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

Harnessing Novel Immunobiology May

2019 www.equilliumbio.com Exhibit 99.1

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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Delivering powerful new treatment

approaches Focused on immuno-inflammatory diseases with high unmet need Driven by an accomplished team rapidly delivering key milestones Our lead asset, itolizumab, is unique; modulating both the activity and trafficking of Teff cells Initial

clinical programs are targeting diseases with limited or no treatment options Successful 2018 IPO; launching multiple clinical PoC studies in 2019

Accomplished Management Team Dan

Bradbury Chairman & Chief Executive Officer Bruce Steel, CFA President & Chief Business Officer Steve Connelly, PhD Chief Scientific Officer Jason Keyes Chief Financial Officer Krishna Polu, MD Chief Medical Officer Christine Zedelmayer

Vice-President of Operations

CD6/ALCAM Role in Immuno-inflammatory

Disease Teff cells play an important role in the pathogenesis of T cell mediated diseases driving autoimmune and allergic inflammation Research implicates CD6/ALCAM pathway in disease pathogenesis Initial Indications Transplant Science Neuro-

Inflammation Systemic Autoimmunity Gastrointestinal Ophthalmic Pulmonary Acute Graft-Versus- Host Disease Chronic Graft-Versus-Host Disease Uncontrolled Asthma Interstitial Lung Diseases Lupus/Lupus Nephritis Scleroderma Behcet's Disease

Rheumatoid Arthritis Psoriatic Arthritis Psoriasis Uveitis Ulcerative Colitis Crohn's Disease Multiple Sclerosis Neuromyelitis Optica Dermatological Solid Organ Rejection Chronic Obstructive Pulmonary Disease Atopic Dermatitis Vasculitis T

cell mediated diseases

Itolizumab (EQ001) -

First-in-class Lead Program Equillium acquired exclusive rights to itolizumab for the U.S. & Canada from Biocon - partnership provides clinical & commercial product, commercial scale production at FDA regulated facility First-in-class

anti-CD6 mAb that inhibits the activity and trafficking of Teff cells by selectively targeting the CD6/ALCAM pathway Unique, multi-modal mechanism with potential disease modifying utility Demonstrated clinical tolerability and efficacy -

approved for the treatment of psoriasis in India Broad potential pipeline in a product', launching multiple clinical studies during 2019

Itolizumab Development Strategy

Equillium is well-capitalized and staffed to execute on key programs aGVHD uncontrolled asthma Indication Phase 1 Phase 1b / 2 Phase 3 Expected Milestones FDA Fast Track Orphan Drug Designation lupus nephritis Uncontrolled moderate to severe asthma

proof-of-concept trial to initiate Q2 2019 Phase 1b/2 aGVHD trial initiated March 2019 Data to inform further development in GVHD, e.g. GVHD prevention, cGVHD Lupus nephritis proof-of-concept trial to initiate H2 2019 Data to inform further

development in lupus

The CD6/ALCAM Pathway

CD6/ALCAM Pathway Central to

Immuno-inflammation T CELL APC / TISSUE CD6 is a co-stimulatory receptor differentially expressed on T cells, 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 is central to the pathogenesis of multiple immuno-inflammatory diseases

Itolizumab Humanized IgG1 Kappa

Binds to domain 1 of human CD6 with 1.3 nM affinity Inhibits ALCAM binding to CD6 Non-depleting, modulatory action Manufacturing and formulation Manufactured in CHO cells at commercial scale IV and SC formulations available 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 Modulates CD6/ALCAM Pathway

CD6 - Central Role in Effector

Cell Development 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" CD6 Low/- CD6 +

CD6 Hi CD6 Th1 Th2 Th17

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

Itolizumab Inhibits Pathogenic T

Cell Activity & Trafficking ACTIVITY TRAFFICKING Decreased proinflammatory cytokine secretion Restoration of regulatory pathways Decreased trafficking of Teff cells into target tissues Inhibits optimal synapse formation co-stimulation,

activation and proliferation

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

Acute graft-versus-host disease

(aGVHD) 8,500 30-70% 53% 0 Allo-HSCT's performed in 2016 4% procedural growth year-over-year Allo-HSCT patients will develop aGVHD Survival rate for steroid responders Number of approved treatments Number of products in development for

first-line aGVHD 2 95% Mortality rate for steroid non-responders A multisystem complication of allogeneic hematopoietic stem cell transplants, or allo-HSCT, caused by Teff cells, recognizing and attacking the recipient's body Product in

development that modulates both the activity and trafficking of Teff cells - itolizumab 1 All numbers are approximate and based on published reports

Itolizumab is a Differentiated aGVHD

Treatment Option Cannabidiol ZEMAIRA ENTYVIO Itacitinib JAKAFI T-Guard DEFITELIO ORENCIA GLASSIA Prevention First-line Steroid-Refractory Itolizumab Phase 3 Phase 3 ready Phase 2b Phase 2 Phase 3 ready

Phase 2 Phase 3 sNDA Phase 1b/2 Phase 3 ready BLA PROCYMAL Acute GVHD 0-100 days post-transplant Dual mode of action inhibits the activity and trafficking of Teff cells Disease-modifying therapy with durable benefit Immunomodulatory and not

immunosuppressive No cytopenias seen in Biocon Phase 3 psoriasis studies Positive Phase 1b data will inform lifecycle opportunity in GVHD prevention and cGVHD First line positioning Itolizumab

Strong Scientific Rationale for

Itolizumab in aGVHD Itolizumab shown to be effective in animal models of GVHD and inflammatory bowel disease (IBD) Ex vivo depletion of CD6+ Teff cells from donor bone marrow prior to allogeneic transplant effectively reduced GVHD incidence CD6+ T

cells in drive Th1/Th17 immune responses and mucosal inflammation in IBD Th17 cells expressing CD6 play a critical role in the pathogenesis of aGVHD Th17 cells are steroid resistant ALCAM expressed on target organs facilitates infiltration of CD6+

Teff cells Studies have shown a high Th17:Treg ratio indicative of a loss of tolerance in aGVHD patients FDA Fast Track for treatment of aGVHD and Orphan Drug Designations for both the prevention and treatment of aGVHD Phase 1b/2 aGVHD trial

initiated in Q1 2019 Data to inform further development in GVHD, e.g. GVHD prevention, cGVHD Translational Validation Clinical Development Scientific Rationale Soiffer et al., 1992. "Prevention of graft-vs-host disease by selective depletion

of CD6-positive T lymphocytes from donor bone marrow." J Clin Oncol 10(7): 1191-1200; Ma et al., 2018. "Critical role of CD6high CD4+ T cells in driving Th1/Th17 cell immune responses and mucosal inflammation in IBD." J

Crohn's and Colitis 13(4): 510-520

EQUATE Study for First-line

Treatment of aGVHD Patients Assess the safety and tolerability of intravenous (IV) dosing of itolizumab Determine optimal IV dose level(s) of itolizumab Primary Objectives Secondary Objectives Characterize the pharmacokinetics (PK) and

pharmacodynamics (PD) of itolizumab Assess the clinical activity of itolizumab (GVHD ORR, NRM, cGVHD, durability) Study Population: Frist-line treatment of newly diagnosed aGVHD patients Study Design Open-label, dose escalation Randomized,

double-blind, placebo controlled Phase 1b topline expected Q1 2020 Phase 1b informs Phase 2 study as well as lifecycle strategy that may include GVHD prevention and cGVHD Assess the clinical activity of itolizumab (GVHD ORR, NRM, cGVHD, durability)

Further characterize the safety, tolerability and PD of intravenous (IV) dosing of itolizumab Phase 1b N=24 (High Risk-MacMillan criteria) Phase 2 N~60 (Grade II - IV)

Uncontrolled moderate to severe

asthma 2.6mm 1.3mm ~50% 0 Severe asthma patients in the U.S. Patients uncontrolled by standard-of-care treatments (long-acting beta-agonists, inhaled corticosteroids, oral corticosteroids) Of uncontrolled patients do not respond to existing biologic

treatments Approved products that cover the full spectrum of disease (Th2 High - Non-Th2 asthma) Products in development that target Non-Th2 asthma 2 A heterogeneous disease characterized by different Teff cell subtypes and other innate immune

cells driving both allergic and autoimmune mechanisms, leading to chronic airway inflammation Product in development that modulates both the activity and trafficking of Teff cells - itolizumab 1 All numbers are approximate and based on

Itolizumab May Address The Full

Spectrum of Uncontrolled Asthma Current therapies target downstream signaling of Th2-associated inflammation Current downstream therapies ineffective in patients with low levels of eosinophils No approved therapies anti-TSLP anti-IgE anti-IL-5 DP2

Agonist CINQAIR anti-IL-4 and IL-13 anti-IL-33 XOLAIR FASENRA DUPIXENT Fevipiprant RG6149 Etokimab GSK3772847 Tezepelumab Th2-High Eosinophils Non-Th2 Neutrophils Th2-Low Low Eosinophils Reciprocally regulated Response to

steroids Marketed Marketed Marketed Marketed NUCALA Marketed Phase 3 Phase 2 Phase 2 Phase 2 Phase 3 anti-CD6/ALCAM Itolizumab Phase 1b/2 GB001 Phase 2

Itolizumab Targets both Th2 and

Non-Th2 Asthma Pathogenesis Modulating CD6-ALCAM pathway attenuates activity and trafficking of Th1 (IFN- ), Th2 (IL-4,5,13), Th17 (IL-17) cells and cytokines in multiple models of autoimmune and allergic inflammation Transcriptional and

histological analyses support the presence of increased CD6, CD4 T cells, and ALCAM in the lungs of severe asthma patients Asthma is a heterogenous disease with CD6+ Th1 (IFN- ), Th2 (IL-4,5,13), Th17 (IL-17) and ILC cells and cytokines

involved in the pathogenesis Th17 and ILC cells are steroid resistant ALCAM expressed on lung tissues facilitates infiltration of CD6+ Teff cells High Th17:Treg ratio associated with asthma exacerbations Uncontrolled moderate to severe asthma

proof-of-concept trial to initiate Q2 2019 Data to inform further development in Th2 and non-Th2 asthma Translational Validation Clinical Development Scientific Rationale Kim et al., 2028. "Activated leukocyte cell adhesion molecule stimulates

the t-cell response in allergic asthma." American Journal of Respiratory and Critical Care Medicine. 197(8); Li et al, 2017. "CD6 as a potential target for treating multiple sclerosis." PNAS 114(10): 2687-2692; Bughani et al.,

2018. "T cell activation and differentiation is modulated by a CD6 domain 1 antibody itolizumab." PLoS One 12(7): e0180088

CD6 Upregulation and ALCAM

Expression in Severe Asthma Patients ***p<0.001, *p<0.05. Fatal asthma Non-asthma ALCAM CD6 overlay epithelium Lamina propria Lamina propria epithelium Examination of gene expression datasets and lung tissue support the presence of increased

CD6, CD4 T cells, and ALCAM in the lungs of severe asthma patients Analysis of two different gene expression datasets support the presence of increased CD6, CD4 T cells, and ALCAM in the lungs of severe asthma patients Fatal asthma patients lung

tissue staining suggests increased numbers of CD6+ cells, upregulation of ALCAM in the lamina propria (mucosa), and co-localization of CD6+ cells with ALCAM expressing tissue Study of the Mechanisms of Asthma (MAST; NCT00595153); Bronchoscopic

Exploratory Research Study of Biomarkers in Corticosteroid-refractory Asthma (BOBCAT) study; Data courtesy of Reynold A. Panettieri, Jr., MD, Rutgers Institute for Translational Medicine and Science

EQUIP Study in Uncontrolled Moderate

to Severe Asthma Assess the safety and tolerability of subcutaneous dosing of itolizumab Determine optimal subcutaneous dose level(s) of itolizumab Primary Objectives Secondary Objectives Characterize the pharmacokinetics (PK) and pharmacodynamics

(PD) of itolizumab Assess the clinical activity of itolizumab (FEV1, ACQ, FeNO, Eos) Phase 1b N=32 Study Design Randomized, double-blind, placebo controlled, dose escalation study Study to initiate Q2 2019 Phase 1b topline expected H2 2020 Study

Population: Uncontrolled moderate to severe asthma patients

Lupus nephritis 100,000 50%-75% 40%

0 9 Lupus nephritis patients in the U.S. Of patients do not respond to frontline treatments Of severe, proliferative patients will progress to end-stage renal disease Approved treatments Products in development Product in development that modulates

both the activity and trafficking of Teff cells - itolizumab 1 A heterogeneous disease that is the most frequent and serious manifestation of systemic lupus erythematosus (SLE) All numbers are approximate and based on published reports