Exhibit 99.1 Corporate Presentation December 2022 1

Forward-Looking Statements Ventyx Biosciences, Inc. (“we,” “us,” “our,” “Ventyx,” or the “Company”) cautions you that statements contained in this presentation regarding matters that are not historical facts are forward-looking statements. These statements are based on the Company’s current beliefs and expectations. Such forward-looking statements include, but are not limited to, statements regarding: clinical development plans and related timing for Ventyx’s product candidates; anticipated timing of data announcements; anticipated efficacy, safety, dosing and clinical differentiation of Ventyx’s product candidates; potential indications for Ventyx's product candidates; market opportunities; the anticipated timing of IND submission for VTX3232; projected catalysts relating to Ventyx’s product candidate pipeline; and anticipated cash runway. The inclusion of forward-looking statements should not be regarded as a representation by Ventyx that any of its plans will be achieved. Actual results may differ from those set forth in this presentation due to the risks and uncertainties inherent in Ventyx’s business, including, without limitation: potential delays in the commencement, enrollment and completion of clinical trials; disruption to our operations from the ongoing global outbreak of the COVID-19 pandemic, including clinical trial delays; the Company’s dependence on third parties in connection with product manufacturing, research and preclinical and clinical testing; the results of preclinical studies and early clinical trials are not necessarily predictive of future results; supply chain constraints; the success of Ventyx’s clinical trials and preclinical studies for its product candidates; interim results do not necessarily predict final results and one or more of the outcomes may materially change as the trial continues and more patient data become available and following more comprehensive audit and verification procedures; regulatory developments in the United States and foreign countries; unexpected adverse side effects or inadequate efficacy of our product candidates that may limit their development, regulatory approval and/or commercialization, or may result in recalls or product liability claims; Ventyx’s ability to obtain and maintain intellectual property protection for its product candidates; Ventyx may use its capital resources sooner than it expects; and other risks described in the Company’s prior communications and the Company’s filings with the Securities and Exchange Commission (SEC), including under the heading “Risk Factors” in the Company’s Quarterly Report on Form 10-Q filed on November 4, 2022, and any subsequent filings with the SEC. You are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date hereof, and Ventyx undertakes no obligation to update such statements to reflect events that occur or circumstances that exist after the date hereof. All forward-looking statements are qualified in their entirety by this cautionary statement, which is made under the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. This presentation includes statistical and other industry and market data that we obtained from industry publications and research, surveys and studies conducted by third parties as well as our own estimates of potential market opportunities. Industry publications and third-party research, surveys and studies generally indicate that their information has been obtained from sources believed to be reliable, although they do not guarantee the accuracy or completeness of such information. Our estimates of the potential market opportunities for our products include several key assumptions based on our industry knowledge, industry publications, third-party research and other surveys, which may be based on a small sample size and may fail to accurately reflect market opportunities. While we believe that our internal assumptions are reliable, such assumptions have not been verified by any third party. The industry in which we operate is subject to a high degree of uncertainty and risk due to a variety of important factors that could cause results to differ materially from those expressed in the estimates made by third parties and by us. Trademarks in this presentation are the property of their respective owners and used for informational and education purposes only. 2

Our Mission: To Become a Leading Immunology Company Underpinned by Strong Drug Discovery and Development Capabilities With Three, Differentiated, Clinical-stage Candidates and a deep pipeline of preclinical programs that target immune-mediated and inflammatory disease indications Our Internally-discovered Small Molecule Drugs allow us to own 100% commercial rights to our entire portfolio with long patent lives for all product candidates Our Experienced Team And Our Internal R&D Engine continue to generate candidates with potential to address diseases with high unmet need 3

Our Leadership Team Management Raju Mohan, PhD Martin Auster, MD Chris Krueger, JD John Nuss, PhD William Sandborn, MD CHIEF EXECUTIVE OFFICER, CHIEF FINANCIAL OFFICER CHIEF BUSINESS OFFICER CHIEF SCIENTIFIC OFFICER PRESIDENT, CHIEF MEDICAL OFFICER FOUNDER Board Of Directors Sheila Gujrathi, MD Jigar Choksey Richard Gaster, MD, PhD Raju Mohan, PhD EXECUTIVE CHAIR, VENTYX PRINCIPAL, THIRD POINT MANAGING PARTNER, VENBIO CHIEF EXECUTIVE OFFICER, VENTYX Aaron Royston, MD Somu Subramaniam William White MANAGING PARTNER, VENBIO MANAGING PARTNER, NEW SCIENCE CHIEF FINANCIAL OFFICER, AKERO VENTURES THERAPEUTICS 4

Broad Pipeline of Candidates With Multiple Near-Term Catalysts Addressing Established Inflammatory and Immunology Markets with a Wholly Owned Product Portfolio Target Program Preclinical Phase 1 Phase 2 Phase 3 Next Anticipated Milestones Initiate Phase 2 trials Q4 2022 TYK2 VTX958 Psoriasis, psoriatic arthritis, Crohn’s disease Report topline Phase 2 data 2023 S1P1R VTX002 Ulcerative Colitis NLRP3 Initiate Phase 2 trial in CAPS Q1 2023 VTX2735 Peripheral CAPS, other potential indications include CV, dermatologic and rheumatologic diseases File IND Q1 2023 NLRP3 VTX3232 CNS-penetrant Initiate Phase 1 trial Q1 2023 Neuroinflammatory diseases Cash, cash equivalents and marketable securities of $412.4M as of September 30, 2022 expected to fund operations into 2025 5

Pipeline Targeting Large Well-Established Markets Indication* Patients In The U.S. Global Drug Revenue* (2020) Target Population Psoriasis 25-30% ~8M ~$20B Dermatology Moderate-to-severe Crohn’s disease 30-40% ~700K ~$13B IBD Moderate-to-severe Ulcerative colitis 30-40% ~1M ~$7B IBD Moderate-to-severe Psoriatic arthritis 40-60% ~1M ~$4B Rheumatology Moderate-to-severe SLE Up to 500K ~$1B Rheumatology Sources: Evaluate Pharma, Company Estimates, Wall Street Research *Global drug revenue refers to the total market across all severity levels Notes: SLE = systemic lupus erythematosus; *Group of indications based on current mid/late-stage trials for BMS’s allosteric TYK2 inhibitor deucravacitinib; global commercial sales totaled $10.65B for biologics targeting IL-12/23 and IL-23 in 2020 6

ORALLY BIOAVAILABLE selective allosteric inhibitor of TYK2

VTX958: Orally Bioavailable, Selective Allosteric Inhibitor of TYK2 Clinically Validated Potential Best-in-Class Large Addressable Target Drug Markets • Established clinical efficacy in IBD, • Selective allosteric TYK2 inhibitor • Multiple autoimmune disorders in psoriasis and psoriatic arthritis with dermatology, IBD, renal and • TYK2 functional selectivity may biologics targeting IL-12 and IL-23* rheumatology total ~$48B** in differentiate clinical profile vs. less 2020 WW sales • Allosteric TYK2 inhibitors target selective TYK2 inhibitors common pathways • High unmet need for safe and • Positive Phase 1 data: effective oral agents in markets • TYK2 inhibition is clinically – Broad therapeutic window dominated by injectable biologics validated in psoriasis, psoriatic – Excellent safety profile arthritis and SLE – Class-leading target coverage • First allosteric TYK2 inhibitor FDA- may position VTX958 for success approved Sept. 9, 2022 -- no boxed warning differentiates across multiple indications TYK2i from JAKi therapeutics *Includes approved drugs Stelara™ (JNJ), Tremfya® (JNJ), Skyrizi™(ABBV), Ilumya™ (Sun Pharma) and others in late-stage development (mirikizumab (LLY), brazikumab (AZN) **Source: Positive Phase 3 efficacy results reported for deucravacitinib in psoriasis at AAD April 2021; positive Phase 2 efficacy results reported for psoriatic arthritis at ACR October 2020 and positive Phase 2 efficacy results reported for SLE at EULAR meeting June 2022 Source: EvaluatePharma 2020 indication sales estimates 8

VTX958 Binds Selectively to the TYK2 Allosteric (JH2) Domain Key Players in JAK/TYK2 Inhibited Active Inactive IL-12, IL-23, IFNα Family Signaling Features of VTX958 JH2 Allosteric Domain JH2 Allosteric Inhibition Much less conserved amongst the JAK family Selectivity for TYK2 JH2 vs. with structurally distinct JAK1 JH2 domain (>4,000 X) binding pockets No binding to JAK2/3 JH2 JH1 Kinase Domain domains Highly conserved within JAK family; inhibitors No binding to TYK2 kinase JH2 targeting the kinase VTX958 JH1 and domain have poor JH1 selectivity No kinase enzyme inhibition of any JAK family member TYK2 ATP Binding to JH1 allows phosphorylation of substrates Selective TYK2 Inhibitor • Targeting the allosteric domain of TYK2 affords inhibitors with selectivity against other JAK isoforms • May Avoid Potential Safety Risks of JAK1/2/3 Inhibition 9

VTX958 is Highly Selective for TYK2 JH2 Domain vs. Deucravacitinib Inhibits TYK2 Pathways (IL-12, IL-23, IFNα) while Avoiding the JAK1/2/3 Pathways TYK2 JH2 domain Structural Rationale for VTX958 Selectivity: • Productive interaction for both VTX958 and deucravacitinib with valine residue in TYK2 JH2 domain • VTX958 has a steric clash with the isoleucine residue (IIe) in the JAK1 JH2 domain – deucravacitinib does not • Key determinant of the high TYK2 selectivity of VTX958 JAK1 JH2 domain JH2 Binding (K ) Deucravacitinib VTX958 d TYK2 0.009 nM 0.058 nM JAK1 0.43 nM 240 nM Fold Selectivity for 48 >4,000 TYK2 vs. JAK1 Source: Ventyx internal data 10

VTX958 Selectively Inhibits IL-12, IL-23 and IFNα Signaling VTX958 Has No Measurable Inhibition VTX958 Potently Inhibits TYK2 Pathways of JAK1-Mediated Pathways Selective and potent inhibition of IL-12/23 and IFNα Lack of inhibition of IL-6, IL-10, IL-22 and other protective axis allows targeting pathways driving immune- cytokines may avoid potential adverse events associated mediated diseases with less selective inhibitors PROINFLAMMATORY INNATE & TH1/TH17 CYTOKINES PLEIOTROPIC CYTOKINES WITH PROTECTIVE FUNCTIONS Psoriasis Patient PBMC IL-12 IL-23 IFNα IL-22 IL-10 IFNγ IL-4 IL-6 DRUG DRUG IC (nM) IC (nM) IC (nM) IC (nM) IC (nM) IC (nM) IC (nM) IC (nM) 50 50 50 50 50 50 50 50 VTX958 VTX958 35 5 12 >10,000 >10,000 >10,000 >10,000 >10,000 deucravacitinib 114 20 350 249 464 deucravacitinib 10 10 5 • Potent activity against IL-23, a key cytokine implicated in psoriasis and other indications KEY TAKEAWAYS • Broad therapeutic window with VTX958 may allow for higher exposures in Phase 2/Phase 3 studies Source: Ventyx internal data; assays conducted in peripheral blood mononuclear cells (PBMC) 11

Summary of VTX958 Phase 1 Results Safety, Exposure and Target Coverage VTX958 well tolerated across all SAD and MAD cohorts VTX958 exhibits class-leading • Achieved TYK2 IC coverage for up to 24 hours with no dose-limiting toxicities 90 TYK2 IC coverage* 90 Robust, dose-dependent • Supports hypothesis that greater pathway inhibition may enable differentiated pharmacodynamic activity in efficacy in clinic ex vivo and in vivo assays *TYK2 IC coverage implies suppression of IL-12, IL-23 and IFNα pathways 90 12

VTX958 Phase 1 Day 10 (Steady State) MAD Results Exposure and Target Coverage Across All Cohorts Target Coverage* (hours) KEY TAKEAWAYS IFNα IL-12 IL-23 MAD Dose • Safely achieved class-leading IC IC IC IC IC IC 90 50 90 50 90 50 TYK2 IC coverage 90 50 mg BID 0 505 07 • IC coverage up to 24 hours 90 for IL-12, IL-23 and IFNα 250 mg QD 4 9 4 9 6 10 • Exposures achieved may 500 mg QD 6 14 6 14 7 16 approach biologic-like suppression of IL-12/23 175 mg BID 16 24 16 24 17 24 pathways 350 mg BID 24 24 24 24 24 24 *Exposures used for target coverage calculations: • IL-12 hWB IC = 865 ng/mL; IC = 130 ng/mL; IFNα hWB IC = 584 ng/mL; IC = 73 ng/mL 90 50 90 50 • IL-12 IC and IC values used for IL-23 IC and IC calibration (hWB assay not available for IL-23) 50 90 50 90 • IL-12 and IL-23 share TYK2-specific heterodimer IL-12Rβ1 13

VTX958 Phase 1 MAD Pre-IFNα Challenge Safety Assessment* VTX958 Placebo 50mg BID 250mg QD 175mg BID 500mg QD 350mg BID All cohorts TEAEs (n=10) (n=6) (n=6) (n=6) (n=6) (n=6) (n=30) Headache 1 (10.0%) - 2 (33.3%) 2 (33.3%) 1 (16.7%) 1 (16.7%) 6 (20.0%) @ Faeces soft 1 (10.0%) 1 (16.7%) 2 (16.7%) 1 (16.7%) - 1 (16.7%) 4 (13.3%) # † Rash papular - - 1 (16.7%) - - 2 (33.3%) 3 (10.0%) Dry mouth - - - - 1 (16.7%) 1 (16.7%) 2 (6.7%) Abdominal pain - 2 (33.3%) - 1 (16.7%) - - 3 (10.0%) ‡ ALT, AST, GGT increase - - - - - 1 (16.7%) 1 (3.3%) • All TEAEs (Treatment Emergent Adverse Events) reported in 2 or more subjects receiving VTX958 prior to IFNα Challenge on day 13 and single subject AEs of interest. IFNα challenge not performed in cohort 5 (350 mg BID), AEs for all 14 days of treatment are presented for Cohort 5. @ Both AEs in a single subject # Single skin papule on lower right cheek judged not drug related; mild; resolved with continued VTX958 dosing † Two subjects in cohort 5 (350 mg BID) experienced mild skin papules judged not drug related one subject with mild face papules that resolved with continued VTX958 dosing one subject with mild face/trunk papules that improved with continued VTX958 dosing ‡ One subject in cohort 5 (350 mg BID) experienced increase in ALT, AST, and GGT, classified as mild; overlapped with COVID diagnosis 14

VTX958 Phase 1 MAD Results: Selected Laboratory Data No significant effects on hematological parameters, lipids, CPK laboratory values Hemoglobin Neutrophils CPK 250 200 150 100 50 0 DAY 1 DAY 2 DAY 5 DAY 7 DAY 10 Platelets Lymphocytes Cholesterol 15 Hemoglobin (g/L) Lymphocytes (10^9/L) (Mean ± SD) (Mean ± SD) Platelets (10^9/L) Neutrophils (10^9/L) (Mean ± SD) (Mean ± SD)

VTX958 Phase 1 MAD Results Robust Dose-Dependent Pharmacodynamic Effects Complete suppression of IL-12 signaling Robust inhibition of TYK2-responsive genes CXCL10, ISG20, IFI27 • Dose-dependent inhibition of IFNγ at all time-points • Genes are direct downstream targets of IFNα and display diverse in response to IL-12/IL-18 dual stimulation onset, amplitude and resolution kinetics • Implies complete suppression of IL-23 signaling • Potent exposure-PD activity on all three genes § IL-12 and IL-23 share TYK2-specific heterodimer IL-12Rβ1 • Response is dose-related through all cohorts tested Ex Vivo Ex Vivo IFNγ response IFNγ response (ELISA) to (ELISA) to IIL-12/IL-18 dual L-12/IL-18 dual stimulation stimulation In Vivo IFNα challenge – Impact on TYK2-mediated genes (% Inhibition* 175 mg BID) Time post- 4h 6h 8h 12h 16h 24h challenge CXCL10 97 82 42 95 95 63 >90% inhibition ISG20 80 69 54 79 101 39 IFI27 78 68 62 60 71 84 BL= baseline *% inhibition shown as placebo adjusted geometric mean *Geometric mean 16

Published TYK2 Target Coverage Data Opportunity for VTX958 to Differentiate with Improved Therapeutic Window Deucravacitinib (BMS) 6 mg & 12 mg QD Target Coverage Deucravacitinib (BMS) 6 mg & 12 mg QD Target Coverage First-generation allosteric TYK2 inhibitor exposures are limited by toxicities 150 • Deucravacitinib 6mg QD (PsO dose) IC 90 achieves IC coverage for ~9 hours (does 50 not reach IC ) 90 100 12 mg QD • Skin toxicities (acne, rash) emerge consistently at higher exposures 6 mg QD Fuller pathway inhibition (improved 50 therapeutic window) expected to drive differentiation IC • Greater coverage of TYK2 IC , IC may 50 50 90 drive improved efficacy 0 • Achievement of durable IC coverage may 0 6 12 18 24 90 be necessary to achieve efficacy in IBD Time post-dose (hours) PK data modeled and graph adapted from Chimalakonda et al., Dermatol. Ther. 2021 Deucravacitinib TYK2 IC of 14 ng/mL from Catlatt et al. EULAR 2017 50 IC values generated assuming a Hill slope of 1. ss= steady state 90 17 Derived Plasma Concentrations, ss (ng/mL)

Deucravacitinib - Skin AEs and Target Coverage Deucravacitinib VTX958 Phase 1 Data Establish Study Skin AE 3 mg BID 6 mg QD 6 mg BID 12 mg QD 12 mg BID Total Differentiation vs. Deucravacitinib P1 MAD HV Any skin related AEs 33% 56% 78% 42% • Deucravacitinib elicits dose- P2 PsO Acne 2% 4% 9% dependent and potentially dose- Pruritis 2% 7% 5% limiting skin toxicities P3 PsO Acne 2% Folliculitis 2% • Skin findings observed with high P2 PsA Acne 3% 2% frequency at exposures > 6 mg Acneiform dermatitis 3% 3% QD (~9h TYK2 IC coverage) 50 Rash 4% 6% P2 Lupus Acne 3% 9% 8% • VTX958 demonstrates potential Rash 2% 3% 8% best-in-class therapeutic window Any skin related AEs 17% 34% 34% – Achieved high TYK2 IC 90 P2 UC Acne 9% coverage without frequent Rash 12% skin AEs TYK2 IC : ~9 h 50 TYK2 IC : ~18 h 50 TYK2 IC : ~0 h 90 TYK2 IC : ~0 h 90 *Deucravacitinib AE data compiled from respective publications and/or company data releases Deucravacitinib Phase 1 MAD dose ranged up to 12mg BID; trial had 7 discontinuations in deucravacitinib arms (8.4%) related to AEs (4 d/c associated with skin toxicities) TYK2 target coverage sourced from Chimalakonda et al., 2021 represents IL-12-stimulated IFNγ production hWB assay 18

Acne, Folliculitis and Rash are not On-Target Effects of IFNα or IL12/23 Inhibition Drug Mechanism of Acne Folliculitis Rash inhibition Anifrolumab (Saphnelo) IFNα < 2% < 2% < 2% Ustekinumab (Stelara) IL12/23 < 1% < 1% < 1% Guselkumab (Tremfya) Anti-IL23 < 1% < 1% < 1% Risankizumab (Skyrizi) Anti-IL23 < 1% < 1% < 1% Source: Prescribing information for each approved drug. 19

VTX958 vs. Competitor Allosteric TYK2 Inhibitors Comparison of Phase 1 Safety and Exposures Data* in Healthy Volunteers VTX958 NDI-034858 Deucravacitinib Phase 1 MAD Phase 1 MAD Phase 1 MAD 100 mg – 700 mg TDD 20 mg – 35 mg QD 2 mg – 24 mg TDD 50 mg – 100 mg QD • Acneiform dermatitis (67%, 17%) • Skin and subcutaneous disorders • Skin and subcutaneous disorders, Adverse Events (42%) including: classified as unrelated (10%) of Interest • Papular rash (25%, 0%) • Rash (20%) • Papular rash (10%) • Grade 3 CPK elevation (1 subject, 20 mg) • Acne (13%) • 1 subject with mild ALT elevation overlapped with Covid (350 mg BID) Relevant Dose 175 mg BID 350 mg BID 30 mg QD 6 mg QD TYK2 IC 24 hours IC 24 hours IC ~24 hours IC ~9 hours 50 50 50 50 Coverage IC 16 hours IC 24 hours IC ~5 hours IC ~0 hours 90 90 90 90 Ventyx: Internal data; Nimbus: JPM 2022 presentation; Deucravacitinib: Chimalakonda et al., Dermatol. Ther. 2021; TDD = total daily dose 20

VTX958 vs. Competitor Allosteric TYK2 Inhibitors Demonstrates Potential Best-in-Class Therapeutic Window Differentiating Parameter VTX958 Deucravacitinib NDI-034858 Relevant Dose / Exposure Comparisons 175 mg BID 6 mg QD 30 mg QD Target Coverage:* TYK2 IC 24 hours 9 hours 24 hours 50 TYK2 IC 16 hours None 5 hours 90 Adverse Events of Interest: Acne, acneiform dermatitis, Skin Findings None Acne, rash folliculitis, rash Rare CPK and triglyceride Neutropenia, CPK elevation, Laboratory Findings None elevations in PsO Phase 3 triglyceride elevations Best-in-class Ph2 UC failed – limited No currently active program– Opportunity in IBD therapeutic window therapeutic window limited therapeutic window Source: Papp et al., 2018 (NEJM); McElwee et al., 2022 (AAD); Gangolli et al., 2022 (SID); internal data *TYK2 target coverage measured with IL-12 assay for VTX958 and deucravacitinib; assay not disclosed for NDI-034858 21

VTX958 Profile Expected to Drive Clinical Differentiation Best-in-Disease Oral Potential in the ~$20B WW Annual Psoriasis Market Psoriasis Competitive Landscape 100% 86-91% 76-90% VTX958 Target Profile 80% Greater TYK2 suppression may produce improved efficacy compared to other 54-59% 60% oral agents, with potential to approach leading biologics 40% 29-33% 20% 0% IL-17 IL-23 p19 Otezla Deucravacitinib Next-Gen Allosteric (Biologic) (Biologic) PDE4 (Oral) TYK2 (Oral) TYK2 Inhibitors (Oral) Note: Solid area represents pbo-adjusted response rate; dashed area indicates total observed response rate; primary endpoint cut-off ranges from Week 10 to Week 16 Sources: Company reports and FDA labels for approved anti-IL-17 and anti-IL-23 biologics; market statistics sourced from EvaluatePharma 22 PASI-75 (% responders) at Primary Endpoint Cut-off

Unlocking the Opportunity in IBD Higher Doses Required for Efficacy in Crohn’s Disease Greater TYK2 pathway inhibition Agent PsO Dose (Induction) Crohn’s Dose (Induction) may be needed for IBD efficacy • Biologics data suggest substantially 150 mg Wks 0, 4 600 mg Wks 0, 4, 8 higher exposures are required for Skyrizi (IL-23) Subcutaneous Intravenous efficacy in Crohn’s vs. PsO • Deucravacitinib Phase 2 in UC failed (6 mg BID dose 0 hours IC coverage) 90 100 mg Wks 0, 4 200 mg Wks 0, 4, 8 Tremfya (IL-23) • Higher doses of VTX958 may approach Subcutaneous Intravenous biologic IL-12/23 pathway suppression • Profile of VTX958 may unlock a major market opportunity in Crohn’s, a >$13B Stelara (IL- 260 mg/390 mg/520 mg Wk 0 45 mg/90 mg Wks 0, 4 global market Subcutaneous, Weight-based Intravenous, Weight-based 12/23) Source: FDA labels for approved drugs/indications, represents adult dosing schedules Tremfya Crohn’s dose sourced from company data release (JNJ) 23

VTX958: Broad Development Opportunities and Commercial Potential • Phase 2 trials will explore a broad dose range, enabling optimal Phase 3 dose selection based on safety and maximizing target coverage – We plan to initiate three Phase 2 trials in Q4 2022 (PsO, Crohn’s and PsA) with additional Phase 2 indications (including SLE) being considered given the unique profile of VTX958 – Phase 2 trials will be dosed with an immediate release (IR) tablet; a modified-release (MR) formulation is in development to approximate BID exposures with a QD oral dose • Bridging study before Phase 3 (Precedent for approved compounds: Rinvoq, Xeljanz, etc.) 24

VTX958 Development Landscape Robust Market Opportunity for a Potential Best-in-Class TYK2 Inhibitor Biologics Oral Agents INDICATION ANTI-IL-23 ANTI-IL-17 APREMILAST DEUCRAVACITINIB VTX958* VTX958 • Excellent safety profile Psoriasis +++ +++ + ++ +++ • Class-leading TYK2 coverage Psoriatic arthritis +++ +++ + ++ +++ • Potentially superior therapeutic window Crohn’s disease N/A +++ — ? +++ • Unique opportunity in IBD Ulcerative colitis Well positioned to N/A ++ — — ++ capitalize on several large, biologic-dominated Lupus N/A N/A — ++ +++ autoimmune markets Therapeutic Moderate Stronger VTX958 target efficacy Ineffective Weaker +++ — + ++ +++ Efficacy Sources: Internal assessment of published efficacy data. *Aspirational target efficacy profile based on VTX958 TYK2 target coverage achieved in Phase 1 healthy volunteer study 25

Robust Market Opportunity for VTX958 • Best-in-class profile of VTX958 may enable clinical differentiation across multiple indications – VTX958 has potential to offer a differentiated clinical profile in PsO, PsA and SLE by dosing to levels that achieve greater TYK2 inhibition relative to competitors – VTX958 may be uniquely positioned among TYK2 inhibitors to address Crohn’s/IBD indications where anti-IL- 12/23 and anti-IL-23 antibodies have proven effective at higher dose levels than in psoriasis ~10.75M Patients in the US ~$48B Global Drug Revenue SLE, 500K Lupus Nephritis, $3B Psoriatic Arthritis, 1M Crohn’s Disease, Lupus Nephritis, 60K Psoriatic Arthritis, $4B $13B Crohn’s Disease, 700K SLE, $1B Ulcerative Colitis, 1M Ulcerative Colitis, $7B Psoriasis, 8M Psoriasis, $20B Sources: CCFA, Evaluate Pharma (2020 indication sales estimates) 26

PERIPHERALLY RESTRICTED S1P1R MODULATOR with potential for treatment of ulcerative colitis

VTX002 Program Summary Phase 2 S1P1R Modulator for Ulcerative Colitis Potentially Differentiated Clinically Validated Target Large Addressable Markets S1P1R Modulator • Selective S1P1R modulator • S1P1R modulators approved for • Ulcerative colitis is lead indication MS and UC with clinical trials totaling up to $7B in worldwide • Differentiated on key parameters ongoing in other indications revenue • Demonstrated pharmacodynamic • BMS’ ozanimod approved for activity in Phase 1 trial UC in May 2021 • Pursuing clinical development plan in both treatment-naïve and biologic-experienced patients 28

VTX002 Differentiates on Multiple Key Parameters vs. Competitors Potential Potential for Dif for Differentiated ferentiated Safety Safety Profile Profile No Drug-Drug No Drug-Drug Interactions Interactions Clinical Clinical P Profile rofile iin UC Patients n UC Patients Sustained lymphocyte reduction up No SAEs, elevated LFTs, abnormal No CYP inhibition; no food effect; to 65% across multiple doses in MAD PFTs or macular edema favorable profile for patients with co- trial morbidities Fast Onset Fast Onset o of f Action Action Ability Ability to Dose to Dose T Tiitrate trate Peripherally Peripherally Restricted Restricted Faster Faster L Lymphocyte ymphocyte Recovery Recovery No long-acting circulating Potential to avoid first-dose cardiac Very low CNS penetration; not a metabolites monitoring in label repurposed MS drug; potential to Optimal half life (t ~20h) avoid macular edema 1/2 Notes: SAE=serious adverse event 29

VTX002 Differentiates on Multiple Key Parameters vs. Competitors Differentiating Parameter Ozanimod Etrasimod VTX002 Receptor Selectivity S1P 1,5 S1P 1,4,5 S1P 1,5 CYP450 Interactions Yes No No Liver Enzyme Elevations Yes No No Active Metabolites Yes No No Half-life 19 h, Met 10-13 d 33 h ~20 h Fast Lymphocyte Recovery Time No Yes Yes First Dose Heart Rate Reduction Yes Yes Yes Dose Titration Yes No Yes First Dose Monitoring No TBD TBD 30

Phase 1 MAD Results: Dose-Dependent Exposure and Lymphocyte Reduction Absolute Lymphocyte Count (ALC) Reductions of 40-50% Correlated with Clinical Efficacy Observed in UC* Pharmacokinetics Pharmacodynamics ****p< 0.0001 **** **** **** **** Placebo 2 mg 10 mg 20 mg 35 mg 45 mg • T of ~20 hours • Demonstrated consistent, sustained reduction of 1/2 lymphocytes up to 65% across multiple dose groups • Dose-proportionate exposure after single and multiple doses of VTX002 with steady-state reached after 4 to 7 days of target-dose exposure 31

Phase 2 Induction Trial in Moderate-to-Severe Ulcerative Colitis BASELINE WEEK 13* WEEK 52 13-Week Treatment Period 39-Week LTE Treatment Period Screening Period * includes 7-day titration R 12-Week Treatment Period VTX002, VTX002, 60 60 mg mg VTX002, VTX002, 60 60 mg mg Trial Design VTX002, VTX002, 30 30 mg mg VTX002, VTX002, 30 30 mg mg N=180; 1:1:1 Placebo Placebo Placebo Placebo WEEK 13 Patients with LOR NR OLE* – VTX002, 60 mg • Powered for primary endpoint of clinical remission KEY TAKEAWAYS • Trial may serve as the first of two pivotal trials required for registration Note: Phase 2 tablet doses of 30mg and 60mg provide comparable VTX002 exposure as Phase 1 suspension doses of 20mg and 40mg, respectively *Induction and OLE non-responder dosing includes 7-day titration period followed by 12 weeks of placebo or VTX002 dose 32

Underpenetrated Market for Biologic Refractory Patients Addressable UC Patient Population in US ~1M UC PATIENTS • Existing agents leave room for new treatments 300K+ MODERATE-TO-SEVERE UC PATIENTS • Novel oral agents may expand penetrance of treated moderate- to-severe UC population beyond VTX002 TARGET POPULATION current ~25-30% ~100K BIOLOGIC-TREATED PATIENTS • S1P well positioned to emerge as leading oral therapeutic class based on its attractive class >50K efficacy/safety profile 33

SELECTIVE NLRP3 INFLAMMASOME INHIBITORS for systemic and CNS indications

Rationale for Targeting the NLRP3 Inflammasome NLRP3 Inflammasome Inhibitors Target IL-1β, a Key Driver of Inflammatory Disease Clinical Validation of In vivo Evidence Genetic Evidence Downstream Target • The NLRP3 inflammasome can • Gain-of-function mutations in the • IL-1β signaling, downstream of become overactive in the presence of NLRP3 gene, associated with inflammasome activation, is a persistent tissue damage or crystal certain severe orphan inflammatory clinically-validated, anti- deposits diseases, are classified as inflammatory target with biologics cyropyrin-associated periodic ® • Inflammasome activation results in • Ilaris ($873M sales in 2020) syndromes (CAPS) release of IL-1β & IL-18 recruiting approved for CAPS and other neutrophils and driving Th17 orphan periodic fever syndromes response • This leads to pyroptosis and further tissue damage NLRP3 = NOD-like receptor family, pyrin domain-containing protein 3; IL-1β = interleukin-1β Sources: Novartis annual report; Ilaris prescribing information 35

NLRP3 Inhibitor Program Summary Peripheral NLRP3 Inhibitor: VTX2735 CNS NLRP3 Inhibitor: VTX3232 • Selective NLRP3 inhibitor • Selective compounds generated with high CNS bioavailability • Well tolerated in GLP safety and tox assessment • Novel and proprietary lead series • Phase 1 completed with attractive • Plan to file IND in Q1 2023 safety/tolerability profile and evidence of • Potential to be first, truly CNS-directed NLRP3 pharmacodynamic activity inhibitor to enter clinic • Phase 2 trial in CAPS planned Q1 2023; additional indications are being evaluated Source: Ventyx internal data 36

VTX2735 Is a Selective & Orally Bioavailable NLRP3 Inhibitor Mouse Pharmacodynamic Assay In Vitro Potency & Selectivity Non-Human Primate PK IV Clearance: 1.6 mL/min/kg; Oral Bioavailability: 80% IL-1β IC (nM) 50 human 2 monocytes On Target human 75 whole blood AIM2 >10000 Off NLRC4 >10000 Target NF-ĸB >10000 • Well-tolerated preclinically in IND-enabling GLP studies KEY • Oral bioavailability (80%) in NHP and dose-proportional TAKEAWAYS exposure that predicts potential for wide safety margins based on PK/PD modeling Source: Ventyx internal data; MCC950 is an NLRP3 inhibitor and a control compound used in in vitro and in vivo studies 37

Summary of VTX2735 Phase 1 Results Excellent Safety and Pharmacodynamic Activity • All AEs considered mild Concentration-Dependent Suppression of Safety • No LFT abnormalities IL-1β Ex Vivo üü • No dose-related increase in frequency of AEs observed • Dose-proportionate increases in exposure PK (C and AUC) max üü • Robust dose and concentration-dependent PD suppression of IL-1β ex vivo üü • Ability to cover IL-1β IC , IC 50 90 Target • Potential wide therapeutic window Data from Day 10 of Phase 1 MAD, 1 to 8h post-dose Coverage üü (safe across wide exposure range) Ex vivo LPS plus ATP-mediated IL-1β release assay *PK: Pharmacokinetics; PD: Pharmacodynamics 38 IL-1β % of baseline

VTX2735 Has Broad Activity Against Multiple NLRP3 Mutations Potential for Differentiation in CAPS Setting What is CAPS? IC in Blood Monocyte Assay (nM) 50 An ultra-orphan auto-inflammatory disease caused by various mutations in NLRP3 and characterized by Most 75% Severe inappropriate release of IL-1β and of all CAPS patients In North America symptoms of recurrent systemic CPD Challenge FCAS1 FCAS2 FCAS3 FCAS4 FCAS.MWS NOMID inflammation L353P (L353P) (L353P) A439V/G564R E525K/V198M F309Y KEY TAKEAWAY VTX2735 LPS 14 24 17 117 56 166 VTX2735 blood assay data from CAPS patients suggest inhibitory MCC950 LPS 1,264 >10K >10K >10K >10K >10K activity across several mutations: FCAS, MWS and NOMID subset of CAPS patients. Source: UCSD (Dr. Hal Hoffman’s lab); CAPS=Cryopyrin-Associated Periodic Syndromes 39

CNS-Penetrant NLRP3 Inhibitor VTX3232 In Vitro Potency & Selectivity Rat PK (PO, 5mg/kg) Dog PK (PO, 5mg/kg) T½ = 4.4 h; Oral Bioavailability = 75% T½ = 8 h; Oral Bioavailability = 100% IL-1β IC (nM) 50 1000 NLRP3 huWB 13 1000 Brain Conc. 100 AIM2 >10000 100 CSF Conc. > 10x ~20 x WB IC 50 WB IC 50 10 at 24 h 10 at 24 h NLRC4 BMDM >10000 WB IC WB IC 50 50 1 1 NF-kb >10000 0 4 8 1216 2024 0 4 8 12 16 20 24 Time (hr) Time (hr) • Novel, potent, brain-penetrant inhibitor of NLRP3 • 13 nM IC in human whole blood IL-1β release assay 50 KEY • Unique structural chemotype vs. peripheral NLRP3 inhibitors TAKEAWAYS • Provisional application filed June 2021 • Phase 1 start in Q1 2023 Source: Ventyx internal data 40 Plasma Conc. (ng/mL) IL-1β (% of DMSO Control) Plasma Conc. (ng/mL)

NLRP3 Program Clinical Development Plan VTX2735 Peripherally-restricted üüüüüü IND-enabling Studies IND Approved Phase 1 Initiate Phase 2 Healthy volunteers CAPS Further indications TBD Complete September 2021 Complete Q1 2023 VTX3232 IND-Enabling Studies CNS-penetrant Inhibitor Potential indications include Parkinson’s, Alzheimer’s, etc. Phase 1 Initiation Q1 2023 41

Our Comprehensive NLRP3 Portfolio Targets a Broad Range of Major Inflammatory Diseases NLRP3 Systemic Diseases Neuroinflammatory Diseases Peripheral NLRP3 inhibitors are designed CNS-directed NLRP3 inhibitors are designed to treat cardiovascular, dermatologic, rheumatic to treat a range of neuro-degenerative and rare genetic diseases disorders, such as Alzheimer’s and Parkinson’s disease • Cardiovascular • Alzheimer’s Disease • Dermatologic • Parkinson’s Disease • Rheumatic • ALS • Rare Genetic Diseases • Multiple Sclerosis Our solution: VTX2735 Our solution: VTX3232 42

Investment Highlights EFFICIENT & PRODUCTIVE IMMUNOLOGY PLATFORM • Internal R&D engine designed to generate candidates to address autoimmune and inflammatory diseases with high unmet need • 100% commercial rights to entire portfolio; long patent life for all product candidates POTENTIALLY DIFFERENTIATED MEDICINES • Multiple selective, oral, small molecule product candidate portfolio: – allosteric TYK2 inhibitor for multiple autoimmune indications – peripherally-restricted S1P1R modulator for ulcerative colitis – peripheral NLRP3 inhibitor for multiple autoimmune indications – CNS-targeted NLRP3 inhibitor for multiple neurodegenerative indications TARGET MAJOR INFLAMMATORY & IMMUNOLOGY DISEASE MARKETS • Our portfolio can address I&I markets, such as psoriasis, IBD, and other indications • Opportunity to disrupt existing markets dominated by biologics with varying degrees of efficacy and safety in order to: ü Capture refractory patients ü Expand market share of moderate-to-severe patient populations with patient-friendly oral therapy CAPITAL-EFFICIENT BUSINESS MODEL • Cash, cash equivalents and marketable securities balance of $412.4M expected to provide cash runway into 2025 43

CONTACT US FOR ADDITIONAL INFORMATION: ir@ventyxbio.com VENTYX BIOSCIENCES, INC. 662 ENCINITAS BOULEVARD, SUITE 250 ENCINITAS, CA 92024 44