Safe Harbor Statement This presentation contains forward-looking statements about Equillium, Inc. (the "Company"). In some cases, you can identify forward-looking statements by the words "will," "expect," "intend," "plan

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Welcome Bruce Steel, CEO Potent

Immune Modulation with Itolizumab Steve Connelly, CSO Advancing Itolizumab in Graft-vs-Host Disease (GVHD) Krishna Polu, CMO John Koreth, M.D., Dana-Farber Steve Connelly, CSO Itolizumab - a Promising Therapeutic to Treat Lupus Nephritis

Krishna Polu, CMO Steve Connelly, CSO Joel Rothman, SVP Development Operations Itolizumab - a Differentiated Approach to Treat Uncontrolled Asthma Steve Connelly, CSO Financials & Corporate Update Jason Keyes, CFO Closing

Remarks Bruce Steel, CEO Q&A Today's Agenda Speakers Bruce Steel, CFA Chief Executive Officer Steve Connelly, Ph.D. Chief Scientific Officer Jason Keyes Chief Financial Officer Krishna Polu, M.D. Chief Medical

Officer John Koreth, M.D., D.Phil. Director of Translational Research, Stem Cell Transplantation Dana-Farber Cancer Institute Joel Rothman SVP of Development Operations Equillium Management Guest Speaker

Our mission is to dramatically improve

the lives of patients through the development of novel immunotherapies World leaders in CD6 biology developing itolizumab, a first-in-class anti-CD6 antibody targeting the CD6-ALCAM pathway Itolizumab is a validated therapeutic with

differentiated mechanism of action (MoA) inhibiting the activity and trafficking of Teff We are advancing development in three severe autoimmune and inflammatory disorders Acute Graft-versus-Host Disease (aGVHD) Lupus/Lupus Nephritis Uncontrolled

Asthma Novel Treatments for Severe Immuno-inflammatory Disorders

Highly differentiated mechanism of

action with potential broad therapeutic utility Itolizumab Development Strategy uncontrolled asthma acute graft-versus-host disease (aGVHD) Indication Phase 1b Phase 2 / 3 Status systemic lupus erythematosus (SLE) / lupus nephritis (LN) FDA Fast

Track and Orphan Drug Designations EQUATE Phase 1b/2 trial actively enrolling Positive interim data reported 2H 2020 Topline data expected 1H 2021 EQUIP Phase 1b trial actively enrolling Topline data expected 2H 2021 FDA Fast Track Designation

EQUALISE Phase 1b trial actively enrolling SLE topline data expected 1Q 2021 LN interim data expected 2H 2021 Regulatory interaction and study initiation expected mid-2021

T Cell Mediated Immuno-inflammatory

Strategic partnership with Biocon

Limited (Biocon): exclusive rights to develop and commercialize itolizumab in the U.S., Canada, Australia, New Zealand Includes supply of commercial-scale drug product manufacturing Three clinical development programs ongoing; initial data promising

Strong cash balance and core institutional shareholders Complete proof-of-concept (PoC) for initial indications Accelerate development on path to approval in first-line aGVHD Broaden asset pipeline to complement itolizumab Potential to be first to

market in first-line treatment of aGVHD Build Company through pipeline expansion Demonstrably improve patient lives by bringing novel immunotherapeutics to market Our Journey to Improve Patient Lives...

Potent Immune Modulation with

CD6 is a co-stimulatory receptor

expressed on T cells, differentially expressed on subsets of innate lymphoid (ILC) and natural killer (NK) cells, but not on T regulatory cells (Treg) Activated leukocyte cell adhesion molecule (ALCAM), is expressed on both antigen-presenting cells

and endothelial/epithelial tissue including the blood-brain-barrier, skin, gut, lung and kidney The binding of CD6-ALCAM is important for: Immune synapse formation Optimal co-stimulation and activation Trafficking into tissues The CD6-ALCAM pathway

modulates T cell activity and trafficking and we believe is central to the pathogenesis of multiple immuno-inflammatory diseases CD6-ALCAM Pathway Central to Immuno-inflammation T CELL APC / TISSUE Consuegra-Fernandez et al., Cell Mol Immunol 2018

CD6 Expression Associated with T

Cell Function Highest levels of CD6 are found on activated T effector cells (Teff) and associated with amplification of the auto-reactive cascade Immune Regulatory "Tolerance" Autoreactive "Autoimmunity" CD6Low/- CD6 +

CD6High CD6 Th1 Th2 Th17 Garcia et al., Cytometry 2014; Bughani et al., PLoS 2017 Signaling Signaling Weak Strong

T eff T reg CD6high High

Proliferation Pathogenic Phenotypes Pro-inflammatory cytokines CD6low/- Low proliferation Regulatory phenotype Anti-inflammatory cytokines CD6High Cells Exhibit Greater Pathogenic Capacity Consuegra-Fernandez et al., Cell Mol Immunol 2018; Ma et

al., J Crohns & Colitis 2019

Increased activation induced cell

death Decreased Teff proliferative responses Impaired Th17 differentiation Attenuation of disease in EAE, EAU & Pso EAE: Experimental Autoimmune Encephalomyelitis EAU: Experimental Autoimmune Uveitis Pso: Psoriasis Reduced infiltration of

Teff cells into tissues Decreased proliferative responses Differentiate more efficiently into FoxP3+ cells following allogeneic stimulation CD6-/- Phenotype of Teff & Treg Cells CD6 -/- Mouse Li et al., PNAS 2017; Zhang et al. J Autoimmun

2018; Consuegra-Fernandez et al., Cell Mol Immunol 2018; Orta-Mascaro et al., JEM 2016

CD6-ALCAM Pathway Central to

Immuno-inflammation ACTIVITY TRAFFICKING Increased proinflammatory cytokine secretion Suppression of regulatory pathways Increased trafficking of Teff cells into target tissues Optimal immune synapse formation, activation and proliferation

An Example of the CD6-ALCAM Pathway

in Disease Ma et al., J Crohns & Colitis 2019

CD6 & ALCAM are Increased in

Intestine of Inflammatory Bowel Disease (IBD) Patients Ulcerative Colitis Crohn's Disease Healthy control CD6 ALCAM Ma et al., J Crohns & Colitis 2019

CD6-ALCAM Pathway is Associated with

Severity of IBD Ma et al., J Crohns Colitis 2019 ***P<0.001 ALCAM CD6 Ulcerative Colitis Crohn's Disease Ulcerative Colitis Crohn's Disease

CD6high Cells are Enriched in

Inflamed GI Tissues ALCAM CD6 Increased CD6/ALCAM expression localizes to inflamed tissue of IBD patients Ulcerative Colitis Crohn's Disease Ulcerative Colitis Crohn's Disease Ma et al., J Crohns Colitis 2019 ***P<0.001

Increased IFN /IL-17 Secretion

Associated with CD6high Cells Pathogenic dual IFN- / IL-17 expressing Th17 cells implicated in multiple autoimmune and inflammatory diseases are associated with levels of CD6 in IBD patients Ma et al., J Crohns Colitis 2019. **p < 0.01, and

***p < 0.001 versus CD6low/ group. #p < 0.05, and ##p < 0.01 versus CD6int group. Data are shown as mean SEM

Itolizumab Humanized IgG1

Kappa Binds to domain 1 of human CD6 with 1.3 nM affinity Inhibits ALCAM binding to CD6 and leads to antigenic modulation Non-depleting, no ADCC, CDC activity Manufacturing and formulation Manufactured in CHO cells at commercial scale Single

formulation allows for IV or subcutaneous (SC) administration Dosing Half-life IV/SC @ 20/24 days respectively; target dosing of bi-weekly to monthly with potential for quarterly maintenance T CELL APC / TISSUE Itolizumab (EQ001) - A First-in-Class

Antigenic Modulation of Cell Surface

CD6 CD6 mean fluorescence intensity on itolizumab treated cells normalized to isotype treated cells 3 independent experiments on Donor 1041 (unstimulated PBMCs) CD6hi CD6lo Same pattern of CD6 loss is observed in both na ve and effector/memory

subsets Pathogenic Non-pathogenic Antigenic modulation

CD6 Blockade Inhibits Teff

Activation and Proliferation Inhibition of activation and proliferation Nair et al., Clin. Exp. Immunol., 2010 Control Itolizumab *p<0.05

CD6 Blockade Inhibits Pathogenic

Teff Activity Betelli et al., J. Exp. Med. 2005; Muranski et al., Blood 2013; Banuelos et al., Cytokine Growth Factor Rev. 2016; Ramesh et al., J.Exp. Med. 2014; Bughani et al., PLoS, 2017 Downregulation of pSTAT3 ROR T Decrease in pathogenic

Th17 cells Pathogenic Th17 cells exhibit increased STAT3 and ROR T and secrete multiple pro-inflammatory cytokines including IL-17A/F, GM-CSF, IFN- , IL22 and IL-23 Loss of glucocorticoid receptor and increase of MDR1 leads to treatment

refractory cells Itolizumab Itolizumab Control Control

CD6 Blockade Inhibits Pathogenic

Teff Activity Lee et al., 2008; Bughani et al., PLoS, 2017 Decrease in pathogenic, dual IFN- / IL-17 expressing T cells Pathogenic dual IFN- / IL-17 expressing Th17 cells implicated in multiple autoimmune and inflammatory diseases IL-17A

Cell-surface CD6 was removed by

incubating peripheral blood mononuclear cells (PBMC) with itolizumab (or isotype) for 24 hours Afterwards, all cell-bound and excess itolizumab was removed PBMCs were then stimulated with anti-CD3 and ALCAM for 24 hours and activation markers were

assessed by flow cytometry CD6low Cells are Hyporesponsive to TCR Stimulation Activation Markers After Stimulation with anti-CD3 + ALCAM Surface Levels of CD6

Animal Model/ Disease Relevance

Method T cell response Key Results Human Tissue Expression CD6 ALCAM TNBS Colitis Inflammatory Bowel Disease TCT 2020 Anti-mCD6 Th1, Th17 Decreased colitis Improved body weight Decreased serum cytokine levels EAE Multiple Sclerosis, NMO Li et al.,

PNAS. 2018 Anti-mCD6 CD6 -/- Th1, Th17 Decreased antigen-specific Th1/Th17 responses Decrease inflammation and demyelination in the CNS (hu) PBMC NSG GvHD, Inflammatory Bowel Disease Ng et al., Blood 2019. TCT 2020 Anti-hCD6 Th1, Th17

Decreased human T cell prevalence Decrease of infiltrating T cells in lung and intestine Improved survival Collagen-Induced Arthritis Rheumatoid Arthritis Li et al., Arthritis & Rheum. 2020 CD6 -/- Anti-mCD6 Th1, Th9, Th17 Decreased

collagen specific Th9 and Th17 Decreased serum pro-inflammatory cytokines and collagen reactive total IgG and IgG1. Reduced joint inflammation Imiquimod-induced Psoriasis Consuegra-Fern ndez et al., Cellular & Molecular

Immunology 2017 CD6 -/- Th1, Th17 Decrease skin inflammation Decrease in proinflammatory cytokines EAU Autoimmune Uveitis Zhang et al., J. Autoimmunity 2018 CD6 -/- Th1, Th17 Decreased retinal inflammation Decreased autoreactive T cell responses

Translational Biology - Summary Tables

Animal Model/ Disease Relevance

Method T cell response Key Results Human Tissue Expression CD6 ALCAM Nephrotoxic Serum Nephritis Antibody-mediated Nephritis ACR 2020 Anti-mCD6 Th1, Th17 Decrease in proteinuria, urinary albumin, BUN Decreased renal infiltration/trafficking by

activated T cells and macrophages MRL/MpJ-Faslpr SLE/Lupus Nephritis ACR 2020 Anti-mCD6 Th1, Th2, Th17 Reduction in lymphadenopathy score, decrease in IFN and TNF- levels in lymph nodes Reduction in size/severity of skin lesions OVA-

& OXA-induced dermatitis Atopic Dermatitis Oh et al., Allergy Asthma Immunol Res. 2019 ALCAM -/- Th2, Th17 Improved skin clinical scores Decreased expression of Th2 cytokines in skin Decreased numbers of activated T cells in skin and draining

lymph nodes OVA-induced food allergy Allergy Kim et al., Clinical & Experimental Immunology 2018 ALCAM -/- Anti-mCD6 Th2 Decreased expression of Th2 cytokines in small intestine Decreased numbers of activated T cells in LN and small intestine

Decrease in total serum IgE OVA-induced asthma Asthma Kim et al., AJRCCM. 2018 ALCAM -/- Anti-mCD6 Th2 Decreased levels of Th2 cytokines in BALF Decreased T cell trafficking to the lung Decrease in total serum IgE Translational Biology - Summary

Upstream, Disease Modifying

Immuno-inflammatory Mechanism Restoration of immune regulation without immunosuppression Inhibition of Teff trafficking into key target organs Synergistic inhibition of multiple Teff cells and cytokines* Itolizumab acts upstream and selectively

targets autoreactive effector T cells, while sparing regulatory T cells to promote immune tolerance and durable disease remission Treg Teff Teff Teff Teff Teff Teff *including but not limited to IFN- , TNF- , IL-4, IL-5, IL-6, IL-13 and

IL-17 Th1 / Th2 / Th17

Advancing Itolizumab in

Graft-vs-Host Disease (GVHD)