An2 Therapeutics, Inc. · NASDAQ:ANTX
An2 Therapeutics — Investor Presentation (September 2026)
50 slides from An2 Therapeutics's investor presentation, September 2026
Slide 1: Investor Overview September 2026
INVESTOR OVERVIEW SEPTEMBER 2026
Slide 2: Forward-Looking Statements
Forward-Looking Statements This presentation contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. In some cases, you can identify forward-looking statements by terms such as “may,” “will,” “should,” “would,” “expect,” “plan,” “anticipate,” “
Slide 3: Unlocking Boron's Promise for Patients
Unlocking Boron’s Promise for Patients Boron-driven B Clinical-stage Focused on Near-term oncology pipeline acute needs catalysts innovation Polycythemia vera Polycythemia vera Oncology 3 proof-of-concept novel oral Polycythemia Startup activities vera PI3Kα and ENPP1 AN2 BORON studies initiating in
Slide 4: Pipeline
Pipeline Product Name Target/Mechanism Research Preclinical Phase 1 Phase 2 Pivotal Epetraborole (EBO) Polycythemia vera Globin synthesis M. abscessus lung disease LeuRS IIT Melioidosis LeuRS AN2-502998 Chagas disease CPSF3 Research Programs Oncology PI3Kα Oncology ENPP1 Bone disorders ENPP1 Tubercu
Slide 5: Advancing toward value-creating milestones over next two years
Advancing toward value-creating milestones over next two years Leveraging proprietary boron chemistry platform to advance pipeline of potentially high-impact programs 2026 2027 2028 Addressable market Polycythemia vera Phase 2 Phase 2 Data 155K Global expansion Initiate U.S. PHASE 2 M. abscessus Pha
Slide 6: Polycythemia Vera
POLYCYTHEMIA VERA Oral epetraborole 6
Slide 7: Oral epetraborole potentially modulates red cell production via a novel MOA
Oral epetraborole potentially modulates red cell production via a novel MOA Investigational Program Summary Candidate Status Form Market Differentiation Enabling data Oral, red-cell Clinical and Epetraborole Phase 2 Oral 155,000 (U.S.) targeting preclinical data Potential once-daily oral administrat
Slide 8: A red-cell-driven disorder with unmet medical needs
A red-cell-driven disorder with unmet medical needs Goals of Treatment Control hematocrit w/o U.S. Prevalence Alleviate symptoms Reduce thrombotic risks phlebotomy dependence without Cytopenias Thrombocytosis Anemia PV biology Treatments ▪ Overproduction of red cells caused by ▪ Phlebotomy and low-d
Slide 9: Early and sustained hematocrit reductions in Phase 2/3 NTM study (n=177)
Early and sustained hematocrit reductions in Phase 2/3 NTM study (n=177) Hematocrit reductions observed throughout epetraborole treatment Phase 2/3 NTM trial Hematocrit (%) Sustained, stable HCT reduction EBO 500mg QD oral (n=105) ▪ HCT reductions were reversible Placebo (n=72) upon treatment discon
Slide 10: Trial replicated data in long-term NHP studies and healthy volunteers
Trial replicated data in long-term NHP studies and healthy volunteers Durable, reversible HCT reduction across epetraborole preclinical and clinical studies Phase 1 Nonhuman primates 4.00 4.0 EBO 250 EBO 500 EBO 750 Control 50mg/kg 150mg/kg 450mg/kg 2.00 2.0 HCT % point change HCT% point change 0.00
Slide 11: Potential for selective red-cell effect and preserved WBCs and platelets
Potential for selective red-cell effect and preserved WBCs and platelets WBCs Data consistent with erythroid-lineage selectivity rather than generalized cytoreduction In prior trials, platelet and WBC counts remained stable and within normal ranges, with no evidence of broad myelosuppression WBCs (1
Slide 12: Potential low-burden oral with targeted control of hematocrit levels
Potential low-burden oral with targeted control of hematocrit levels A well tolerated, red-cell selective option could offer additional flexibility to individualize hematocrit control 57% on hydroxyurea lack control after 3 months Epetraborole target profile Potential clinical applications Uncontrol
Slide 13: Global Phase 2 design and early anticipated data readout
Global Phase 2 design and early anticipated data readout Study design consistent with prior PV programs, allows for early assessment of key efficacy measures MAJOR OUTCOME MEASURES 1. Percent of patients maintaining “clinical PART 1 PART 2 success” defined as Open-label Open-label Open-label Double-
Slide 14: Anticipated PV timeline
Anticipated PV timeline Subject to regulatory review and enrollment rates 3Q & 4Q26 2027 U.S. IND Clinical data updates & FPI periodically throughout 2027 14
Slide 15: Mycobacterium Abscessus Complex Lung Disease
MYCOBACTERIUM ABSCESSUS COMPLEX LUNG DISEASE Oral epetraborole
Slide 16: M. abscessus: chronic lung disease with no approved drugs
M. abscessus: chronic lung disease with no approved drugs Investigational Program Summary Candidate Status Form Market Current Therapies Target Profile 84-patient Phase 2 IIT 50,000 (U.S., Epetraborole initiated Oral Europe, Japan) Off-label only, IV, significant toxicities Once-daily oral Progressi
Slide 17: Building on MAC experience with strong enabling data for M. abscessus
Building on MAC experience with strong enabling data for M. abscessus Differentiated Target Product Profile Well-Controlled, Decision-Enabling Study Design ▪ Potential once-daily oral therapy would reduce ▪ 84-patient randomized, controlled IIT in MAB treatment burden in an IV-heavy treatment landsc
Slide 18: Prior MAC trial informs development strategy in MAB
Prior MAC trial informs development strategy in MAB Order of magnitude lower in vitro MICs in MAB support potential for PK/PD target attainment MAB MIC BY NUMBER MAB MIC50/90: Insights from prior MAC trial 4 OF ISOLATES ▪ MIC in MAB orders of magnitude below MICs 90 85 observed in EBO-301 TR-MAC pop
Slide 19: Oral EBO matched gold-standard imipenem in preclinical mouse model
Oral EBO matched gold-standard imipenem in preclinical mouse model Off-label IV imipenem is current backbone therapy for Comparable activity to imipenem suggests LeuRS is a MAB highly attractive target in MAB ATCC 19977 M9530 M9501 CFU per ml (lung) CFU per ml (lung) CFU per ml (lung) 6 8 8 5 6 6 4
Slide 20: Oral epetraborole demonstrated bactericidal activity in mouse model
Oral epetraborole demonstrated bactericidal activity in mouse model The bacteriostatic profile of oral omadacycline in the EBO shows bactericidal activity in an in vivo mouse same in vivo model translated into positive Phase 2 model of MAB lung disease compared to omadacycline data in treatment-naïv
Slide 21: Phase 2 IIT study underway
Phase 2 IIT study underway STUDY OBJECTIVES EBO Regimen 1 (2:1) EBO 500mg PO QD n=28 ▪ Proof of concept in MAB lung disease ▪ Identify optimal dose and enable Placebo QD n=14 potential Phase 3 registrational trial vs. ENDPOINTS EBO Regimen 2 EBO 750mg PO QD n=28 ▪ Sputum culture conversion (2:1) ▪ S
Slide 22: Anticipated MAB timeline
Anticipated MAB timeline Subject to enrollment rates January 2026 March 2026 Late 2027 IIT IND Trial initiated Topline data 22
Slide 23: Chagas Disease
CHAGAS DISEASE (American trypanosomiasis) Oral AN2-502998
Slide 24: In Chagas disease, a silent parasite infects the heart, other critical organs
In Chagas disease, a silent parasite infects the heart, other critical organs Investigational Program Summary Candidate Status Form Market Current Therapies Target Profile Phase 2 initiation 300,000 (U.S.) AN2-502998 anticipated 2026 Oral 7-10M (Global) No FDA-approved drugs for adults Curative, ora
Slide 25: Expanding recognition of Chagas disease in the U.S.
Expanding recognition of Chagas disease in the U.S. IN THE NEWS United States Chagas Disease, or deadly ”kissing bug” ~300,000 disease, has spread in the U.S. Here’s what to know CBS NEWS | SEPTEMBER 9, 2025 No FDA-approved treatment Deadly ‘Kissing Bug’ Disease Chagas Has For adults with chronic Sp
Slide 26: Large U.S. patient population without an approved treatment
Large U.S. patient population without an approved treatment Standard of Care in U.S. Benznidazole or Nifurtimox Pediatric only in USA/FDA; most cases are in Significant tolerability and safety issues in adults adults: ~80% TEAE rate, ~15% discontinuation Long treatment duration (40-120 days) Potenti
Slide 27: A novel antiparasitic targeting CPSF3
A novel antiparasitic targeting CPSF3 Oral AN2-502998 AN2-502998's presumed mechanism of action: inhibition of CPSF3 in the T. cruzi parasite. CPSF3 target is essential in T. cruzi parasite mRNA processing. Inhibition of T. cruzi CPSF3 leads to parasite death.1 ▪ CPSF3 is a validated target for tryp
Slide 28: Phase 1 FIH and NHP efficacy with 28-day treatment support advancement to Phase 2
Phase 1 FIH and NHP efficacy with 28-day treatment support advancement to Phase 2 ✓ NHP EFFICACY STUDY PHASE 1 FIH STUDY* 100% AN2-502998 generally well tolerated at exposure levels consistent with NHP efficacy thresholds PARASITE ELIMINATION with 28-days of AN2-502998 treatment SAD: 6 dose levels M
Slide 29: Efficacy evaluation in NHPs with naturally-acquired T. cruzi infection
Efficacy evaluation in NHPs with naturally-acquired T. cruzi infection potential translation to human efficacy Only compound to have demonstrated curative activity in NHPs with long-term, NHPs in Native naturally acquired infection of diverse T. cruzi genetic types Transmission ▪ Higher translationa
Slide 30: Favorable infrastructure potentially enables fast, targeted patient access in the U.S. if approved
Favorable infrastructure potentially enables fast, targeted patient access in the U.S. if approved ________________ 1 ________________ ________________ 2 ________________ ________________ 3 ________________ Defined and scalable patient Favorable coverage and access Long-term exclusivity & population
Slide 31: A market poised for transformation – comparable to Hep C Story
A market poised for transformation – comparable to Hep C Story Chagas disease exhibits similar structural attributes that historically unlocked Hepatitis C market with Harvoni and Sovaldi: silent, slowly proliferating, irreversible critical-organ damage, high mortality HEPATITIS C CHAGAS Early sympt
Slide 32: Anticipated timeline for Chagas
Anticipated timeline for Chagas Subject to regulatory review and enrollment duration 2Q 2026 2026 2H 2027 Phase 1 & Phase 2 Phase 2 topline data NHP data initiate 32
Slide 33: Oncology Programs
ONCOLOGY PROGRAMS Research 33
Slide 34: Two high-potential lead targets enabled by boron chemistry
Two high-potential lead targets enabled by boron chemistry PI3Kα (CANDIDATE EXPECTED 2026) ENPP1 (CANDIDATE DECLARED FOR SOLID TUMORS) Targeting third-generation design with true pan-mutant Alleviate immune suppression to enhance efficacy of coverage, high selectivity over wild type checkpoint inhib
Slide 35: Oncology: PI3Kα
ONCOLOGY PI3Ka AN2Therapeutics
Slide 36: Opportunity for 3rd gen pan-mutant PI3Kα with WT-sparing selectivity
Opportunity for 3rd gen pan-mutant PI3Kα with WT-sparing selectivity TISSUES AFFECTED BY PI3Kα is part of a key signaling pathway that controls how cells PI3Kα MUTATIONS manage metabolism and survival Mutations in the PIK3CA gene can lead to uncontrolled cell growth and cancer metastasis PI3Kα is th
Slide 37: PI3Kα mutations are a large market opportunity; selectivity over WT proven to reduce SAEs
PI3Kα mutations are a large market opportunity; selectivity over WT proven to reduce SAEs and lead to longer mPFS Targetable PI3Kα driver mutations take two major forms: kinase and helical Kinase Helical Highly prevalent in cancer patients Helical 17% 25% of all cancers of endometrial cancer Kinase
Slide 38: Helical selectivity, ~50% of mutations, will define next-gen compounds
Helical selectivity, ~50% of mutations, will define next-gen compounds 1st generation 2nd generation 3rd generation Alpelisib/Inavolisib RLY2608, STX-478 AN2 ON MARKET CLINICAL STAGE OPPORTUNITY True pan-mutant coverage Kinase dominant; High selectivity across PAN-MUTANT/WILD- diminished helical kin
Slide 39: AN2 boron-based mutant-selective inhibitors designed to bind covalently to an allosteric site of PI3Kα
AN2 boron-based mutant-selective inhibitors designed to bind covalently to an allosteric site of PI3Kα p110α ATP-site (non-WT sparing) GENENTECH + NOVARTIS Covalent Allosteric Inhibitor Best multi-mutant inhibitor AN2 THERAPEUTICS H1047X E545X/E542X Kinase Allosteric Site 1 ABD ONKURE Kinase Alloste
Slide 40: In vivo efficacy superior to alpelisib without glucose disregulation
In vivo efficacy superior to alpelisib without glucose disregulation TV 600 Tumor Volume (mm3) ▪ Superior mouse efficacy in xenograft model 400 against H1047R vs. apelisib ▪ 27X selective for H1047R mutant over WT 200 ▪ No effects on glucose regulation 0 3 6 9 12 15 18 21 Days for treatment G1: Vehi
Slide 41: AN2 boron heterocycles – opportunity for best-in-class molecules
AN2 boron heterocycles – opportunity for best-in-class molecules AN2-495877 KINASE AND HELICAL SELECTIVITY ▪ Novel covalent binding to PI3Kα allosteric site with 1000 916 potentially differentiated on/off rate and kinetics 43X 13X 6.5X ▪ Pan-mutant potency targeting 5-100 fold selectivity over WT 80
Slide 42: Oncology: ENPP1
ONCOLOGY ENPP1 AN2Therapeutics
Slide 43: ENPP1 is highly expressed across various solid tumor types
ENPP1 is highly expressed across various solid tumor types High incidence of ENPP1 overexpression in colon, lung, pancreas and breast 6% 5% Colon Lung 5% 4% Pancreas Breast cBioportal; TCGA dataset 43
Slide 44: Tumors evade the immune system via increased ENPP1 expression
Tumors evade the immune system via increased ENPP1 expression High ENPP1 immune inhibition ENPP1 inhibition immune activation 1. ENPP1 sits on the outer membrane of the cancer cell lying in 1. Damaged cancer cells alert the immune system via cGAMP wait for the cGAMP messenger dinucleotide chemical m
Slide 45: ENPP1 inhibitors ≠ STING agonists: different enzymes, different biology
ENPP1 inhibitors ≠ STING agonists: different enzymes, different biology STING agonists ENPP1 inhibitors MECHANISM Directly force STING into its active conformation, Block ENPP1, preserving endogenous cGAMP and enabling producing a rapid, global inflammatory burst natural, sustained STING activation
Slide 46: High ENPP1 expression leads to worse outcomes
High ENPP1 expression leads to worse outcomes PUBLICATION ▪ Phase 1a dose escalation completed PNAS IMMUNOLOGY AND INFLAMMATION ▪ All dose levels safe and well tolerated ENPP1 is an innate immune • >17 months on therapy at 800mg BID checkpoint of the anticancer (ongoing) cGAMP-STING pathway in • No
Slide 47: Clinical candidate AN2-503321: potential for single-agent efficacy vs PD-1 and CTLA4 inhibitors
Clinical candidate AN2-503321: Potential for single-agent efficacy compared to PD-1 and CTLA4 checkpoint inhibitors in EMT6 (breast cancer) model AN2-503321 was well-tolerated and showed TGI at two highest doses tested, comparable to the inhibition observed with Anti-PD-1 antibody alone Tumor volume
Slide 48: AN2-503321 and Stingray SR-8541A in CT26 (colorectal cancer) model
AN2-503321 and Stingray SR-8541A in CT26 (colorectal cancer) model AN2-503321 EFFICACY DATA SR-8541A EFFICACY DATA – EXTRAPOLATED1 1500 cGAMP IC50 = 3.59 nM^ 3000 cGAMP IC50 = 1.16 nM 2 73% TGI 2 Tumor Volume (mm3) 74% TGI Tumor Volume (mm3) 1000 2000 Vehicle 2500 500 Vehicle 1000 2500 AN2-503321-MC
Slide 49: AN2-503321: promising results in colorectal model
AN2-503321: promising results in colorectal model Tumor Response to Anti-CTLA4 vs. Mean tumor volumes AN2-503321 with Anti-CTLA4 3000 Vehicle Dosing stopped Tumor Volume (mm3) Tumor Rechallenge AN2-503321 30mg/kg, BID 3000 2000 Anti-CTLA4, 10 mg/kg, BIW Anti-CTLA4, 10 mg/kg, BIW 1000 AN2-503321 30mg
Slide 50: Unlocking Boron's Promise for Patients
Unlocking Boron’s Promise for Patients Menlo Park, CA | IR@an2therapeutics.com
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