Forward Looking Statements This presentation contains "forward-looking statements" that involve substantial risks and uncertainties for purposes of the safe harbor provided by the Private Securities Litigation Reform Act

Synlogic DESIGNED FOR LIFE June 2019

Corporate Presentation Exhibit 99.1

Forward Looking Statements This

presentation contains "forward-looking statements" that involve substantial risks and uncertainties for purposes of the safe harbor provided by the Private Securities Litigation Reform Act of 1995. All statements, other than statements

of historical facts, included in this presentation regarding strategy, future operations, future financial position, future revenue, projected expenses, prospects, plans and objectives of management are forward-looking statements. In addition, when

or if used in this presentation, the words "may," "could," "should," "anticipate," "believe," "estimate," "expect," "intend," "plan,"

"predict" and similar expressions and their variants may identify forward-looking statements. Examples of forward-looking statements include, but are not limited to, the approach we are taking to discover and develop novel therapeutics

using synthetic biology; statements regarding the potential of our platform to develop therapeutics to address a wide range of diseases, including: inborn errors of metabolism, liver disease, inflammatory and immune disorders, and cancer; the future

clinical development of Synthetic Biotic medicines; the potential of our technology to treat hyperammonemia and phenylketonuria; the expected timing of our anticipated clinical trial initiations; the benefit of orphan drug and fast track status; the

adequacy of our capital to support our future operations and our ability to successfully initiate and complete clinical trials; the results of our collaborations; and the difficulty in predicting the time and cost of development of our product

candidates. Actual results could differ materially from those contained in any forward-looking statement as a result of various factors, including, without limitation: the uncertainties inherent in the preclinical development process; our ability to

protect our intellectual property rights; and legislative, regulatory, political and economic developments, as well as those risks identified under the heading "Risk Factors" in our filings with the SEC. The foregoing review of important

factors that could cause actual events to differ from expectations should not be construed as exhaustive and should be read in conjunction with statements that are included herein and elsewhere, including the risk factors included in our Annual

Report on Form 10-K filed with the SEC on May 9, 2019. The forward-looking statements contained in this presentation reflect our current views with respect to future events. We anticipate that subsequent events and developments will cause our views

to change. However, while we may elect to update these forward-looking statements in the future, we specifically disclaim any obligation to do so. These forward-looking statements should not be relied upon as representing our view as of any date

subsequent to the date hereof.

Harnessing nature and technology to

create LIVING medicines designed to significantly improve patients' LIVES Synthetic BioticTM Medicines Designed For Life

v Synthetic BioticTM Medicines A Novel

Class of Engineered Living Medicines Designed genetic circuits to execute biological functions Degradation of disease-causing metabolites Production of therapeutic molecules Bacterial chassis Non-pathogenic Amenable to genetic manipulation PATHWAYS,

COMBINATIONS, BIOMARKERS PROGRAMMABLE POTENCY AND CONTROL LOCAL ACTIVITY, REDUCED SYSTEMIC TOXICITY BIOTIC SYNTHETIC

Synthetic Biotic Portfolio: Breadth and

Potential Initial Applications Designed to Target Different Sites of Action in Metabolic and Immunomodulatory Diseases Oral Administration IMMUNOMODULATION METABOLIC DISEASES Immuno-Oncology Inflammatory and Autoimmune Small or Large Intestine

"Cold" Solid Tumors Small or Large Intestine Rare Metabolic Disease Broad Metabolic Disease

Builds off validated pilot program

initiated in 2017 Provides access to Ginkgo's industrial scale, high-throughput strain optimization and screening Enables screening and identification of higher quality optimized candidates, increasing potential for success Delivers novel

tools for increased candidate potency Includes equity investment at a premium, extending runway through multiple milestones Platform Collaboration to Accelerate Development of Synlogic's Synthetic Biotic Medicines

Platform Collaboration to Accelerate

Development of Synlogic's Synthetic Biotic Medicines Industry leader in the construction and editing of microbial strains and organisms Leaders in non-therapeutic commercial applications of synthetic biology Comprehensive database of microbial

genome sequences and unparalleled automated foundry Top-tier platform companies and collaborations High-quality investor base Rapid prototyping and screening enables efficient iteration through 1000's of microbial strains

Investing in Development of a Robust

Pipeline for Range of Diseases Hyperammonemia - Urea Cycle Disorder Research IND-Enabling Studies Phase 1 Phase 2 Phenylketonuria Additional Rare Metabolic Diseases Hyperammonemia - Hepatic Encephalopathy (HE) Inflammatory Bowel Disease

Immuno-Oncology Solid Tumors Additional Oncology Applications SYNB1020 SYNB1618 SYNB1020 SYNB1891 Rare Metabolic Diseases Broad Metabolic Disease Immunomodulation

UREA CYCLE DISORDERS (UCD) SYNB1020 for

Hyperammonemia Indications Characterized by Systemic Ammonia Accumulation Neuropsychiatric complication in patients with end-stage liver disease (cirrhosis) Liver dysfunction leads to ammonia accumulation Toxic to brain, leading to HE crisis &

hospitalization Patients: 165,000 diagnosed overt patients in US Up to 70% of patients with cirrhosis characterized as covert (subclinical) Treatment: Lactulose: laxative with significant side effects Rifaximin: reduction in overt HE recurrence

Genetic defects in Urea Cycle Deficiency in one of the six enzymes Nitrogen accumulates as toxic ammonia leading to metabolic crisis Patients: ~2,000 diagnosed in US; similar in EU Treatment: Ammonia scavengers: Buphenyl (sodium

phenylbutyrate), Ravicti (glycerol phenylbuterate) Low protein diet with amino acid supplements Target Profile to Address Unmet Need: Reduce episodes of hospitalization Improve cognitive outcomes, Quality of Life Target Profile to Address

Unmet Need: Maintain blood ammonia in normal range, avoid crisis Protein liberalization: 50-100% more per day Oral administration HEPATIC ENCEPHALOPATHY (HE)

Arginine Urea SYNB1020 Mechanism of

Action: Under normal conditions, the urea cycle metabolizes ammonia into urea In UCD and HE, ammonia is not efficiently metabolized via urea cycle. SYNB1020 provides an alternative mechanism Conversion of Toxic Ammonia into Beneficial Arginine for

the Treatment of UCD and HE Ammonia/NH4Cl Urea Cycle Ammonia Arginine Arginine argD argF argI argG carA carB argR argE argC argB argH Metabolic Conversions FNR FNR argAfbr Glutamate Converts ammonia to Arginine Engineered Probiotic Bacteria: E. coli

Nissle Components of Synthetic Genetic Circuit Can re-enter the Urea Cycle Ammonia metabolism blocked in disease

In vivo data in mouse models and

healthy volunteers demonstrate mechanism of action SYNB1020 data recently published in Science Translational Medicine PLASMA NITRATE URINARY NITRATE MOUSE MODEL

SYNB1020 Clinical Data in Healthy

Volunteers Dose-dependent Increase in SYNB1020 in Feces, Clearance on Cessation of Dosing DOSE-DEPENDENT INCREASE IN FECES CLEARANCE Dosing period = 14 days Dosing period = 14 days Samples collected daily

SYNB1020 Clinical Development

Hepatic Encephalopathy Phase 1b/2a in Patients with Cirrhosis and Elevated Ammonia Hepatic Encephalopathy Clinical Trial Randomized, double-blind placebo-controlled study ongoing at multiple sites in the US Primary outcome: establish

safety/tolerability in patients with cirrhosis and elevated ammonia Secondary outcome: reduction of ammonia Phase 1b / 2a PROGRAM Hepatic Encephalopathy Mild Cirrhosis Patients, MELD1<12, Open label, TID for 6 days Sentinel cohort for safety N =

6 Cirrhosis Patients: MELD < 20 & Elevated Ammonia; RCT, TID for 6 days Proof of Mechanism N up to 40 Safety Evaluation Part 1 Part 2 1. MELD score: scoring system model for end-stage liver disease Urea Cycle Disorders (Plans to continue

development in UCD dependent on data from Ph 1b/2a HE study)

PKU is a rare inherited amino acid

metabolism disorder Causes build up of amino acid phenylalanine (Phe) in the body Today, less than half of adults are at or below target Phe levels of 120-360 mmol / L If left untreated, symptoms include cognitive impairment, convulsions, behavioral

problems, skin rash Patients: 16,500 diagnosed in US, similar in EU5 Treatment: Phenylalanine is found in all proteins therefore low protein diet is followed (no meat, dairy, nuts, eggs) KUVAN (sapropterin dihydrochloride): PAH cofactor.

20-40% of patients are responders PalynziqTM (pegvaliase-pqpz): injectable, pegylated, bacterial enzyme (phenylalanine ammonia-lyase or PAL) for treatment of adult patients SYNB1618 for Phenylketonuria (PKU) Target Profile to Address Unmet Need:

Manage Phe below target levels to prevent irreversible cognitive damage Increase natural protein intake: classic PKU patients' natural protein intake is typically less than 10g Oral dosing without systemic toxicity Goal: Managing Plasma Phe

SYNB1618 Mechanism of Action Amino

acids from dietary proteins (absorption and recirculation) Phe PKU Healthy Phenylalanine Hydroxylase (PAH) converts Phe into Tyrosine Tyrosine Accumulation of Phe to toxic levels Impaired PAH SYNB1618 Manage Phe levels When Phe is not efficiently

metabolized (PKU) SYNB1618 provides an alternative mechanism PAL3: produces TCA which is converted to HA in the liver and is excreted in urine LAAD: produces phenylpyruvate (PP) Phenylalanine (Phe) Hippuric Acid (HA) Engineered Probiotic Bacteria:

E. coli Nissle Components of Synthetic Genetic Circuit trans-Cinnamic Acid (TCA) PheP: High-Affinity Uptake trans-Cinnamic Acid (TCA) pheP PAL3 Metabolic Conversions FNR FNR FNR FNR Phenylalanine LAAD AraC AraC Phenylalanine (Phe) Phenylpyruvate

SYNB1618 Preclinical

Characterization Biomarkers Demonstrate Activity of SYNB1618 in Mouse Model of PKU and Healthy NHPs IN VIVO EFFICACY IN (PKU) PAHenu2/enu2 MOUSE DOSE RESPONSE IN HEALTHY NHPs Nat. Biotechnol. 2018 Oct;36(9):857-864 Development of synthetic live

bacterial therapeutic for the human metabolic disease phenylketonuria Vincent M Isabella et al, Synlogic, Inc.

SYNB1618 in the Clinic: Safety There

were no treatment-related serious adverse events, no systemic toxicity or infections Treatment-emergent adverse events were either mild or moderate in severity, and reversible. Most adverse events were GI-related Single dose MTD was defined as

2x1011 CFU. Doses above this level were associated with dose-limiting GI adverse events All subjects cleared the bacteria. There was no evidence of colonization, and no subject required antibiotics Interim Analysis of Phase 1/2a SAD/MAD Study

Demonstrates Safety and Clearance in Healthy Volunteers Based on pharmacodynamic data and tolerability profile, a dose of 7x1010 CFU was identified for the second part of the study in PKU patients 56 healthy volunteers Received at least one dose of

SYNB1618 or placebo Adults Age range: 18-62 yrs old

SYNB1618 in the Clinic: Activity

Statistically Significant Dose-dependent Activity of SYNB1618 in Healthy Volunteers SYNB1618 or placebo Protein shake / meal D5-Phe Measure over 6hrs: Plasma: Phe/D5-Phe TCA/D5-TCA Urine: HA/D5-HA TCA AUC SINGLE DOSE RESPONSE MAD URINARY HA AND

D5-HA Key: HA: Hippurate, D5-HA: labeled HA, CFB: change from baseline, CFP: change from placebo

SYNB1618 Clinical Development Phase

1/2a in Healthy Volunteers with Patient Cohort Phase 1 / 2a Phase 1 / 2a SAD / MAD Healthy Volunteers SD / MD PKU Patients PROGRAM PKU Clinical Trial Design Randomized, double-blind placebo-controlled study ongoing at multiple sites in the US

Primary outcome: establish safety/tolerability following single and multiple doses in HV and PKU patients Secondary outcome: SYNB1618 kinetics in feces Exploratory: change from baseline in plasma and urinary biomarkers Single Ascending Dose (SAD)

Healthy Volunteers 6 cohorts, N = 24 Multiple Ascending Dose (MAD) 7 days Healthy Volunteers; 4 cohorts, N = 32 MTD Dose ID Single Dose (SD) PKU Patients N = 4 Multiple Dose (MD) 7 days PKU Patients; N up to 20 Dose Confirm

2019 SYNLOGIC. ALL RIGHTS

RESERVED. | Immuno-Oncology

CHECKPOINT INHIBITORS HAVE TREATMENT

FAILURES Synlogic Vision for Immuno-Oncology Expand the Benefits of Immunotherapy Broadly Across Tumor Types Other tumors, where CPIs are not indicated, show little-to-no response to checkpoint inhibitors Failure Rates for Select FDA Approved CPI

Monotherapy 55% NSCL 1st line 60% Melanoma 1st line 71% Bladder 1st line 87% Cervical / Gastric 2nd line Non-responders For indications where immune checkpoint inhibitors are indicated, 55-87% of patients fail to respond Nature often gives us hints

to her profoundest secrets, and it is possible that she has given us a hint in which, if we will but follow, may lead us on to the solution of this difficult problem. " " Bacteria Recognized as Earliest Immunotherapy DR. WILLIAM B. COLEY

IMMUNO-ONCOLOGY PIONEER Enable broad response and remission through engagement of multiple immunomodulatory pathways to enhance tumor inflammation and promote robust T cell responses

Dual Innate Immune Activator:

Synthetic Biotic Medicine Producing STING Agonist (SYNB1891) Synthetic biology applied to confer activities for efficacy and control for safety Designed as a dual innate immune activator: combined benefit of bacterial chassis and STING agonist The

dacA gene is integrated into genome under the control of inducible promoter (Pfnr) to produce c-di-AMP (CDA) Dual biosafety feature via auxotrophies - no proliferation in tumor, systemic circulation or environment Learnings inform future

combinations ANAEROBIC ENVIRONMENT dacA Pfnr ATP + ATP Cyclic-di-AMP (STING Agonist) 02 Auxotrophies Diaminopimelic acid (DAP) Thymidine

SYNB1891 In Vitro Characterization

Interferon Production Across Multiple Human STING Alleles - Activity Greater than Naked STING Agonist HUMAN PRIMARY DENDRITIC CELLS REPORTER HUMAN MONOCYTIC LINE Human STING Alleles STING Knockout

SYNB1891 In Vivo Characterization d1

107, 5x107 or 108 CFU, i.t. (SYNB1891-PT1) A20 tumors ~100 mm3, randomize groups d7 d4 d18 Dose-dependent Anti-tumor Activity of SYNB1891 Prototype Strain (PT1) as a Single Agent Control Control SYNB1891-PT1 (1 x 107) SYNB1891-PT1 (5 x 107)

SYNB1891-PT1 (1 x 108) = Dose

SYNB1891 In Vivo Characterization

SYNB1891 Prototype Strain (PT1) Leads to Systemic Anti-tumor Immunity SYNB1891-PT1 dose Re-challenge d1 108 CFU, i.t. (Bacteria) A20 tumors ~80-100 mm3, randomize groups d7 d4 d35 d63 Rechallenge (2e5 A20 cells) d1

Dual Innate Immune Activator

SYNB1891 Designed to Locally Inflame the TME and Systemically Drive Tumor Antigen-Specific Immunity Tumor Colonization without Leakage Enhanced Activity vs. Naked STING Agonist Intracellular Activation of STING and Bacterial-Induced Immune Pathways

Within APCs Dose-dependent Anti-tumor Activity Immunological Memory Clinical trial material manufactured IND Submission 2H19 STING Agonism in Target Cells that Drive Efficacy Sparing Cells Where STING Agonism is Detrimental Activation of Multiple

Innate Immune Pathways Low Systemic Risk PROMISE OVER OTHER APPROACHES PROGRESS TOWARDS THE CLINIC

A Tumor Can Evade Multiple Critical

Aspects of the Cancer-Immunity Cycle Killing Recognition Infiltration Antigen release Presentation Priming and activation T cell trafficking Insufficient activity/proliferation Immuno-suppression Insufficient trafficking Insufficient priming