased PET avidity

AML: one patient with minimal residual disease (0.7% abnormal blasts at baseline) obtained a complete molecular remission after 4 infusions of TTI-621 and remains in continued remission for 15+ weeks

Rituximab combination: 3 of 6 lymphoma patients who have had at least one interval PET/CT restaging obtained partial metabolic responses as demonstrated by decreased tumor activity on PET/CT scans

TTI-621-01 Anti-tumor Activity: Clinical Responses Observed Across Myeloid and Lymphoid Malignancies

Although preliminary, we believe that the multiple clinical responses across varied hematologic malignancies seen to date are encouraging

TTI-621-02: Phase 1 Study in Patients with Solid Tumorsand Mycosis Fungoides (T cell lymphoma)

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Phase 1 study of intratumoral TTI-621 in patients with percutaneously accessible solid tumors or mycosis fungoides (NCT02890368)

Rationale for intratumoral route of administration:

Compelling preclinical efficacy in xenograft models Achieve high local target saturation Can perform serial, on-treatment biopsies to

characterize the effects of TTI-621 on the tumor microenvironment (e.g., macrophages, T cells)

First patient dosed in Q1/2017

Plan to provide update 2H/2017

DLBCL (Toledo) xenograft model

TTI-621 intratumoral injections (0.2 mg/mouse, arrowheads)

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Expanding our CD47 Pipeline with TTI-622

TTI-621 TTI-622

Human IgG1 Fc Human IgG4 Fc

Blocks CD47 and delivers a strong activating signal through FcγRs

Blocks CD47 and delivers a modest activating signal through FcγRs

TTI-621 is the most potent SIRPαFc format

TTI-622 is less likely to deplete platelets, enabling higher exposures

Both agents may have unique combination opportunities

Both agents are differentiated from antibodies by a lack of binding to human erythrocytes

Human SIRPα

SIRPαFc – Broad Clinical Effort in Multiple Malignancies

TTI-621-01 Trial:

Focus on emerging signals of clinical activity and signal seek in additional hematologic malignancies and selected solid tumors

Explore combinations with monoclonal antibodies and other anti-cancer agents

Determine if dose intensification can lead to greater receptor occupancy and ultimately, greater clinical benefit

TTI-621-02 Trial:

Probe the biological effects of TTI-621 on the tumor microenvironment following intratumoral administration

Explore combinations with monoclonal antibodies and other anti-cancer agents

TTI-622:

Submit IND by year end 2017

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Trillium’s Innovative Chemistry Platform –Creating Differentiated New Medicines with Fluorine

Block sites of metabolism to increase half-life and reduce toxicity

Electronegativity alters chemical properties to improve binding & potency

Lipophilicity improves oral absorption and blood-brain-barrier (BBB) penetration

Approximately 25% of all marketed drugs contain fluorine

Innovative proprietary chemistry allows access to an unprecedented class of novel fluorinated molecules

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Epidermal growth factor receptor (EGFR) is a receptor tyrosine kinase involved in the pathogenesis of many cancers

Amplification of EGFR locus is the most common genetic aberration in glioblastoma (GBM)1

Aberrant receptor expression correlates with poor clinical prognosis for GBM patients2

Pharmacological inactivation of EGFR and mutant variants inhibit tumor growth in GBM patients3

EGFR is a Drug Target in Brain Cancer

1Parsons et al. Science. 20082Shinojima et al. Cancer Res. 20033Johns et al. Clin Cancer Res. 2007; Karpel-Massler et al. Mol Cancer Res. 2009

Brain Metastasis

Lung and CRC metastasize to brain

Primary Brain Tumors

>50% of GBMs have amplified/mutated EGFR

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Approved EGFR Inhibitors Exhibit Poor CNS Penetration

EGFR-targeted drugs approved by FDA

HNSCC: head and neck squamous cell carcinoma

There are numerous EGFR-targeted drugs on the market; none are FDA approved for CNS tumors

Clinical testing of EGFR inhibitors in brain cancers has yielded mixed results

Poor blood-brain barrier (BBB) penetration (<5%) limits efficacy of existing agents

There is an urgent unmet medical need for novel BBB-penetrant EGFR inhibitors

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TTI-2341 Exhibits Superior BBB Penetration vs. Afatinib

Brain Exposure Following a Single 20 mg/kg Oral Dose in Male SD Rats (n=4)

TTI-2341 brain AUC and Cmax values are 6-fold higher than afatinib

TTI-2341 (but not afatinib) was quantifiable in the brain up to 24 hours post 7-day repeat dosing

TTI-2341 has >10-fold higher Kpuu (unbound drug brain-to-plasma ratio) than afatinib

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TTI-2341 is a novel covalent inhibitor of wild type and mutant EGFR developed with Trillium’s proprietary fluorine chemistry

Compared to the benchmark compound afatinib, TTI-2341 exhibits:

Similar in vitro potency

Superior in vitro ADME properties

Greater oral bioavailability

Enhanced BBB penetration

TTI-2341 is amenable to radiolabeling with 18F for use as a PET imaging probe

Future development steps have been identified, IND submission can be achieved in approximately 18 months with appropriate resources

Summary – TTI-2341 as a Potential Best-in-class Brain-penetrant Covalent EGFR Inhibitor

Projected 12-month Catalysts

Present initial clinical data from the TTI-621 heme Phase 1a trial – Q4/2016

Presentation of additional preclinical combination data (Q2/2017)

Guidance on the bromodomain inhibitor program – 1H/2017

Update on the EGFR inhibitor program – 1H/2017

Initial clinical data from the TTI-621 solid tumor trial – 2H/2017

Additional clinical data from the TTI-621 heme Phase 1b trial expansion cohorts –2H/2017

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Experienced Leadership & Veteran Board of Directors

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Executive Title Joined Trillium

Dr. Niclas Stiernholm President & Chief Executive Officer 2002

Dr. Robert Uger Chief Scientific Officer 2003

Dr. Eric Sievers Chief Medical Officer 2015

Dr. Penka Petrova Chief Development Officer 2003

Mr. James Parsons Chief Financial Officer 2003

Dr. Malik Slassi Senior Vice President, Discovery Research 2016

MANAGEMENT

BOARD OF DIRECTORS

Executive Recent Affiliation

Dr. Calvin Stiller, Chair Chair

Dr. Henry Friesen Chair

Dr. Niclas Stiernholm CEO

Dr. Michael Moore CEO

Executive Recent Affiliation

Dr. Robert Kirkman CEO

Dr. Thomas Reynolds CMO

Mr. Luke Beshar CFO

Capitalization and Intellectual Property

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SHARES OUTSTANDING

CASH AND MARKETABLE SECURITIES

INSTITUTIONALOWNERSHIP

INTELLECTUAL PROPERTY

16.7M Common & Preferred

$41.3M CAD as of March 31, 2017; $30M USD raised June 2017 (~$40M CAD)

~70%

• Two SIRPaFc patent families covering method of use and composition of matter through 2030 and 2033

• Eleven patent families covering fluorine small molecule therapeutics and medical uses through 2035 and beyond

Investment Highlights

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Immuno-oncology company developing a next generation checkpoint inhibitor, engaging multiple arms of the immune system

Lead programs targets CD47, a “do not eat” signal tumor cells exploit to escape destruction by the immune system

Phase 1b enrolling 13 cohorts of advanced hematologic malignancies and select solid tumors; Second trial in solid tumors and mycosis fungoides is currently recruiting

Multiple anti-tumor responses observed across both myeloid and lymphoid malignancies

Proprietary fluorine-based medicinal chemistry platform generating a pipeline of pre-clinical oncology assets