Form 8-K - Current report

UNITED STATES

SECURITIES AND EXCHANGE COMMISSION

Washington, D.C. 20549

FORM 8-K

CURRENT REPORT

Pursuant to Section 13 or 15(d)

of the Securities Exchange Act of 1934

Date of Report (Date of earliest event reported): May 23, 2024

SAGIMET BIOSCIENCES INC.

(Exact name of registrant as specified in its charter)

Delaware

001-41742

20-5991472

(State or other jurisdiction

of incorporation)

(Commission

File Number)

(I.R.S. Employer

Identification No.)

Sagimet Biosciences Inc.

155 Bovet Road, Suite 303,

San Mateo, California 94402

(Address of principal executive offices, including zip code)

(650) 561-8600

(Registrant’s telephone number, including area code)

Not Applicable

(Former Name or Former Address, if Changed Since Last Report)

Check the appropriate box below if the Form 8-K filing is intended to simultaneously satisfy the filing obligation of the registrant under any of the following provisions:

¨	Written communications pursuant to Rule 425 under the Securities Act (17 CFR 230.425)

¨	Soliciting material pursuant to Rule 14a-12 under the Exchange Act (17 CFR 240.14a-12)

¨	Pre-commencement communications pursuant to Rule 14d-2(b) under the Exchange Act (17 CFR 240.14d-2(b))

¨	Pre-commencement communications pursuant to Rule 13e-4(c) under the Exchange Act (17 CFR 240.13e-4(c))

Securities registered pursuant to Section 12(b) of the Act:

Title of each class	Trade Symbol(s)	Name of each exchange on which registered
Series A Common Stock, $0.0001 par value per share	SGMT	The Nasdaq Global Market

Indicate by check mark whether the registrant is an emerging growth company as defined in Rule 405 of the Securities Act of 1933 (§ 230.405 of this chapter) or Rule 12b-2 of the Securities Exchange Act of 1934 (§ 240.12b-2 of this chapter).

Emerging growth company x

If an emerging growth company, indicate by check mark if the registrant has elected not to use the extended transition period for complying with any new or revised financial accounting standards provided pursuant to Section 13(a) of the Exchange Act. ¨

Item 7.01

Regulation FD Disclosure

On May 23, 2024, Sagimet Biosciences Inc. (the “Company”), updated information reflected in a slide presentation, which is attached as Exhibit 99.1 to this Current Report on Form 8-K and is incorporated herein by reference. Representatives of the Company will use the updated presentation in various meetings with investors from time to time.

The information in Item 7.01 of this Current Report on Form 8-K, including the information set forth in Exhibit 99.1, is being furnished and shall not be deemed “filed” for purposes of Section 18 of the Securities Exchange Act of 1934, as amended (the “Exchange Act”), nor shall Exhibit 99.1 furnished herewith be deemed incorporated by reference in any filing under the Securities Act of 1933, as amended, or the Exchange Act, except as shall be expressly set forth by specific reference in such a filing.

Item 9.01

Financial Statements and Exhibits

(d) Exhibits

Exhibit No.		Document
99.1		Investor Presentation of Sagimet Biosciences Inc., dated May 23, 2024
104		Cover Page Interactive Data File (embedded within the Inline XBRL document).

SIGNATURE

Pursuant to the requirements of the Securities Exchange Act of 1934, as amended, the registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.

	Sagimet Biosciences Inc.

Date: May 23, 2024	By:	/s/ David Happel
		David Happel
		Chief Executive Officer

Exhibit 99.1

Targeting Metabolic Dysfunction with Novel Therapies to Treat M ASH, Acne and Cancer May 202 4

Forward Looking Statements 2 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 statements of historical facts or statements that relate to present facts or current conditions, including but not limited to, statements regarding possible or assumed future results of operations, business strategies, research and development plans, regulatory activities, the presentation of data from clinical trials, Sagimet’s clinical development plans and related anticipated clinical development milestones, market opportunity, competitive position and potential growth opportunities are forward - looking statements. These statements involve known and unknown risks, uncertainties and other important factors that may cause our actual results, performance or achievements to be materially different from any future results, performance or achievements expressed or implied by the forward - looking statements. In some cases, you can identify forward - looking statements by terms such as “may,” “will,” “should,” “would,” “expect,” “plan,” “anticipate,” “could,” “intend,” “target,” “project,” “believe,” “estimate,” “predict,” “potential,” or “continue” or the negative of these terms or other similar expressions. The forward - looking statements in this presentation are only predictions. These forward - looking statements speak only as of the date of this presentation and are subject to a number of risks, uncertainties and assumptions, some of which cannot be predicted or quantified and some of which are beyond our control, including, among others: the clinical development and therapeutic potential of denifanstat or any other drug candidates we may develop; our ability to advance drug candidates into and successfully complete clinical trials , the risk the topline clinical trials may not be predictive of, and may differ from final clinical data and later - stage clinical trials; that unfavorable new clinical trial data may emerge in other clinical trials of denifanstat , including Phase 3 clinical trials; that clinical trial data are subject to differing interpretations and assessments, including by regulatory authorities; our relationship with Ascletis , and the success of its development efforts for denifanstat ; the accuracy of our estimates regarding our capital requirements; and our ability to maintain and successfully enforce adequate intellectual property protection. These and other risks and uncertainties are described more fully in the “Risk Factors” section of our most recent filings with the Securities and Exchange Commission and available at www.sec.gov . You should not rely on these forward - looking statements as predictions of future events. The events and circumstances reflected in our forward - looking statements may not be achieved or occur, and actual results could differ materially from those projected in the forward - looking statements. Moreover, we operate in a dynamic industry and economy. New risk factors and uncertainties may emerge from time to time, and it is not possible for management to predict all risk factors and uncertainties that we may face. Except as required by applicable law, we do not plan to publicly update or revise any forward - looking statements contained herein, whether as a result of any new information, future events, changed circumstances or otherwise.

Dave Happel President & CEO • Cognoa : President & CEO Chrono Therapeutics: President & CEO Senior E xecutive and C ommercial roles at Horizon, Raptor, Dynavax, Chiron • M.B.A. – Indiana State University; B.A. C hemistry – Indiana University George Kemble Executive Chairman • AstraZeneca (formerly MedImmune, Aviron): SVP R esearch for B iologics & G eneral M anager of California operations, VP V accine R esearch & D evelopment for V accines • Ph.D. – Stanford University, D ept of M icrobiology & I mmunology Eduardo Martins CMO • Abbvie (formerly Allergan), Eiger BioPharmaceuticals , Gilead, Genentech, Dynavax, Intermune, SciClone • D.Phil. – University of Oxford M.D. – Federal University of Rio de Janeiro, Brazil Thierry Chauche CFO • Provention Bio, Alexion Pharmaceuticals, Intercept Pharmaceuticals, Novartis • MBA – The Wharton School of the University of Pennsylvania • M.S. - Ecole Des Ponts ParisTech Elizabeth Rozek General Counsel • Cognoa , Basilea Pharmaceutica, US Department of Justice • J.D. – University of California Berkeley M.A. – University of California San Diego B.A. – Brown University Proven Team with Development and Commercialization Experience Across Hepatology, Metabolic Disease and Oncology 3

Sagimet Investment Highlights Critical role of FASN enzyme in M ASH x Key enzyme in de novo lipogenesis – responsible for excess liver fat in MASH x FASN inhibition directly improves the 3 key drivers of M ASH – liver fat, inflammation, fibrosis x Differentiated MOA to treat growing underserved patient population x FASCINATE - 2 Phase 2b positive topline results • NASH resolution without worsening of fibrosis with ≥2 - point reduction in NAS (p=0.002) • ≥2 - point reduction in NAS without worsening of fibrosis (p=0.0001) • Fibrosis improvement by ≥ 1 stage with no worsening of NASH (p=0.005) x Blood test confirms drug response x Predictive biomarkers identify likely responders x Opportunity to personalize treatment and optimize outcomes Acne x Clinical proof of concept established in Phase 1 x Positive Phase 2 topline results announced in May 2023 by license partner Ascletis x Ascletis Phase 3 in severe acne vulgaris ongoing Cancer x Clinical proof of concept established in Phase 1 x Phase 3 rGBM trial enrollment for interim analysis completed in September 2023 by Ascletis Denifanstat: FASN inhibitor with compelling clinical data Precision medicine is key differentiator Strong rationale for FASN in acne and cancer Strong financial position x Upsized IPO completed in July 2023 raised $86.2 million of net proceeds x Follow - on financing completed in January 2024 raised net proceeds of $104.7 million. x Cash, cash equivalents and marketable securities were $193.7 million as of March 31, 2024, expected to fund current operations through 2025 4

Therapeutic Area Stage of Development Indication Expected Milestone / Status Preclinical Phase 1 Phase 2 Phase 3 Metabolic disease • Phase 2b successfully completed; MASH Phase 3 study planned to start 2H 2024 MASH - F2/F3 • Phase 1 hepatic impairment results 1Q 2024 Dermatology Acne • IND - enabling studies completed; evaluating timing to file IND • Phase 3 clinical study initiated 4 Q 2023 * Oncology Solid tumors • Patient selection and trial design in FASN - dependent tumor types ongoing Recurrent glioblastoma ( GBM ) • Phase 3 enrollment of 120 patients achieved in 3Q 2023; interim analysis planned * Development Pipeline : Indications and Clinical Milestones 5 * Trials conducted in China by Ascletis, who has licensed development and commercialization rights to all indications in Greater China TVB - 2640 TVB - 2640 TVB - 2640 (ASC40) TVB - 2640 (ASC40) TVB - 3567

M ASH: A Burgeoning Epidemic • Only one recently approved drug in U.S., and no approved drugs in Europe • Complex disease, heterogeneous patient population • Improving regulatory clarity, but liver biopsy still required • Many molecules moved forward on weak mechanism and data • Inappropriate biomarkers for mechanism that did not translate to clinical benefit • Safety: triglyceride elevations, LDL elevations, liver injury Disease challenges Drug development challenges x Designed for once - daily, oral dosing x Rigorous and de - risked development strategy x Direct DNL inhibition demonstrated in Phase 1b x Improvements observed across biomarkers in Phase 2a x Topline data of successfully completed Phase 2b announced in 1Q 20 24 x Precision medicine approach to improve patient outcomes Denifanstat Patients in 2016 1 United States 85.3 million MASLD Metabolic Dysfunction - Associated Liver Disease Hepatocellular carcinoma MASH Metabolic Dysfunction - Associated Steatohepatitis MASH mod - adv fibrosis F2 - F3 Cirrhosis F4 11 thousand annual cases among NAFLD population 1.4 million compensated and decompensated 17.3 million 5.7 million 1 Estes, et al. 2018; http://dx.doi.org/10.1016/j.jhep.2018.05.036 DNL = de novo lipogenesis 6

Denifanstat in M ASH 7

Denifanstat : Differentiated Mechanism Believed to Target Key Drivers of M ASH Adapted from Wegermann et al, Clinical Liver Disease, Vol 11, No 4, April 2018, DOI: 10.1002/cld.709 Denifanstat has independent mechanisms designed to: ඹ Block steatosis via inhibiting de novo lipogenesis in hepatocytes ය Reduce inflammation via preventing immune cell activation ර Blunt fibrosis via inhibiting stellate cell activation 8

Denifanstat: Well Tolerated at 25/50mg Doses in FASCINATE - 1 • No dose - related significant adverse events relative to placebo • No serious AEs • Majority of AEs were Grade 1; no Grade ≥3 drug - related AEs 9

FASCINATE - 2 Phase 2b Biopsy Trial Design Measuring Histological Improvement 10 FASCINATE - 2 Phase 2b trial design • Biopsy confirmed F2 - F3 NASH patients • 52 weeks, 2:1 50mg or placebo, double - blind Primary endpoints Other selected endpoints • NAS ≥2 points improvement w/o worsening of fibrosis OR • NASH resolution + NAS ≥2 improvement w/o worsening of fibrosis • Improvement in liver fibrosis ≥1 stage without worsening of NASH (Bx) • Digital AI pathology • MRI - PDFF: absolute decrease, % change from baseline, % pts ≥30% reduction from baseline (responders) AI: Artificial Intelligence, Bx; biopsy, MRI - PDFF; magnetic resonance imaging derived proton density fat fraction, NAS; NAFLD Ac tivity Score.

FASCINATE - 2 Baseline Characteristics Typical F2/F3 MASH Population Modified intent - to - treat population ( mITT ) includes all patients with paired biopsies. Data are mean (SD) or n (%) 11 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/m 2 36.5 (+/ - 6.7) 34.6 (+/ - 6.1) Type 2 diabetes 27 (60%) 55 (68%) ALT (alanine aminotransferase) U/L 67 (+/ - 33) 57 (+/ - 29) AST (aspartate aminotransferase) U/L 52 (+/ - 27) 48 (+/ - 29) Liver Fat Content (MRI - PDFF) , % 19.0 (+/ - 7.0) 16.6 (+/ - 7.1) Baseline liver biopsy NAS ≥ 5 34 (76%) 63 (78%) Baseline liver biopsy F2/F3 22 (49%) / 23 (51%) 34 (42%) / 47 (58%) Statin (at baseline) 21 (47%) 38 (47%) GLP1 - RA (at baseline) 4 (9%) 12 (15%) LDL , mg/dL 103 ( +/ - 39) 96 ( +/ - 34) Triglycerides , mg/dL 153 ( +/ - 67) 173 ( +/ - 79) ELF (Enhanced Liver Fibrosis) Score 9.8 ( +/ - 0.8) 9.6 ( +/ - 0.8) FAST ( Fibroscan AST) Score 0.6 (0.19) 0.6 (0.20)

Primary Endpoints: Liver Biopsy Denifanstat Achieved Statistical Significance Cochran - Mantel - Haenszel Test – One sided at the 0.05 significance level. mITT population. * ≥1 - point improvement in ballooning or inflammation. 12 20% 52% Placebo n=45 Denifanstat n=81 % response NAS ≥ 2 points improvement* w/o worsening of fibrosis p=0.0001 13% 36% Placebo n=45 Denifanstat n=81 % response NASH resolution + NAS ≥ 2 improvement w/o worsening of fibrosis p=0.0022

Secondary Endpoints: Liver Biopsy Denifanstat Achieved Statistical Significance 13 Resolution of NASH w/o worsening of fibrosis p= 16% 38% Placebo n=45 Denifanstat n=81 % response p=0.0021 Cochran - Mantel - Haenszel Test – One sided at the 0.05 significance level. mITT population 18% 41% Placebo n=45 Denifanstat n=81 % response Improvement in liver fibrosis ≥ 1 stage w/o worsening of NASH p=0.0051

Independent Fibrosis Analysis by AI - based Digital Pathology Supporting Evidence that Denifanstat Significantly Reduced Fibrosis 14 0.10 - 0.30 Placebo n=45 Denifanstat n=81 LS mean change qFibrosis Continuous Value Change from Baseline p=0.0023 Cochran - Mantel - Haenszel Test – One sided at the 0.05 significance level. LS means; least squares mean. HistoIndex platform. mITT population.

Patient Subset on Stable GLP1 - RA at Baseline: Liver Biopsy Denifanstat Improves NASH Resolution and Fibrosis 15 Resolution of NASH w/o worsening of fibrosis Improvement in liver fibrosis ≥ 1 stage w/o worsening of NASH 0% 42% Placebo n=4 Denifanstat n=12 % response 0% 42% Placebo n=4 Denifanstat n=12 % response p=0.034 p=0.103 Cochran - Mantel - Haenszel Test – One sided at the 0.05 significance level. mITT population

Biomarkers of Fibrosis Denifanstat Decreased FAST Score and ELF Mixed - effects Model for Repeated Measures – Two sided at the 0.05 significance level. mITT population. *Baseline ELF > 9.8 (mean). 16 p= p= - 0.11 - 0.12 - 0.40 - 0.41 Week 26 Week 52 LS mean change Placebo n=22/23 Denifanstat n=32/30 ELF* Change from Baseline - 0.10 - 0.10 - 0.20 - 0.30 Week 26 Week 52 LS mean change Placebo n=42/40 Denifanstat n=76/73 FAST Change from Baseline p<0.0001 p<0.0001 p>0.05 p>0.05

Secondary Endpoint: Liver Fat by MRI - PDFF Denifanstat Achieved Statistical Significance 17 21% 65% Placebo n=38 Denifanstat n=69 % response MRI - PDFF ≥ 30% Relative Reduction, Week 52 p<0.0001 MRI - PDFF Relative Change from Baseline 5% - 8% - 25% - 31% Week 26 Week 52 LS mean change Placebo n=37/38 Denifanstat n=68/72 p=0.0008 p=0.0036 > 30% reduction: Cochran - Mantel - Haenszel Test. Relative reduction: Mixed - effects Model for Repeated Measures . mITT population

Secondary Endpoints: Liver Enzymes Denifanstat Decreased ALT and AST Levels 18 ALT Percent Change from Baseline AST Percent Change from Baseline Mixed - effects Model for Repeated Measures – Two sided at the 0.05 significance level. mITT population - 2.80 - 16.30 - 23.10 - 30.60 Week 26 Week 52 LS mean change Placebo n=45/43 Denifanstat n=80/80 p=0.015 p=0.030 0.00 - 12.00 - 20.60 - 26.80 Week 26 Week 52 LS mean change Placebo n=45/43 Denifanstat n=79/80 p=0.018 p=0.027

Cardiometabolic health Denifanstat Decreased LDL - c Levels 19 LDL - c* Change from Baseline p>0.05 p>0.05 Triglycerides Median values 70 90 110 130 150 170 190 210 230 250 0 4 8 13 26 39 52 TG, mg/dL Weeks Placebo Denifanstat - 1.60 - 9.10 - 12.60 - 19.10 Week 26 Week 52 Mean change, mg/dL Placebo n=27 Denifanstat n=32 mITT population. *For LDL - c, baseline > 100 mg/dL. Mixed - effects Model for Repeated Measures – Two sided at the 0.05 significance le vel. n=45 n=80 p>0.05 p>0.05 Small increase driven by increased polyunsaturated fatty acids in triglycerides • Positive cardiometabolic profile • Known result of FASN inhibition

FASCINATE - 2: Safety Denifanstat was Generally Well Tolerated 20 Parameter Placebo n=56 Denifanstat N=112 Any TEAE (treatment emergent adverse event) 45 (80.4%) 96 (85.7%) TEAE related to study drug 20 (35.7%) 51 (45.5%) Most common TEAE related to study drug in ≥ 5% of patients by system organ class eye disorders 9 (16.1%) 17 (15.2%) gastrointestinal disorders 5 (8.9%) 13 (11.6%) skin and subcutaneous tissue disorders 4 (7.1%) 25 (22.3%) TEAE leading to study drug discontinuation 3 (5.4%) 22 (19.6%) TEAE with CTCAE Grade 3 (Severe) or higher* 3 (5.4%) 13 (11.6%) SAE (none related to treatment) 3 (5.4%) 13 (11.6%) Fatal TEAE 0 0 * No treatment - related AE was Grade 3 or higher

MASH Development Program 18

Progression from Phase 2b to Phase 3 Phase 2b – baseline Fibrosis stage Phase 2b – 26 weeks Non - invasive interim Phase 2b – 52 weeks Histology • Using Phase 2b results including AI pathology scores to design and power Phase 3 • Held end of Phase 2 Meeting with FDA in May 2024; in discussion with FDA regarding development plans and study protocol Primary endpoint s • NAS ≥2 improvement w/o worsening of fibrosis; or NASH resolution + NAS ≥2 improvement w/o worsening of fibrosis Secondary endpoints • Fibrosis ≥1 stage improvement w/o worsening of NASH • Digital AI pathology Interim cohort F2 – 46.2% F3 – 53.8% Interim results released Nov 2022 Topline data released Jan 2024 Enrollment completed Sep 2022 Phase 3 Fibrosis endpoint - human 22 ^ddK^/^ /E&>DDd/KE >/WKdKy//dz &/ZK^/^ DdK>/ ,>d, >ŝǀĞƌ&Ăƚ ; DZ/ Ͳ W&& Ϳ WZK Ͳ ϯ >& < Ͳ ϭϴ ĞƌĂŵŝĚĞƐ >d >> &'& Ϯϭ E/&E^dd MASH Phase 3 study planned to start 2H 2024

We Believe Denifanstat is Differentiated in the Evolving M ASH Landscape Mechanism FASN inhibitors THRß A gonists FGF - 21 GLP - 1 agonists PPAR agonists ACC inhibitors FXR agonists Category DNL pathway Nuclear receptor Growth factor GLP - 1 Nuclear receptor DNL pathway Nuclear receptor Route Oral Oral Oral Oral Oral Status Phase 2 complete Phase 3 to start 2H 2024 Approved March 2024 Phase 2 complete Phase 2 complete Phase 3 ongoing Phase 2 complete Phase 3 complete Challenges • Perceived market pressure from incretin class of weight loss drugs • Diarrhea • Potential hormonal axis changes • Bone loss • Injectable • Nausea and diarrhea • Potential neutralizing antibodies • Higher COGS • GI side effects including nausea • Lack of fibrosis improvement to date • Muscle wasting • Weight gain, edema, GI side effects, anemia • Possible liver injury • Combinations only • MOA causes triglyceride increases • Lack of fibrosis improvement as monotherapy • Mixed results from several programs • MOA causes pruritus and LDL - cholesterol increases 23

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%. Blood test for predictive marker denifanstat denifanstat • MASH is a multi - faceted disease and patients may benefit from being matched with optimal treatments • Two approaches using blood tests are undergoing further evaluation • Drug response: 1 - 2 months after taking drug, tripalmitin identifies patients responding to drug treatment • Predictive marker: before taking drug, signature of 6 blood metabolites enriches for responders 1 Blood test for drug response (e.g. tripalmitin) Clinical response rate denifanstat Clinical response rate On - treatment 1 - 2 months Pre - treatment 21

Strong Monotherapy Opportunity for Denifanstat in M ASH Expansion as backbone of combinations Illustrative potential combo mechanisms FXR GLP - 1, PPAR, FGF21 DGAT2 →→ThR HSP47, integrins NLRP3 Chemokines, ARO - HSD x Oral, once - daily tablet ideal for chronic administration • Tablets generally more affordable than complex biologics x Potential to treat broad patient population • Including those with thyroid challenges x Novel mechanism that acts directly upon liver x Encouraging safety profile to date Denifanstat data support success as first line monotherapy • Denifanstat’s potential x Complementary to other mechanisms x Potential for fixed dose combinations with other oral medications x Preclinical combination studies ongoing • MASH agents: anti - fibrotic, other metabolic agents • Co - morbidities: diabetes and other cardiovascular agents Broaden market opportunity through combinations with denifanstat as backbone 22

Additional Expansion Opportunities in M ASH • Compensated cirrhotic patients ( MASH F4) • Denifanstat directly targets stellate cells • Hepatocytes continue to be functional, and patients frequently have increased liver fat • Next steps • Characterize PK profile in patients with impaired hepatic function – Phase 1 results in 1Q 24 • Positive impact on fibrosis in FASCINATE - 2 • Phase 2b/3 trial in M ASH - F4 • Pediatric M ASH • 23% of children with NAFLD have M ASH at the time of diagnosis • Next steps • Compile safety data across all denifanstat studies in young adults including FASCINATE - 2 • Nonclinical toxicology study in juvenile animals – plan to initiate in 2024 • Phase 2 trial in pediatric M ASH 1 Estes, et al. 2018; http://dx.doi.org/10.1016/j.jhep.2018.05.036 F 4 compensated and decompensated 23 Cirrhosis 1

Other Indications 24

FASN Hyper - Activity Plays a Key Role in Multiple Diseases Beyond M ASH Cancer cell Membrane synthesis, intracellular signaling, protein modification FASN in cancer 1. Supports tumor survival 2. Enables tumor proliferation 3. Establishes resistance to drugs FASN in M ASH 1. Drives steatosis 2. Activates pro - inflammatory cells 3. Activates stellate cells leading to fibrosis Sebocyte Sebum production FASN in acne 1. Sebum production 2. Sebum composition 25

DNL Pathway Plays a Role in the Pathogenesis of Acne FASN is an attractive therapeutic target for acne • Acne is associated with excess sebum production by sebocyte cells in the skin • Acne resolution is associated with reduced sebum production • Sebocytes upregulate and rely on DNL/FASN to make sebum • >80% of key sebum lipids such as palmitate and sapienic acid produced by DNL/FASN Phase 2 – acne by Ascletis in China Phase 1 – sebum analysis by Sagimet • Denifanstat inhibited lipogenesis in skin • Dose - dependent • Proof of mechanism 26 EFFICACY RESULTS – 12 WEEKS Placebo n=45 25 mg n=45 50 mg n=44 75 mg n=45 Total lesions - 34.9% - 49.5% ** - 51.5% ** - 48.4% ** Inflammatory lesions - 36.5% - 54.7% ** - 56.7% ** - 49.4% * Non - inflammatory lesions - 35.0% - 44.4% - 46.6% - 46.5 IGA (2 - grade improvement) 15.6% 31.1% 31.8% 22.2% * p <0.05 ** p <0.01 Well tolerated across dose groups

FASN is Integral to Tumor Cell Proliferation and Survival Reprogramed metabolism is one of the hallmarks of cancer • Certain cancers are dependent on DNL/FASN for proliferation especially downstream of driver oncogenes • eg. KRASM in non - small cell lung cancer (NSCLC) • Strategy – > exploit this vulnerability using FASN inhibition in the combination setting to cause death Dietary fatty acids cannot compensate for de novo synthesized palmitate Specific oncogenic drivers are FASN - dependent Prevents lipid peroxidation and stress induced death Palmitate RTK e.g. MET, VEGFR Saturated fatty acids for lipid rafts and membranes Protein modification and localization/ function Receptor localization and signaling Acetyl - CoA Malonyl - CoA pS6 mTOR AKT PI3K KRAS - 4A B - tubulin WNT Lipid rafts FASN Completed Phase 1 provides foundation • 136 patients received denifanstat • Heavily pretreated Phase 1 population • Recommended Phase 2 dose defined • Promising clinical activity consistent with proposed mechanism • KRASM NSCLC patients had significantly longer duration on study with denifanstat than KRASWT (p<0.02), and 91% KRASM had stable disease FASN - dependence 27

FASN - Dependent Tumor Types Identified that Meet Core Criteria Program focused on 4 selected tumor types Preclinical ongoing • Combination with KRAS inhibitor in mouse models x Encouraging Phase 1 results with denifanstat Translational ongoing • Patient selection bioinformatics x Positive preclinical results Phase 1 pending start • Investigator Sponsored Trial at Weill Cornell, in combination with enzalutamide x Positive preclinical results Phase 3 ongoing • By Ascletis in China, in combination with bevacizumab x Positive Phase 2 investigator sponsored trial results NSCLC KRASM HCC FASN - dependent Prostate FASN - dependent GBM If positive, favor clinical collaboration with a KRASM industry partner If patient selection is tractable, Sagimet would sponsor a clinical study Phase 1 results will inform clinical decision by Sagimet Phase 3 results will inform clinical decision by Sagimet x FASN - dependent mechanism x Preclinical or clinical POC shown x Unmet clinical need x Tractable clinical path including patient selection Core criteria Tumor type Status Next milestone GBM (glioblastoma), HCC (hepatocellular carcinoma), KRASM (mutant KRAS), NSCLC (non small cell lung cancer) 28

Strong Financial Position and Intellectual Property Portfolio Financial highlights Nasdaq: SGMT x Upsized IPO completed in July 2023 raised $86.2 million of net proceeds x Follow - on financing completed in January 2024 raised net proceeds of $ 104.7 million. x Cash , cash equivalents and marketable securities were $193.7 million as of March 31, 2024, expected to fund current operations through 2025 Strong patent estate x Denifanstat method of use: 2036 x Denifanstat c omposition of matter: 2032 ( Issued in all key commercial territories) x Opportunities exist to lengthen patent exclusivity of either composition patent or method of use patent for up to 5 years via Patent Term Extension (US) or SPC (Europe) x Currently building out global patent portfolio to further protect commercialization of denifanstat via patent applications directed to formulations, methods of use, and synthetic methods, with potential to extend exclusivity further 32 0 1

Therapeutic Area Stage of Development Indication Expected Milestone / Status Preclinical Phase 1 Phase 2 Phase 3 Metabolic disease • Phase 2b successfully completed; MASH Phase 3 study planned to start 2H 2024 MASH - F2/F3 • Phase 1 hepatic impairment results 1Q 2024 Dermatology Acne • IND - enabling studies completed; evaluating timing to file IND • Phase 3 clinical study initiated 4 Q 2023 * Oncology Solid tumors • Patient selection and trial design in FASN - dependent tumor types ongoing Recurrent glioblastoma ( GBM ) • Phase 3 enrollment of 120 patients achieved in 3Q 2023; interim analysis planned * Development Pipeline : Indications and Clinical Milestones 33 * Trials conducted in China by Ascletis, who has licensed development and commercialization rights to all indications in Greater China TVB - 2640 TVB - 2640 TVB - 2640 (ASC40) TVB - 2640 (ASC40) TVB - 3567

Cover	May 23, 2024
Cover [Abstract]
Document Type	8-K
Amendment Flag	false
Document Period End Date	May 23, 2024
Entity File Number	001-41742
Entity Registrant Name	SAGIMET BIOSCIENCES INC.
Entity Central Index Key	0001400118
Entity Tax Identification Number	20-5991472
Entity Incorporation, State or Country Code	DE
Entity Address, Address Line One	155 Bovet Road
Entity Address, Address Line Two	Suite 303
Entity Address, City or Town	San Mateo
Entity Address, State or Province	CA
Entity Address, Postal Zip Code	94402
City Area Code	650
Local Phone Number	561-8600
Written Communications	false
Soliciting Material	false
Pre-commencement Tender Offer	false
Pre-commencement Issuer Tender Offer	false
Title of 12(b) Security	Series A Common Stock, $0.0001 par value per share
Trading Symbol	SGMT
Security Exchange Name	NASDAQ
Entity Emerging Growth Company	true
Elected Not To Use the Extended Transition Period	false