Sagimet Biosciences Inc. - Series A · NASDAQ:SGMT
Sagimet Biosciences Inc. - Series A — Sagimet Biosciences — Investor Presentation (November 2025)
51 slides from Sagimet Biosciences Inc. - Series A's investor presentation, Nov 13, 2025
Slide 1: Targeting Metabolic Dysfunction with Novel Therapies to Treat MASH, Acne & Cancer
Targeting Metabolic Dysfunction with Novel Therapies to Treat M ASH, Acne & Cancer November 2025
Slide 2: Forward-Looking Statements and Disclaimer
2 November 2025 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
Slide 3: Leadership Team with Proven Development and Commercialization Experience
3 November 2025 Leadership Team with Proven Development and Commercialization Experience Dave Happel 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
Slide 4: Sagimet at a Glance
4 November 2025 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
5 November 2025 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 it completed its
Slide 6: Development Pipeline: Multiple Indications and Clinical Milestones
6 November 2025 Expected Milestone / Status Stage of Development Indication Therapeutic Area Phase 3 Phase 2 Phase 1 Preclinical Phase 2b met histology primary and multiple secondary endp oints , data announced 1Q2024 ; FDA Breakthrough Therapy designation; Phase 3 F2/F3 ready MASH Metabolic Disease
Slide 7: MASH: A Burgeoning Epidemic
7 November 2025 MASH • Complex disease with h eterogeneous 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
Slide 8: FASN Inhibition Addresses Three Independent Mechanisms of MASH Development and Progression
8 November 2025 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 li
Slide 9: FASN Inhibition Directly Blocks Human Liver Stellate Cell Function
9 November 2025 FASN Inhibition Directly Blocks Human Liver Stellate Cell Function Stellate cells require DNL for fibrogenesis Denifanstat blocks stellate cell activation Denifanstat directly inhibits fibrogenic activity 1 Primary human stellate cell assay Denifanstat • Stimulated by TGF - beta to a
Slide 10: Treatment Goals for MASH Across Fibrosis Staging
10 November 2025 Treatment Goals for MASH Across Fibrosis Staging F4 (Compensated) F3 F2 F1 MASH STAGING 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
12 November 2025 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
Slide 13: FASCINATE-2: Baseline Characteristics
13 November 2025 FASCINATE - 2: Baseline Characteristics Were Typical of the F2/F3 MASH Population Denifanstat , n=81 Placebo, n=45 Parameter 56.1 (+/ - 10.8) 59.6 (+/ - 10.9) Age , years 48 (59%) 27 (60%) Sex , female 73 (90%) 41 (91%) Race , White 27 (33%) 15 (33%) Ethnicity , Hispanic or Latino 3
Slide 14: Primary Endpoints: Liver Biopsy
14 November 2025 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
Slide 15: Secondary Endpoints: Liver Fibrosis and MASH Resolution
15 November 2025 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 Den
Slide 16: Secondary Endpoints: Liver Fibrosis
16 November 2025 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 p - value Denifanstat Placebo Subgroup Fibrosis Endpoints 0.040** 30% 14% ITT > 1 stage im
Slide 17: Statistically Significant VCTE Improvement at Weeks 26 and 52
17 November 2025 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 magni
Slide 18: Additional Fibrosis Analysis Using AI-based Digital Pathology
18 November 2025 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 Pl
Slide 19: qFibrosis Zonal Analysis
19 November 2025 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 Cirrhotic (F4) Patients
20 November 2025 Differentiated Mechanism of Action • In vitro data demonstrates that denifanstat reduces pro - fibrotic signaling in stellate cells , suggesting that denifanstat has the potential to remove fibrotic scar tissue and reestablish the basal extracellular matrix ( ECM ) scaffold even in
Slide 21: 85% of qF4 Patients on Denifanstat Showed Fibrosis Reductions
21 November 2025 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 pa
Slide 22: FASCINATE-2: Safety
22 November 2025 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 comparabl e to placebo • AE of hair thinning stabilized with a 2 - to - 4 week dose pause and t
Slide 23: Denifanstat Decreased Liver Fat by MRI-PDFF and Reduced FAST Score
23 November 2025 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 Signif
Slide 24: Secondary Endpoints: Liver Enzymes
24 November 2025 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 mea
Slide 25: Cardiometabolic Health
25 November 2025 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 . 1 For LDL - c, baseline > 100 mg/dL. Denifanstat Decreased LDL - c Levels and Increased Polyunsaturated Triglycerides LDL -
Slide 26: Denifanstat Reduced De Novo Lipogenesis
26 November 2025 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 tripalm
Slide 27: Precision Medicine: Blood Tests May Lead to Improved Patient Outcomes
27 November 2025 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
Slide 28: Combination Therapy Development Program for MASH
Combination Therapy Development Program for MASH
Slide 29: Combination of FASN Inhibitor and Semaglutide in MASH Mouse Model
29 November 2025 Combination of FASN Inhibitor and Semaglutide Improved Histological Features in MASH Mouse Model - SMA: a marker of activated hepatic stellate cells NC VEH FASN SEMA COMBO 0 5 10 s c o r e Phenotypic Fibrosis Composite Score * ** NS Fibrosis NC VEH FASN SEMA COMBO In a mouse model,
Slide 30: Patient Subset on Stable GLP1-RA at Baseline
30 November 2025 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
Slide 31: Mechanism of Action Supports Combination Therapy Opportunity
31 November 2025 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. Presente
Slide 32: Potential Benefits of Combination Therapy in Advanced MASH Patients
32 November 2025 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 t rial design and patient populations. As a result, cross - trial comparisons cannot b
Slide 33: Potential Clinical Development Program for Denifanstat and Resmetirom Combination
33 November 2025 Step 1 - Phase 1 PK trial for combination of denifanstat and resmetirom • PK to evaluate any drug/drug interaction • Assess safety/tolerability • Confirm optimal combination dose levels for later clinical efficacy study in MASH Step 2, subject to consultation with regulatory authori
Slide 34: Attractiveness of a Potential Denifanstat/Resmetirom Combination
34 November 2025 Attractiveness of a Potential Denifanstat / Resmetirom Combination • Phase 1 clinical trial to evaluate the pharmacokinetics ථ (PK) and tolerability of a combination of denifanstat and resmetirom initiated in September 2025; data readout expected 1H 2026 • If the outcome of this Pha
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
36 November 2025 FASN Also Plays a Key Role in Other Diseases With Significant Unmet Need FASN in cancer Supports t umor survival Enables t umor proliferation Establishes r esistance to drugs FASN in acne Increases sebum production Exacerbates sebum composition Cancer cell Membrane synthesis, intrac
Slide 37: Acne Pathogenesis and Potential Role of FASN Inhibitors
37 November 2025 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 Pathogene
Slide 38: Acne Market Overview
38 November 2025 Blackheads Whiteheads Papules & Pustules Cysts & Nodules Acne Market Overview Global acne market is expected to reach $17B in next decade 1 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 pat
Slide 39: Acne Treatment Algorithm
39 November 2025 Moderate to Severe Disease Mild 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
40 November 2025 Clinical Data Support Mechanism of Action of a FASN Inhibitor in Acne • FASN inhibitor demonstrated a >90% reduction in sebum lipids by day 15 1,2 • FASN inhibitor maintained the reduced level of sebum lipids through the entire study 1,2 • FASN inhibitor demonstrated a dose responsi
Slide 41: Ascletis Acne Phase 3 Clinical Trial Design
41 November 2025 Ascletis Acne Phase 3 Clinical Trial Design • Moderate to severe acne • Multi - center placebo controlled • 1 :1 randomization • D ouble - blind • Once daily oral dosing • 480 patients in China Primary endpoints at week 12 • % patients who receive IGA success (defined as at least a
Slide 42: Ascletis Acne Phase 3 Trial: All Primary and Secondary Endpoints Met
42 November 2025 Ascletis Acne Phase 3 Clinical Trial: All Primary and Secondary Endpoints Met Placebo (n=240) 50mg denifanstat (n=240) Baseline Characteristics 102.1 102.2 Total lesion count 43.1 42.1 Inflammatory lesion count 85.8 85.8 IGA=3 (moderate), % 14.2 14.2 IGA=4 (severe), % p value 50mg d
Slide 43: Ascletis Acne Phase 3 Clinical Trial Safety Data
43 November 2025 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 incide
Slide 44: Second FASN Inhibitor TVB-3567 Entered FIH Phase 1
44 November 2025 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 = S
Slide 45: Potential Clinical Development Program for TVB-3567 in Acne
45 November 2025 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 dos
Slide 46: Attractiveness of FASN Inhibition in Acne
46 November 2025 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 initiatin
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
48 November 2025 FASN Also Plays a Key Role in Other Diseases With Significant Unmet Need FASN in cancer Supports t umor survival Enables t umor proliferation Establishes r esistance to drugs FASN in acne Increases sebum production Exacerbates sebum composition Cancer cell Membrane synthesis, intrac
Slide 49: FASN Is Integral to Tumor Cell Proliferation and Survival
49 November 2025 FASN Is Integral to Tumor Cell Proliferation and Surviv al KRASM – KRAS mutant. KRASWT - KRAS wild type FASN dependence • Certain cancers are dependent on DNL/FASN for proliferation especially downstream of driver oncogenes • Strategy kill tumor cells and/or avoid drug resistance by
Slide 50: Cancer Program Focuses on 4 FASN-Dependent Tumor Types
50 November 2025 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. Wan
Slide 51: Sagimet at a Glance
51 November 2025 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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