Sagimet Biosciences Inc. - Series A · NASDAQ:SGMT
Sagimet Biosciences Inc. - Series A — Sagimet Biosciences — Investor Presentation (December 2025)
51 slides from Sagimet Biosciences Inc. - Series A's investor presentation, Dec 18, 2025
Slide 1: Targeting Metabolic Dysfunction with Novel Therapies to Treat MASH, Acne & Cancer
Targeting MetabolicDysfunction with Novel Therapies to Treat MASH, Acne&Cancer December 2025
Slide 2: Forward-Looking Statements and Disclaimer
December 2025 2 Forward-Looking Statements and Disclaimer This presentation contains forward-looking statements within the meaning of, and made pursuant to the safe harbor provisions of, The Private Securities Litigation Reform Act of 1995. All statements contained in this document, other than state
Slide 3: Leadership Team with Proven Development and Commercialization Experience
December 2025 3 Leadership Team with Proven Development and Commercialization Experience DaveHappel President&CEO >20 years of experience in executive leadership in biotech and pharma Brought multiple innovative healthcare products to the market Eduardo Martins Chief Medical Officer >20 years of lea
Slide 4: Sagimet at a Glance
December 2025 4 Sagimet at a Glance • Our lead molecule, denifanstat, is a novel fatty acid synthase (FASN) inhibitor with a differentiated MOA with the potential to target multiple underserved diseases • Strong clinical data demonstrates denifanstat’s proof of concept across multiple disease states
Slide 5: Strong IP, Cash Position, and Collaboration Potential
December 2025 5 Strong IP, Cash Position, and Collaboration Potential • Denifanstat met all primary and secondary endpoints in Phase 3 clinical trial in patients with moderate to severe acne vulgaris in China conducted by license partner for China, Ascletis • Ascletis announced that Denifanstat NDA
Slide 6: Development Pipeline: Multiple Indications and Clinical Milestones
December 2025 6 Therapeutic Area Indication Stage of Development Expected Milestone / Status Preclinical Phase 1 Phase 2 Phase 3 Metabolic Disease MASH Phase 2b met histology primary and multiple secondary endpoints, data announced 1Q2024; FDA Breakthrough Therapy designation; Phase 3 F2/F3 ready Ph
Slide 7: MASH: A Burgeoning Epidemic
December 2025 7 MASH • Complex disease with heterogeneous patient population • Significant opportunity for differentiated MOA MASH: A Burgeoning Epidemic Note: MASH, or metabolic dysfunction-associated steatohepatitis, was formerly known as NASH, or nonalcoholic steatohepatitis. 1. Estes C, et al. J
Slide 8: FASN Inhibition Addresses Three Independent Mechanisms of MASH
December 2025 8 Sagimet’s lead drug candidate, denifanstat, is a specific and potent inhibitor of FASN that functions through three independent mechanisms in MASH: FASN Inhibition Addresses Three Independent Mechanisms of MASH Development and Progression Blocking steatosis via inhibiting de novo lip
Slide 9: FASN Inhibition Directly Blocks Human Liver Stellate Cell Function
December 2025 9 FASN Inhibition Directly Blocks Human Liver Stellate Cell Function Stellate cells require DNL for fibrogenesis Denifanstat blocks stellate cell activation Denifanstat directly inhibits fibrogenic activity1 Primary human stellate cell assay Denifanstat • Stimulated by TGF-beta to acti
Slide 10: Treatment Goals for MASH Across Fibrosis Staging
December 2025 10 Treatment Goals for MASH Across Fibrosis Staging MASH STAGING F1 F2 F3 F4 (Compensated) Risk Staging based on: • Fat • Inflammation • Fibrosis • Liver & CV Events Primary Treatment Objectives Primary Therapeutic Interventions (based on Primary Objectives) Improve Glycemic Control /
Slide 11: Strong MASH Data Creates Opportunities to Reach Advanced Patient Populations
Strong MASH Data Creates Opportunities to Reach Advanced Patient Populations
Slide 12: FASCINATE-2: Biopsy Trial Design Focused on Histological Endpoints
December 2025 12 FASCINATE-2: Biopsy Trial Design Focused on Histological Endpoints AI: Artificial Intelligence, MRI-PDFF; magnetic resonance imaging derived proton density fat fraction, NAS; NAFLD Activity Score. • Biopsy confirmed F2-F3 MASH patients (n=168) • 52 weeks, 2:1 randomization to 50mg o
Slide 13: FASCINATE-2: Baseline Characteristics
December 2025 13 FASCINATE-2: Baseline Characteristics Were Typical of the F2/F3 MASH Population Parameter Placebo, n=45 Denifanstat, n=81 Age, years 59.6 (+/- 10.9) 56.1 (+/- 10.8) Sex, female 27 (60%) 48 (59%) Race, White 41 (91%) 73 (90%) Ethnicity, Hispanic or Latino 15 (33%) 27 (33%) BMI, kg/m2
Slide 14: Primary Endpoints: Liver Biopsy
December 2025 14 Loomba R, et al. Lancet Gastroenterol Hepatol. 2024;9(12):1090-1100 Primary Endpoints: Liver Biopsy Cochran-Mantel-Haenszel Test – two sided at the 0.05 significance level. * ≥1-point improvement in ballooning or inflammation. Denifanstat Achieved Statistical Significance at Week 52
Slide 15: Secondary Endpoints: Liver Fibrosis and MASH Resolution
December 2025 15 Loomba R, et al. Lancet Gastroenterol Hepatol. 2024;9(12):1090-1100 Secondary Endpoints: Liver Fibrosis and MASH Resolution Cochran-Mantel-Haenszel Test – Two sided at the 0.05 significance level Denifanstat Achieved Statistical Significance at Week 52 18% 41% Placebo n=45 Denifanst
Slide 16: Secondary Endpoints: Liver Fibrosis
December 2025 16 Secondary Endpoints: Liver Fibrosis *One sided at the 0.05 significance level, **Two sided at the 0.05 significance level Denifanstat Achieved Statistically Significant Improvement of Fibrosis Fibrosis Endpoints Subgroup Placebo Denifanstat p-value >1 stage improvement in fibrosis w
Slide 17: Statistically Significant VCTE Improvement at Weeks 26 and 52
December 2025 17 Denifanstat Achieved Statistically Significant VCTE Improvement at Weeks 26 and 52 FASCINATE-2 Phase 2b Sagimet Biosciences data on file. FASCINATE-2 posthoc analysis. mITT population. Chi-square test. VCTE: Vibration-controlled transient elastography. VCTE <=30% means magnitude of
Slide 18: Additional Fibrosis Analysis Using AI-based Digital Pathology
December 2025 18 Additional Fibrosis Analysis Using AI-based Digital Pathology Digital Imaging Showed that Denifanstat Significantly Reduced Fibrosis in Advanced Patients Pre-Treatment Pt A NASH-CRN Fibrosis stage F3 Post-Treatment Pt A NASH-CRN Fibrosis stage F1 Denifanstat 0.10 -0.30 Placebo n=45
Slide 19: qFibrosis Zonal Analysis
December 2025 19 qFibrosis Zonal Analysis Demonstrated that Denifanstat Improves Parameters Linked to Liver Outcomes Zone 1 Zone 2 Zone 3 Central Vein Portal Vein HA BD Response at the individual zonal parameter level was defined as ”at least” 30% relative decrease from baseline. 2. Rinella M, et al
Slide 20: Denifanstat Potential in Patients with MASH Cirrhosis (F4)
December 2025 20 Differentiated Mechanism of Action • In vitro data demonstrates that denifanstatreduces pro-fibrotic signaling in stellatecells, suggesting that denifanstat has the potential to remove fibrotic scar tissue and reestablish the basal extracellular matrix (ECM) scaffold even in patient
Slide 21: 85% of qF4 Patients on Denifanstat Showed Fibrosis Reductions
December 2025 21 85% of qF4 Patients on Denifanstat Showed 1 to 2-Stage Reductions in Fibrosis • AI may detect fibrosis regression at an earlier point in time, compared to conventional pathology • qF4 population (defined on AI platform by HistoIndex) are likely the most advanced subgroup of F3 patie
Slide 22: FASCINATE-2: Safety
December 2025 22 FASCINATE-2: Safety Denifanstat Was Generally Well-Tolerated • No DILI (drug-induced liver injury) signal and no muscle wasting were detected, and GI (gastrointestinal) effects were comparable to placebo • AE of hair thinning stabilized with a 2-to-4 week dose pause and then reverse
Slide 23: Denifanstat Decreased Liver Fat by MRI-PDFF and Reduced FAST Score
December 2025 23 Denifanstat Decreased Liver Fat by MRI-PDFF and Reduced FAST Score >30% reduction: Cochran-Mantel-Haenszel Test. Relative reduction: Mixed-effects Model for Repeated Measures. mITT population. Two sided at the 0.05 significance level. Denifanstat Achieved Statistical Significance 21
Slide 24: Secondary Endpoints: Liver Enzymes
December 2025 24 Secondary Endpoints: Liver Enzymes Mixed-effects Model for Repeated Measures – Two sided at the 0.05 significance level. mITT population Denifanstat Decreased ALT and AST Levels ALT Percent Change from Baseline AST Percent Change from Baseline -2.70 -16.20 -23.10 -30.60 LS mean chan
Slide 25: Cardiometabolic Health
December 2025 25 Cardiometabolic Health mITT population. Mixed-effects Model for Repeated Measures – Two sided at the 0.05 significance level. *p<0.05, **p<0.01, ***p<0.001. 1For LDL-c, baseline > 100 mg/dL. Denifanstat Decreased LDL-c Levels and Increased Polyunsaturated Triglycerides LDL-c1 Change
Slide 26: Denifanstat Reduced De Novo Lipogenesis
December 2025 26 Denifanstat Reduced De Novo Lipogenesis Two sided at the 0.05 significance level, ITT population Tripalmitin: • A saturated triglyceride which is a biomarker of DNL inhibition • Reduced by denifanstat as early as week 4 of treatment Next steps • Continue the development of tripalmit
Slide 27: Precision Medicine: Blood Tests May Lead to Improved Patient Outcomes
December 2025 27 Precision Medicine: Blood Tests May Lead to Improved Patient Outcomes 1. Signature has 6 metabolites: ursodeoxycholic acid, DL-2-aminocaprylic acid, sarcosine, glycoursodeoxycholic acid, D(-)-2-aminobutyric acid, PC(0-18:0/22:4). Accuracy 79%, PPV 88%, NPV 63%. • MASH is a multi-fac
Slide 28: Combination Therapy Development Program for MASH
Combination Therapy Development Program for MASH
Slide 29: FASN Inhibitor and Semaglutide Combination in MASH Mouse Model
December 2025 29 Combination of FASN Inhibitor and Semaglutide Improved Histological Features in MASH Mouse Model α-SMA: a marker of activated hepatic stellate cells Fibrosis NC VEH FASN SEMA COMBO In a mouse model, combination treatment showed: 1) an additive effect on fibrosis reduction, 2) a dire
Slide 30: Patient Subset on Stable GLP1-RA at Baseline
December 2025 30 Patient Subset on Stable GLP1-RA at Baseline: Liver Biopsy Cochran-Mantel-Haenszel Test – One sided at the 0.05 significance level. mITT population GLP patients were on stable dose for 6 months prior to first biopsy FASCINATE-2 Phase 2b - Denifanstat Improved MASH Resolution and Fib
Slide 31: Mechanism of Action Supports Combination Therapy Opportunity
December 2025 31 Mechanism of Action Supports Combination Therapy Opportunity MOA- Mechanism of Action 1. Tsai WW, et al. Presented at: EASL 2024; June 5-8, 2024; Milan, Italy. https://sagimet.com/wp-content/uploads/2024/06/2024-EASL-poster-GAN-model-final.pdf Tsai WW, et al. Presented at: EASL 2024
Slide 32: Potential Benefits of Combination Therapy in Advanced MASH Patients
December 2025 32 Potential Benefits of Combination Therapy in Advanced MASH Patients Note: These data are placebo-adjusted, derived from different clinical trials at different points in time, with differences in trial design and patient populations. As a result, cross-trial comparisons cannot be mad
Slide 33: Clinical Development Program for Denifanstat and Resmetirom Combination
December 2025 33 Phase 1 pharmacokinetics (PK) trial for combination of denifanstat and resmetirom completed in December 2025 • Combination of denifanstat and resmetirom was generally well-tolerated over the duration of the study, with no safety signals • No Serious Adverse Events (SAEs), no clinica
Slide 34: Attractiveness of a Potential Denifanstat/Resmetirom Combination
December 2025 34 Attractiveness of a Potential Denifanstat/Resmetirom Combination • Phase 1 PK clinical trial of a combination of denifanstat and resmetirom completed in December 2025 • Phase 2 trial of denifanstat/resmetirom combination in F4 MASH patients is planned to initiate in 2H 2026 • Global
Slide 35: FASN Inhibition Offers Potential Benefit in Multiple Indications: Acne
FASN Inhibition Offers Potential Benefit in Multiple Indications: Acne
Slide 36: FASN Also Plays a Key Role in Other Diseases With Significant Unmet Need
December 2025 36 FASN Also Plays a Key Role in Other Diseases With Significant Unmet Need FASN in cancer Supports tumor survival Enables tumor proliferation Establishes resistance to drugs FASN in acne Increases sebum production Exacerbates sebum composition Cancer cell Membrane synthesis, intracell
Slide 37: Acne Pathogenesis and Potential Role of FASN Inhibitors
December 2025 37 Multifactorial pathogenesis of acne involves 4 key aspects: • Increased sebum in sebaceous glands (80% of lipids produced through DNL) • Abnormal or excessive follicular hyper-keratinization • Accelerated bacterial growth (C. acnes) • Localized inflammatory response Acne Pathogenesi
Slide 38: Acne Market Overview
December 2025 38 Blackheads Whiteheads Papules & Pustules Cysts & Nodules Acne Market Overview Global acne market is expected to reach $17B in next decade1 5.1 million US acne patients are treated by dermatologists annually (total US acne market is 50 million people) 2,3 • Acne is the #1 or #2 patie
Slide 39: Acne Treatment Algorithm
December 2025 39 Mild Disease Moderate to Severe Disease Acne Treatment Algorithm • Most acne patients receive skin care routines that include OTC cleansers and moisturizers to address AEs associated with their treatment Disease management involves flare and prevention intervention Treatment include
Slide 40: Clinical Data Support Mechanism of Action of a FASN Inhibitor in Acne
December 2025 40 Clinical Data Support Mechanism of Action of a FASN Inhibitor in Acne • FASN inhibitor demonstrated a >90% reduction in sebum lipids by day 151,2 • FASN inhibitor maintained the reduced level of sebum lipids through the entire study1,2 • FASN inhibitor demonstrated a dose responsive
Slide 41: Ascletis Acne Phase 3 Clinical Trial Design
December 2025 41 Ascletis Acne Phase 3 Clinical Trial Design • Moderate to severe acne • Multi-center placebo controlled • 1:1 randomization • Double-blind • Once daily oral dosing • 480 patients in China Primary endpoints at week 12 • % patients who receive IGA success (defined as at least a 2-poin
Slide 42: Ascletis Acne Phase 3: All Primary and Secondary Endpoints Met
December 2025 42 Ascletis Acne Phase 3 Clinical Trial: All Primary and Secondary Endpoints Met Baseline Characteristics 50mg denifanstat (n=240) Placebo (n=240) Total lesion count 102.2 102.1 Inflammatory lesion count 42.1 43.1 IGA=3 (moderate), % 85.8 85.8 IGA=4 (severe), % 14.2 14.2 Efficacy endpo
Slide 43: Ascletis Acne Phase 3 Clinical Trial Safety Data
December 2025 43 Ascletis Acne Phase 3 Clinical Trial Safety Data Denifanstat 50mg was generally well tolerated during the 12-week study Treatment-emergent adverse events (TEAEs): • TEAE incidence rates were comparable between denifanstat and placebo • Only two categories of TEAEs had an incidence r
Slide 44: TVB-3567 Phase 1 Trial in Healthy and Acne Participants
December 2025 44 A double-blind, randomized, placebo-controlled trial to assess the safety, tolerability, pharmacokinetics and pharmacodynamics of single and multiple ascending doses of TVB-3567 in healthy and acne participants • Includes sebum analysis as pharmacodynamic readout Note: SAD = Single
Slide 45: Potential Clinical Development Program for TVB-3567 in Acne
December 2025 45 Potential Clinical Development Program for TVB-3567 in Acne Step 1 - Phase 1 first-in-human pharmacokinetic (PK) clinical trial of TVB-3567 in healthy volunteers • PK and pharmacodynamics (PD) evaluation to confirm profile • Assess safety/tolerability • Confirm potential doses for a
Slide 46: Attractiveness of FASN Inhibition in Acne
December 2025 46 Attractiveness of FASN Inhibition in Acne • First-in-human Phase 1 clinical trial of TVB-3567 initiated in June 2025 for development in acne • Upon completion of TVB-3567 Phase 1, will consult with regulatory authorities regarding Phase 2 trial design, with goal of initiating TVB-35
Slide 47: FASN Inhibition Offers Potential Benefit in Multiple Indications: Oncology
FASN Inhibition Offers Potential Benefit in Multiple Indications: Oncology
Slide 48: FASN Also Plays a Key Role in Other Diseases With Significant Unmet Need
December 2025 48 FASN Also Plays a Key Role in Other Diseases With Significant Unmet Need FASN in cancer Supports tumor survival Enables tumor proliferation Establishes resistance to drugs FASN in acne Increases sebum production Exacerbates sebum composition Cancer cell Membrane synthesis, intracell
Slide 49: FASN Is Integral to Tumor Cell Proliferation and Survival
December 2025 49 FASN Is Integral to Tumor Cell Proliferation and Survival KRASM – KRAS mutant. KRASWT- KRAS wild type FASN dependence • Certain cancers are dependent onDNL/FASN for proliferation especiallydownstream of driver oncogenes • Strategy kill tumor cells and/or avoid drug resistance by com
Slide 50: Cancer Program Focuses on 4 FASN-Dependent Tumor Types
December 2025 50 GBM Prostate HCC NSCLC KRASM Cancer Program Focuses on 4 FASN-Dependent Tumor Types GBM (glioblastoma), HCC (hepatocellular carcinoma), KRASM (mutant KRAS), NSCLC (non small cell lung cancer) 1. ClinicalTrials.gov. NCT05743621. https://clinicaltrials.gov/study/NCT05743621. 2. Wang H
Slide 51: Sagimet at a Glance
December 2025 51 Sagimet at a Glance • Our lead molecule, denifanstat, is a novel fatty acid synthase (FASN) inhibitor with a differentiated MOA with the potential to target multiple underserved diseases • Strong clinical data demonstrates denifanstat’s proof of concept across multiple disease state
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