Sagimet Biosciences Inc. - Series A · NASDAQ:SGMT
Sagimet Biosciences Inc. - Series A — Sagimet Biosciences — Corporate Update (March 2026)
52 slides from Sagimet Biosciences Inc. - Series A's corporate update, Mar 11, 2026
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 March 2026
Slide 2: Forward-Looking Statements and Disclaimer
2 March 2026 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 sta
Slide 3: Leadership Team with Proven Development and Commercialization Experience
3 March 2026 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 lea
Slide 4: Sagimet at a Glance
4 March 2026 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 Un
Slide 5: Strong IP, Cash Position, and Collaboration Potential
5 March 2026 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 • Denifanstat was well - tolerated in Ascleti
Slide 6: Development Pipeline: Multiple Indications and Clinical Milestones
6 March 2026 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 ready (F2/F3 MASH) MASH Metabolic Dis
Slide 7: MASH: A Burgeoning Epidemic
7 March 2026 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. J
Slide 8: FASN Inhibition Addresses Three Independent Mechanisms of MASH
8 March 2026 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 lipog
Slide 9: FASN Inhibition Directly Blocks Human Liver Stellate Cell Function
9 March 2026 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 acti
Slide 10: Treatment Goals for MASH Across Fibrosis Staging
10 March 2026 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 / Imp
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 March 2026 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 50
Slide 13: FASCINATE-2: Baseline Characteristics
13 March 2026 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 34.6
Slide 14: Primary Endpoints: Denifanstat Achieved Statistical Significance at Week 52
14 March 2026 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 We
Slide 15: Secondary Endpoints: Liver Fibrosis and MASH Resolution
15 March 2026 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 Denifa
Slide 16: Secondary Endpoints: Liver Fibrosis
16 March 2026 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 impro
Slide 17: Statistically Significant VCTE Improvement at Weeks 26 and 52
17 March 2026 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 magnitud
Slide 18: Additional Fibrosis Analysis Using AI-based Digital Pathology
18 March 2026 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 Place
Slide 19: qFibrosis Zonal Analysis
19 March 2026 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. P
Slide 20: Denifanstat Potential in Patients with MASH Cirrhosis (F4)
20 March 2026 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 pat
Slide 21: 85% of qF4 Patients on Denifanstat Showed Fibrosis Reductions
21 March 2026 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
22 March 2026 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 then
Slide 23: Denifanstat Decreased Liver Fat by MRI-PDFF and Reduced FAST Score
23 March 2026 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 Significa
Slide 24: Secondary Endpoints: Liver Enzymes
24 March 2026 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 c
Slide 25: Cardiometabolic Health
25 March 2026 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 - c
Slide 26: Denifanstat Reduced De Novo Lipogenesis
26 March 2026 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 tripalmiti
Slide 27: Precision Medicine: Blood Tests May Lead to Improved Patient Outcomes
27 March 2026 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
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
29 March 2026 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, com
Slide 30: Patient Subset on Stable GLP1-RA at Baseline
30 March 2026 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 an
Slide 31: Mechanism of Action Supports Combination Therapy Opportunity
31 March 2026 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 a
Slide 32: Potential Benefits of Combination Therapy in Advanced MASH Patients
32 March 2026 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 be m
Slide 33: Phase 1 PK Trial of Denifanstat and Resmetirom Completed
33 March 2026 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 clinical
Slide 34: Attractiveness of a Potential Denifanstat / Resmetirom Combination
34 March 2026 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
36 March 2026 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, intracell
Slide 37: Acne Pathogenesis and Potential Role of FASN Inhibitors
37 March 2026 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 Pathogenesis
Slide 38: Acne Market Overview
38 March 2026 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 patien
Slide 39: Acne Treatment Algorithm
39 March 2026 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 includes t
Slide 40: Clinical Data Support Mechanism of Action of a FASN Inhibitor in Acne
40 March 2026 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 responsive
Slide 41: Ascletis Acne Phase 3 Clinical Trial Design
41 March 2026 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 2 -
Slide 42: Ascletis Acne Phase 3 Trial: All Primary and Secondary Endpoints Met
42 March 2026 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 deni
Slide 43: Ascletis Acne Phase 3 Clinical Trial Safety Data
43 March 2026 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
Slide 44: Ascletis Acne Open Label Phase 3 Trial
44 March 2026 Ascletis Acne Open Label Phase 3 trial Denifanstat generally well - tolerated in the open label clinical trial Ascletis data on file. Safety and efficacy endpoints of 50 mg denifanstat oral, once daily for 52 weeks versus placebo for 12 weeks an d 50mg denifanstat oral once daily for 4
Slide 45: TVB-3567 Phase 1 Trial Design
45 March 2026 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 = Sing
Slide 46: Potential Clinical Development Program for TVB-3567 in Acne
46 March 2026 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
Slide 47: Attractiveness of FASN Inhibition in Acne
47 March 2026 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, plan to consult with regulatory authorities regarding Phase 2 trial design, with goal of initiatin
Slide 48: FASN Inhibition Offers Potential Benefit in Multiple Indications: Oncology
FASN Inhibition Offers Potential Benefit in Multiple Indications: Oncology
Slide 49: FASN Also Plays a Key Role in Other Diseases With Significant Unmet Need
49 March 2026 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, intracell
Slide 50: FASN Is Integral to Tumor Cell Proliferation and Survival
50 March 2026 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 co
Slide 51: Cancer Program Focuses on 4 FASN-Dependent Tumor Types
51 March 2026 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 52: Sagimet at a Glance
52 March 2026 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 U