Legal Disclaimers Statements in this presentation (the "Presentation") for RAPT Therapeutics, Inc. (the "Company," "we," or "our") that are not statements of historical fact are forward-looking statements. Such forward-l

Transforming the Treatment of Cancer

and Inflammation Corporate Presentation January 2020 Exhibit 99.1

Legal Disclaimers Statements in this

presentation (the "Presentation") for RAPT Therapeutics, Inc. (the "Company," "we," or "our") that are not statements of historical fact are forward-looking statements. Such forward-looking statements

include, without limitation, statements regarding our research and clinical development plans; current and future drug candidates; business strategy and plans; regulatory pathways; and our ability to complete certain milestones. Words such as

"believe," "anticipate," "plan," "expect," "will," "may," "upcoming," "milestone," "potential," "target" or the negative of these terms or similar expressions are intended to identify forward-looking statements, though not all forward-looking

statements necessarily contain these identifying words. These forward-looking statements are based on the current beliefs of the Company's management with respect to future events and trends and are subject to known and unknown risks and

uncertainties, including those described in the "Risk Factors" section of our Form 10-Q filed with the Securities and Exchange Commission on December 11, 2019, that may cause our actual performance or achievements to be materially

different from any future performance or achievements expressed or implied by the forward-looking statements in this Presentation. These forward-looking statements should not be taken as forecasts or promises nor should they be taken as implying any

indication, assurance or guarantee that any assumptions on which such forward-looking statements have been made are correct or exhaustive or, in the case of such assumptions, fully stated in the Presentation. You are cautioned not to place undue

reliance on these forward-looking statements, which speak only as of the date this Presentation is given. Although we believe that the beliefs and assumptions reflected in the forward-looking statements are reasonable, we cannot guarantee future

performance or achievements. Except as required by law, we undertake no obligation to update publicly any forward-looking statements for any reason after the date of this Presentation.

DISCOVERY Focused on Oral Drugs

Targeting Critical Immune Drivers of Disease FLX475 (Oncology): Selectively targets immunosuppressive tumor Treg Encouraging clinical activity in Phase 1 study Phase 2 PoC readout Q2 2020 RPT193 (Allergic Disease): Oral agent targets inflammatory

Th2 cells Robust PK/PD with favorable safety in Ph1 study PoC readout Q3 2020 GCN2 (Oncology): Turns on an antitumor metabolic switch in TME HPK1 (Oncology): Unlocks T cell activation to tumor antigens CLINICAL Diversified pipeline Large

market opportunities Significant inflection points in 2020 Strategic collaborations Proprietary discovery engine

Diversified Pipeline with Significant

Inflection Points in 2020 PROGRAM DISCOVERY PRECLINICAL PHASE 1 PHASE 2 PHASE 3 Anticipated Program Milestone CCR4 FLX475 Oncology PoC: Q2 2020 RPT193 Inflammation PoC: Q3 2020 GCN2 Oncology Select Candidate: 2020 HPK1 Oncology Asthma and Other

Allergic Diseases Monotherapy Combination w/ Keytruda Atopic Dermatitis PoC: Proof of Concept * ** * Clinical collaboration with Merck ** Regional collaboration and license with Hanmi in Korea and China - Ph2 gastric cancer trial to be

initiated after combination RP2D selected Gastric Cancer

Proprietary Drug Discovery and

Development Engine R Drug discovery Clinical development to POC Rapid Interrogating clinically-relevant big datasets to identify targets and biomarkers Driven by data to improve chances of clinical success Critical immune drivers of cancer and

inflammation A Analytics P Patient selection T Targeting

Experienced Leadership Team and

Scientific Advisory Board Leadership Board of Directors Scientific and Clinical Advisors Investors Brian Wong, MD, PhD Chief Executive Officer Dirk Brockstedt, PhD Chief Scientific Officer William Ho, MD, PhD Chief Medical Officer Paul Kassner, PhD

Vice President, Quantitative and Computational Biology David Wustrow, PhD Senior Vice President, Drug Discovery and Preclinical Development Sylvia Wheeler Wheelhouse Life Sciences Advisors, Investor Relations and Corporate Affairs Rodney Young Chief

Financial Officer David V. Goeddel, PhD Managing Partner, The Column Group Michael F. Giordano, MD Former SVP and Head of Development, Oncology & Immuno-Oncology, Bristol-Myers Squibb Mary Ann Gray, PhD President, Gray Strategic Advisors, LLC

Linda Kozick Former VP and Head of Immuno-Oncology/Oncology Product & Portfolio Strategy, Bristol-Myers Squibb William Rieflin, JD Executive Chairman, NGM Biopharmaceuticals Inc. Wendye Robbins, MD President and CEO, Blade Therapeutics Inc.

Brian Wong, MD, PhD CEO, RAPT Therapeutics Alexander Rudensky, PhD Chairman, RAPT Scientific Advisory Board, Chairman, Immunology Program, Sloan-Kettering Institute Antoni Ribas, MD, PhD Professor, Medicine, Hematology/Oncology & Director, UCLA

Scott J. Antonia, MD, PhD Instructor in the Department of Medicine, Duke University School of Medicine Drew Pardoll, MD, PhD Professor, Johns Hopkins University Philip Greenberg, MD Professor, Medicine (Oncology) & Immunology, University of

Washington Robert Zamboni, PhD Adjunct Professor of Chemistry, McGill University David V. Goeddel, PhD Founder & CEO Tularik; Founder & Partner The Column Group Oncology Allergy / Immunology Emma Guttman-Yassky, MD, PhD Professor and Vice

Chair for Research at the Department of Dermatology, Director of the Center for Excellence in Eczema, and Director of the Laboratory of Inflammatory Skin Diseases at the Icahn School of Medicine at Mount Sinai Medical Center Jasmina Jankicevic, MD

Consulting Dermatologist, Premier Research Thomas Bieber, MD Professor of Dermatology and Allergy, University of Bonn, Germany Andrew Blauvelt, MD, MBA Dermatologist and President of Oregon Medical Research Center

CCR4 Drives Tumor Progression and

Allergic Inflammation Regulatory T cells (Treg) are recruited into the tumor via CCR4 and block antitumor immunity Th2 cells are recruited via CCR4 into tissues and drive allergic inflammation CCR4 Treg CCR4 Th2 Eosinophilia Skin and airway

thickening High IgE IL-4 IL-5 IL-13 Cancer Atopic Dermatitis, Asthma CCR4 Ligands CD8 T Cell Antitumor immunity CCR4 Ligands

FLX475: CCR4 Antagonist for Oncology

FLX475: Oral CCR4 Antagonist with

Phase 2 PoC Anticipated in Q2 2020 Designed to selectively block tumor Treg while sparing normal tissues and beneficial immune cells Phase 1/2 study ongoing with PoC readout anticipated in Q2 2020 Demonstrated preliminary evidence of clinical

activity Collaborations with Merck and Hanmi to enable global development program Issued U.S. composition of matter patent with coverage at least through 2037 Blocks interaction with CCR4 ligands CCL22 and CCL17 on Treg

Treg Allows Tumors to Evade the

Immune System Treg are a major barrier to effective antitumor immunity Treg numbers correlate with poor clinical outcome across most tumor types Act as powerful suppressors of the immune response Patients with genetic defects in Treg exhibit severe

autoimmunity The CCR4 pathway specifically drives Treg accumulation in the tumor but not in healthy tissues Cancer Tumor Treg CD8 T Cell Suppression

Identification and Characterization

of "Charged" Tumors "Charged" tumors: Tumors expressing high levels of CCR4 ligands and Treg Non-Small Cell Lung Cancer Triple Negative Breast Cancer Head and Neck Cancer Virally-Associated Cancers "Charged"

tumors tend to be "hot" with high levels of Treg likely holding back the antitumor immune response Potential for tissue-agnostic accelerated approval in virally- associated tumors - Data from in-house analysis of TCGA database combined

with other data sets; Confirmed in > 400 tumor microarrays - The graph above reflects a logarithmic scale on each axis Treg CCR4 Ligands Gastric EBV+ NPC EBV+ NSCLC Sq. TNBC Cervical HPV+ HNSCC NSCLC Ad. "Heat" (CD8 Signature)

Virally-Associated Non-Virally-Associated

A Large Proportion of Multiple Tumor

Types are "Charged" Tumor Type Prevalence* (U.S.) Virally Associated Percent Viral Estimated Percent "Charged"** Non-Small Cell Lung Cancer 268,600 N/A N/A 60-80% Triple Negative Breast Cancer 145,500 N/A N/A Head and Neck

Squamous Cell Carcinoma 143,000 25%-60% Nasopharyngeal Cancer 105,000*** >95% >90% of virally associated tumors Hodgkin Lymphoma 28,500 30%-50% Cervical Cancer 46,800 >95% Non-Hodgkin Lymphoma 225,000****

Widely variable among subtypes * Based on 2012 Globocan registries 5-year prevalence (2008-2012 estimates) ** Data from in-house analysis *** World-wide prevalence **** Based on 2018 Globocan registries 5-year prevalence (2013-2018

CCR4 Antagonist: Single Agent

Activity in a Mouse Model of a "Charged" Tumor CD8 : Treg Ratio Single Agent Efficacy Tumor Volume (mm3) Days post-inoculation CD8 : Treg ratio Vehicle CCR4 Antagonist Checkpoint Inhibitor Combination *** ** **** * **

P<0.01 *** P<0.001 * P<0.05 **** P<0.0001 ** 400 600 200 0 800 0 20 40 60 Vehicle CCR4 Antagonist Checkpoint Inhibitor Combination Pan02 "Charged" Tumor

Accumulation of Treg in the TME is a

General Adaptive Immune Resistance Mechanism to Treatment Pre CAR-T Post CAR-T CD8 FoxP3 O'Rourke et al. Science Trans. Med. (2017) Sharma et al. Clinical Cancer Research (2019) Accumulation of Treg has also been observed in both post

anti-PD-1 and after conventional therapies such as radiation or chemotherapy Anti-CTLA-4 Therapy CAR-T Cell Therapy

CCR4 Antagonist Synergizes with

Checkpoint Inhibitors Vehicle CPI 1/10 Tumor-Free CPI + CCR4 Antagonist 5/10 Tumor-Free Treatment initiation Median tumor volume (mm3) Days post-inoculation ** p<0.01 Combination Efficacy 500 1000 0 1500 0 10 20 30 Vehicle Checkpoint Inhibitor

CCR4 antagonist + CPI *** Inhibition of Treg Migration Number of Treg 250 200 150 150 100 50 0 -50 CT26 tumor model p<0.001

FLX475 Clinical Development Status

Monotherapy 25 mg - 100 mg QD (Mixed tumors including "Charged") Combination w/ Keytruda 50 mg - 100 mg QD (Mixed tumors including "Charged") 3+3 design Recommended Phase 2 Dose current stage Endpoints: Safety, PK,

Biomarkers, Objective Response Rate Phase 1 Healthy Volunteer Study (Completed) Phase 1 Cancer Dose Escalation RP2D Selected

Phase 1 Summary Healthy Volunteer

Study 104 healthy human volunteers Target engagement achieved in majority of subjects at 75 mg Excellent safety and tolerability at targeted exposures Oncology Dose Escalation Recommended Phase 2 Dose (Monotherapy): 100 mg Dose escalation for

combination cohorts ongoing No new safety findings Encouraging evidence of clinical activity

Confirmed Partial Response in a

Checkpoint Inhibitor-Refractory NSCLC Patient Treated with 50 mg FLX475+Keytruda* 4L NSCLC patient that progressed on prior atezolizumab therapy Confirmed partial response (PR) by RECIST 1.1 criteria. Patient remains on study. Week 14 Screening Week

8 -37.5% (PR) -47% (PR) Baseline *Based on radiological analysis conducted at the clinical investigator site

FLX475 Phase 2 Trial: PoC Expected

in Q2 2020 FLX475 Monotherapy N=10 FLX475 w/ Keytruda N=10 N=10 N=10 N=10 N=10 N=10 N=10 Nasopharyngeal (EBV+) Non-Small Cell Lung (CPI Experienced) Hodgkin/Non-Hodgkin (EBV+) Head & Neck (CPI Na ve) Cervical (HPV+) (CPI Na ve)

TN Breast (CPI Na ve) Head & Neck (CPI Na ve) Head & Neck (CPI Experienced) PoC Q2 2020 Patients have failed at least one line of therapy Endpoints: Safety, PK, Biomarkers, Objective Response Rate CPI = Checkpoint Inhibitor Gated

2-stage design: if positive ORR in a cohort, enroll additional 19 patients

RPT193: CCR4 Antagonist for Allergic

RPT193: Oral CCR4 Antagonist for

Allergic Diseases with PoC Anticipated in Q3 2020 Targeting atopic dermatitis, asthma, others Oral convenience could provide substantial competitive advantage to injectables and topical agents Completed IND-enabling studies and healthy volunteer

data suggest a favorable safety profile Phase 1 trial ongoing with PoC in atopic dermatitis anticipated in Q3 2020 Normal Human Skin AD Lesional Skin

RPT193 Acts on a Well Validated

Pathway in Asthma and Atopic Dermatitis (AD) RPT193 Inhibits Th2 migration into inflamed tissues anti-IL5/R Ab (Benralizumab, AZ) (Mepolizumab, GSK) anti-IL13 Ab (Lebrikizumab, Dermira) Airway/Skin Allergen IL-5 anti-IL4R Ab (Dupilumab,

Regeneron/Sanofi) CCR4 Th2 CCL17 CCL22 IL-4 IL-13 Inflammation Thickening Cough/Itch X Cytokines Alarmins: TSLP, IL25, IL33 Th2 cells are recruited via CCR4 into inflamed tissues

RPT193 Dupilumab* JAK inhibitors

Safety Preclinical and healthy volunteer data suggest a favorable safety profile Generally safe and well tolerated Conjunctivitis Immunosuppressive Potential black box warning for infections, malignancies and thromboembolic events Route of

Administration Oral, daily dosing Injectable Oral Efficacy Preclinical data suggest efficacy similar to dupilumab* Durable clinical efficacy Activity in AD and asthma Similar to dupilumab* RPT193 Potential Advantages Favorable Characteristic

Unfavorable Characteristic * DUPIXENT

Potency of CCR4 Inhibitors in an In

Vitro Th2 Chemotaxis Assay RPT193 AZD2098 GSK2239633 CCL22-Induced Th2 Chemotaxis IC50 ~370nM IC50 ~3 M IC50 ~3 M

RPT193 Demonstrates Similar Efficacy

to Biologics in Atopic Dermatitis Model Skin Analysis Sensitization Allergen Challenge Treatment: Vehicle, RPT193, Anti-IL-4R, or Anti-IL-13 Days 0 1 7 8 9 10 11 12 Delta Skin Thickness (mm) Days

RPT193 Demonstrates Broader Activity

than Anti-IL-13 in an Allergic Asthma Model p<0.05 Eosinophils Eosinophils in BALF (x106) Neutrophils Neutrophils in BALF (x106) OVA RPT193 Anti-IL-13 Vehicle Vehicle OVA RPT193 Anti-IL-13 IL-5 IL-5 (pg/ml) Vehicle OVA RPT193 Anti-IL-13 24 hrs

after day 23 challenge BALF collection and cell count Sensitisation OVA Day 1 Lung OVA Challenge Days 20-23 Oral RPT193 on Days 19 - 23 Anti-IL-13 on Day 19 Boost OVA Day 14 p<0.001 p<0.001

RPT193 Phase 1a/1b Healthy

Volunteer/ Atopic Dermatitis Trial Mod-Severe AD Readout 4 weeks Placebo-controlled 2:1 ~30 AD Patients ~40-50 Healthy Volunteers Escalating Dose RPT193: Seamless Clinical Trial Design to PoC and Beyond Phase 1a SAD RPT193 Phase 2 Trials Escalating

Dose Phase 1a MAD Phase 1b Atopic Dermatitis Phase 2b Atopic Dermatitis Phase 2a Asthma and Other Allergic Diseases Endpoints: Safety, PK, Biomarkers, Efficacy (EASI) Single Dose PoC Q3 2020

Phase 1a HV Data Supports Once-Daily

Dose 100 mg once-daily dose exceeds target exposures and receptor occupancy Favorable safety profile to date (n=56) Target Receptor Occupancy Exceeded at 100 mg Dose-Proportional Oral PK with ~24 Hr. Half-Life

RPT193 - dose level 1 ~40 - 60

AD Patients per cohort Proposed Phase 2b Double Blind, Placebo-Controlled Trial Placebo control RPT193 - dose level 2 RPT193 - dose level 3 1:1:1:1 Screening Treatment Period (12-16 wks) Key inclusion criteria: Age 18 years

Mod-Severe AD EASI of 16 BSA of 8 IGA 3 R Primary Endpoints: Mean % change from baseline in EASI at week 12 or 16 Secondary Endpoints: IGA and EASI response rates