Exhibit 99.1 Investor Overview June 2025 A N 2 T H E R A P E U T I C S . C O M

Forward-Looking Statements This presentation contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Forward-looking statements expressed or implied in this presentation include, but are not limited to, statements regarding: anticipated milestones, catalysts, value-creation opportunities, and inflection points, and potential of the Company’s boron chemistry platform and pipeline programs; cash runway, and cash burn reduction and ability to achieve catalysts/inflection points within cash runway; patentability and patent and exclusivity periods; design, initiation, and timing of the Company’s clinical trials and results, market size and revenue opportunity and medical needs; the Company’s intellectual property; and other statements that are not historical fact. These statements are based on AN2’s current estimates, development pathways for AN2’s product candidates; expectations, plans, objectives, and intentions, are not guarantees of future performance and inherently involve significant risks and uncertainties. Actual results and the timing of events could differ materially from those anticipated in such forward-looking statements as a result of these risks and uncertainties, which include, but are not limited to, risks and uncertainties related to: AN2’s ability to implement its plans for its internal boron chemistry platform and pipeline programs; timely enrollment of patients in AN2’s clinical trials; AN2’s ability to procure sufficient supply of its product candidates for its clinical trials; the potential for results from clinical trials to differ from preclinical, early clinical, preliminary or expected results; significant adverse events, toxicities or other undesirable side effects associated with AN2’s product candidates; the significant uncertainty associated with AN2’s product candidates ever receiving any regulatory approvals; continued funding by the National Institute of Allergy and Infectious Disease (NIAID) of AN2’s development program for melioidosis; AN2’s ability to obtain, maintain or protect intellectual property rights related to its current and future product candidates; implementation of AN2’s strategic plans for its business and product candidates; the sufficiency of AN2’s capital resources and need for additional capital to achieve its goals; global macroeconomic conditions and global conflicts and other risks, including those described under the heading “Risk Factors” in AN2’s Annual Reports on Form 10-K and Quarterly Reports on Form 10-Q, and AN2’s other reports filed with the U.S. Securities and Exchange Commission (SEC). These filings, when made, are available on the investor relations section of AN2’s website at www.an2therapeutics.com and on the SEC’s website at www.sec.gov. Forward-looking statements contained in this presentation are made as of this date, and AN2 undertakes no duty to update such information except as required under applicable law. 2

Advancing Novel Product Candidates With Our Boron Chemistry Platform Clinical-Stage Boron Chemistry National Defense & Platform Opportunities Global Health • Unique model that leverages non- • Founded by AN2 team originally from • Chagas: Phase 1 start up activities dilutive funding sources to advance Anacor underway; complete in 2H/2025 important global health and national • Established record of platform • Melioidosis: Phase 2 start anticipated defense programs, some with dual productivity at Anacor 2H/2025 opportunities - Novel targets • First oncology candidate expected to • Funding/scientific partners include advance into development 2H/2025 NIAID, Gates Foundation, University - 15+ development candidates of Georgia, DNDi - 2 FDA approved drugs, 1 pending (EMA) • M. abscessus: Enabling data from EBO-301 informs path for potential - Anacor sold to Pfizer for $5.2B further development Disciplined Capital Management • $78.5M cash, cash equivalents and investments (unaudited) as of 3/31/25 • Runway into 2028 3

Product Portfolio Provides Multiple Paths to Significant Value Creation Program Potential Worldwide Opportunity Chagas disease $1B+/yr Phase 1 start up activities underway with product candidate in development for chronic, life-threatening illness; ~300K PRV patients in U.S.; ~6-7M globally Melioidosis PRV potential, endemic country sales High priority biothreat and government High mortality with no approved treatments stockpiling Emerging oncology programs ENPP1 (immuno-oncology) >$1B/yr/program PI3Kα (targeted therapy) 4

Validated Boron-Based Drug Discovery is Uniquely Suited to Deliver Novel Drug Candidates that Have Potential to be First in Class, if Approved I N F L A M M A T O R Y O N C O L O G Y R E S P O N S E Undruggable Targets: first-in-class • LeuRS: epetraborole,GSK656 • CPSF3: AN2-502998, acoziborole Significant potential through differentiated binding modes, excellent drug-like design properties and oral PK (e.g. oncology targets: ENPP1, PI3Kα) Demonstrated track record of two boron-based FDA-approved drugs (Anacor) and one pending P A R A S I T E S B A C T E R I A L D I S E A S E S 5

Broad Pipeline of Novel Clinical & Preclinical Programs Discovered Internally from our Boron Chemistry Platform Pathogen Target RESEARCH PRECLINICAL PHASE 1 PHASE 2 Status & Anticipated Inflections AN2-502998 Initiated Ph1 start up activities; complete Chagas disease Ph1 2H/2025; initiate Ph2 2026; target T. cruzi CPSF3 (chronic) data 2027 Epetraborole Observational trial data 2Q/2025; Ph2 study planned 2H/2025; target topline Ph2 Melioidosis – acute IV B. pseudomallei LeuRS data YE 2026; initiate Ph3 2027; NIH funded Ph2 POC (non-dilutive) planning 2H/2025 NTM - oral LeuRS M. abscessus Boron Platform PI3Kα Solid Tumors (oncology) First oncology candidates(s) on track to enter preclinical development in 2025; potential POC within cash runway Solid Tumors (oncology ENPP1 Solid Tumors (oncology) Multiple targets Lead op stage, development candidate Tuberculosis & malaria LeuRS anticipated 2026 *programs with light blue arrows leverage nondilutive funding 6

AN2-502998 for Chagas Disease 7

Chagas Disease: Hidden Threat to the Heart Parasitic disease caused by Trypanosoma cruzi (T. cruzi) Usually spreads through contact with triatomine bugs (“kissing bugs”). Other transmission routes include: congenital, blood-borne, organ-derived, oral T. cruzi parasite lives in heart, GI, and other muscle tissue for decades Significant morbidity and mortality if untreated Can cause arrhythmia, cardiac arrest, cardiomyopathy, heart failure, emboli, megaesophagus, megacolon, and other conditions CDC - Chagas Disease - Detailed FAQs; Cleveland Clinic: Causes, Symptoms, Treatments 1. Bern C, et al. Chagas Disease in the United States: a Public Health Approach. Clin Microbiol Rev. 2019 Nov 27;33(1):e00023-19. doi: 10.1128/CMR.00023-19. 8 Image: Bern C. Chagas' Disease. N Engl J Med. 2015 Jul 30;373(5):456-66. doi: 10.1056/NEJMra1410150. 8

Global Threat Hiding in Plain Sight in the U.S. Estimated Prevalence ~300K U.S. 6-7M GLOBAL ~100K EU & UK ~4-5M countries in Latin America Global: WHO Chagas Fact Sheet (4 April 2024); dndi.org/diseases/chagas/facts USA: Irish A, et al. Updated Estimates and Mapping for Prevalence of Chagas Disease among Adults, United States. Emerg Infect Dis. 2022 Jul;28(7):1313-1320. doi: 10.3201/eid2807.212221; Manne-Goehler J, et al. Estimating the burden of chagas disease in the United States. PLoS Negl Trop Dis 2016; 10:e0005033 9 Europe & UK: Basile L, et al, Working Group on Chagas Disease Collective. Chagas disease in European countries: the challenge of a surveillance system. Euro Surveill. 2011;16(37):pii=19968. https://doi.org/10.2807/ese.16.37.19968-en

Expanding U.S. Prevalence Growing impact in the U.S.: ~300K infected T. cruzi & ‘kissing bug’ vector present in ~27 U.S. states CDC estimates that 5.5%–7.5% of confirmed infections in blood donors are related to locally acquired infection $1B+ estimated peak sales potential Confirmed’ and ‘Indeterminate’ Chagas Disease Among Blood Donors in the United States (2007-2019). Source: AABB Chagas Biovigilance Network. https://www.aabb.org/docs/default-source/default-document-library/resources/chagas-graph-builder.html Higuita N et al. Chagas disease in the United States: a call for increased investment and collaborative research. The Lancet Regional Health – Americas, Volume 34, 100768. June 2024. Manne-Goehler, J. et al. Access to care for Chagas disease in the United States: A health systems analysis. Am J Trop Med Hyg. 2015; 93:108-113 10 https://asm.org/articles/2021/april/chagas-disease-in-the-u-s-what-we-know-about-the-k

No Approved Treatments for Adults with Chagas Disease in U.S. Two products in the U.S. approved for pediatrics only: benznidazole and nifuritmox No FDA-approved therapies for adults Rarely used; most cases are found in adults where safety and with Chagas disease efficacy in Chagas has not been established AN-502998 Potential Product Profile Long treatment duration (40-120 days) • Potential cure • Oral treatment Significant tolerability and safety issues: ~80% TEAE rate, ~15% discontinuation, genotoxic • Favorable non-clinical safety to date 1. Aldasoro E, et al, 2018. What to expect and when: benznidazole toxicity in chronic Chagas’ disease treatment. J Antimicrob Chemother 73: 1060–1067 2. Lascano F, et al Review of pharmacological options for the treatment of Chagas disease. Br J Clin Pharmacol 2022;88:383–402. https://doi.org/10.1111/bcp.14700. 3. Molina I, et al, 2015. Toxic profile of benznidazole in patients with chronic Chagas disease: risk factors and comparison of the product from two different manufacturers. AAC. 59: 6125–6131 4. Viotti R, et al, 2014. Towards a paradigm shift in the treatment of chronic Chagas disease. Antimicrob Agents Chemother 58:635–639. doi: 10.1128/AAC.01662-13 5. Molina I, et al. Randomized Trial of Posaconazole and Benznidazole for Chronic Chagas’ Disease. N Engl J Med 2014;370:1899–908. https://doi.org/10.1056/nejmoa1313122. 6. Bosch-Nicolau P, et al. Efficacy of three benznidazole dosing strategies for adults living with chronic Chagas disease (MULTIBENZ): an international, randomized, double-blind, phase 2b trial. Lancet Infect Dis 2024. https://doi.org/10.1016/s1473-3099(23)00629-1. 7. FDA Labels: BENZNIDAZOLE tablets, for oral use (fda.gov) & LAMPIT (nifurtimox) tablets label (fda.gov) 11

AN2-502998: Phase 1 Candidate with Curative Potential for Chronic Chagas Disease - Oral, small molecule benzoxaborole • Novel target (CPSF3) is essential part of complex involved in 1 T. cruzi RNA processing • Chemical class with 2 FDA-approved drugs (crisaborole and tavaborole) • Target proof-of-concept through benzoxaborole acoziborole, human African trypanosomiasis drug candidate with ~95% 2 cure rate in Ph 2/3 study - In vitro potency against a spectrum of genetically diverse 1 strains of T. cruzi • Killed both actively dividing and dormant intracellular T. cruzi faster than benznidazole 1 - Cured T. cruzi infection in mouse models - Exclusivity potential into mid-2040s with pending, granted, and filed cases AN2-502998 is formerly known as AN15368. 1. Padilla, A.M., et al. Discovery of an orally active benzoxaborole prodrug effective in the treatment of Chagas disease in non-human primates. Nat Microbiol 7, 1536–1546 (2022) 12 2. Betu Kumeso VK, et al. Efficacy and safety of acoziborole in patients with human African trypanosomiasis caused by Trypanosoma brucei gambiense: a multicentre, open-label, single-arm, phase 2/3 trial. Lancet Infect Dis. 2023 Apr;23(4):463-470..

AN2-502998 Cured Chronic T. cruzi Infection in Nonhuman Primates AN2-502998: only compound, of which we are aware, to have demonstrated curative activity in nonhuman primates (NHPs) with 1 long-term, naturally acquired infection of diverse T. cruzi genetic types NHPs naturally acquire T. cruzi-infection and develop chronic disease comparable to chronic Chagas disease in humans T. cruzi-infected NHP study data mirrored human clinical trial results for 2,3,4 benznidazole and E1224 (Eisai) up to 1-yr post-treatment For benznidazole and E1224, mouse models did not predict the clinical trial failure, hence the importance of studying drug candidates in 5 naturally infected NHPs to de-risk translation to human efficacy Ongoing studies of AN2-502998 in naturally infected NHPs to enable Ph 2 dose selection # 1 AN2-502998 was dosed at 30 mg/kg x 60 days in rhesus macaques ; half followed for >4 years * Benznidazole (15 mg/kg BID x 60 days) and E1224 (20 mg/kg x 60 days) NHP study was in cynomolgus macaques ^ Parasites screened by blood PCR and hemoculture for 52 weeks 1 Padilla, A.M., et al. Discovery of an orally active benzoxaborole prodrug effective in the treatment of Chagas disease in non-human primates. Nat Microbiol 7, 1536–1546 (2022) 2. Torrico F, et al. E1224 Study Group. Treatment of adult chronic indeterminate Chagas disease with benznidazole and three E1224 dosing regimens: a proof-of-concept, randomised, placebo-controlled trial. Lancet Infect Dis. 2018 Apr;18(4):419-430. 3. Bosch-Nicolau, P et al. Efficacy of three benznidazole dosing strategies for adults living with chronic Chagas disease (MULTIBENZ): an international, randomised, double-blind, phase 2b trial. Lancet Infect Dis. 2024 Apr;24(4):386-394. 13 4. Molina I, et al. 2014. Randomized trial of posaconazole and benznidazole for chronic Chagas' disease. N Engl J Med 370:1899–1908. doi: 10.1056/NEJMoa13131224 5. Tarleton RL. Avoiding Clinical Trial Failures in Neglected Tropical Diseases: The Example of Chagas Disease. Clin Infect Dis 2022;76:1516–20. https://doi.org/10.1093/cid/ciac884.

Chagas Disease: Drug Development Landscape Novartis Eisai Merck Failed in clinic Phase 2 planned Failed in clinic Phase 1 FIH E1224 protease inhibitor (posaconazole) Start up activities (ravuconazole) underway 14

Chagas Disease: Potential for Ph 2 PoC Within Projected Runway Planned timeline Collaborating with DNDi Chagas Clinical Research Platform for Phase 2 2027 Initiated YE-2025 2026 Phase 1 Start Phase 2 Phase 1 FIH Phase 2 Up Activities Data Complete Initiate 2027 2025 2026 Developed under license agreement with University of Georgia Research Foundation. Agreement includes pre-NDA milestones of approximately $0.4M, sharing of proceeds from the potential sale of any PRV, and low single-digit royalties on commercialization 15

Epetraborole in Melioidosis 16

Melioidosis - Under-Reported, High Unmet Medical Need Disease High Mortality - New approaches needed to address Caused by the Gram-negative bacterium significant unmet clinical need Burkholderia pseudomallei • Mortality: 89,000/year • Third most common cause of death from an infectious disease in SE Asia after HIV/AIDS & TB • ~40% mortality 90-day all cause in AN2 observational trial recently conducted using IV standard of care treatment in • Incidence (estimated): 165,000 cases/year hospital settings • Potential emerging pathogen in U.S. B. pseudomallei endemic in US (Gulf Coast of MS, US Virgin Islands and Puerto Rico) Melioidosis endemic but underreported Melioidosis predicted to be endemic but never reported Not a surveillance priority 17 Limmathurotsakul D, et al ‘Predicted global distribution of Burkholderia pseudomallei and burden of melioidosis’ Nat Microbiol. 2016 January 1; 1(1)

Market Opportunity: Melioidosis 100% Funded to date Market potential by the U.S. Government (non-dilutive) • High priority biothreat • Priority review voucher target (second highest potential behind anthrax, plague, • Government(s) stockpiling smallpox) • Treatment sales (e.g., • Military force protection Thailand, India, China, • U.S. civilian population Brazil) • Government funded: $18M NATIONAL SECURITY High Priority Biothreat 18

Potential to Reduce Mortality in Patients vs. SOC Alone • Epetraborole showed cidal activity against multiple isolates (10) in an acute pulmonary murine infection model of B. pseudomallei MSHR435 melioidosis when subcutaneous (SC) dosing was delayed EBO 1 µg/mL; CAZ 8 µg/mL 12-hours after infection • MIC of 1 µg/mL against 242 recent clinical isolates from 90 NE Thailand • Epetraborole plus ceftazidime (CAZ) exhibited improved activity vs EBO or CAZ alone in a macrophage and murine infection models of infection (PLoS Negl. Trop Dis 17:e0011795) • EBO showed an additive effect to CAZ in macrophages and murine infection models (PLoS Negl. Trop Dis 17: e0011795) PLoS Negl Trop Dis 17: e0011795 19 Lung Log CFU 10

Goal: Significantly Reduce Mortality in Melioidosis Patients Planned timeline Anticipated primary endpoint will be to • 200 patients enrolled at 3 sites in 12 months 1 2 evaluate mortality (Thailand and Laos) • Confirmed high mortality (~27% 28-day; ~50% (epetraborole + ceftazidime/meropenem vs. placebo + ceftazidime/meropenem) 90-day all-cause) Oct. ‘24 2Q25 2H25 YE 2026 2027 Completed enrollment Observational trial data Initiate Phase 2* Initiate Phase 3* Topline data of observational trial 2024 2025 2026 2027 20 *Subject to regulatory allowance to proceed with trial and continued U.S. government funding and timelines

Oncology Programs 21

Boron’s Validated Binding Modes Enable Access to Undruggable Targets Diverse, covalent and non-covalent binding modes Empty p-orbital allows for unique • Tunable tetrahedral or trigonal geometry binding modes not • Covalently binds amino acids (e.g., S, T, Y, K) possible with • Binds ribose covalently carbon-based • H-bonding • Metal coordination chemistry Integrated into approved and clinical compounds: Validated chemical • 5 approved boron containing medicines space with • 15 boron compounds listed in active clinical dev. multiple FDA • Tunable PK – can be oral, IV, sub-q, and topical approved drugs • Differentiated structures facilitate strong IP 22

Oncology ENPP1 23

ENPP1 – Promising Immuno-Oncology Target • Blocking ENPP1 has two essential roles: – Turns “cold” tumors “hot”, triggering innate immune system response – Inhibition of tumor metastasis • Potential synergy with checkpoint inhibitors PD-1 (e.g., Keytruda), PD-L1, and CTLA4 • Broad use across solid tumors with high unmet need (e.g., breast, lung, colorectal) • Ideally suited for boron chemistry: Boron serves as a phosphate mimic and binds to the bi-metallic zinc ions in the catalytic site 24

ENPP1 - Immune System’s “On/Off” Switch No ENPP1 High ENPP1 Innate anti-tumor immunity combats cancer growth Immune response interrupted expression expression • Inhibiting ENPP1 on the cancer cells allows cGAMP to signal • AN2 boron heterocycles demonstrated excellent in vitro to the immune cells potentially causing immune activation and physical chemical properties enabling improved solubility, eliciting an antitumor response → “cold” to “hot” tumor permeability, and PK • Ideal target for boron-chemistry with covalent binding to metals • AN2's extensive expertise in boron-based drug discovery in ENPP1 active site enables efficient progress to clinical development candidates Li et al., Cancer Discovery 2020; Wang et al., PNAS 2023 25

ENPP1 - Emerging Oncology Target Wang et. Al., PNAS, 2023 ENPP1 expression in different cancer types Li et. al., Cancer Discovery, 2020 Colon 6.08% of 592 cases 397/10,953 (4%) of NSCLC queried patients* 5.33% of 994 cases Breast 3.88% of 1082 cases High expression of ENPP1 translates to poorer outcomes • ENPP1 is a relevant target in many cancer types, including breast, colon and lung High ENPP1 (n=59 patients) Low ENPP1 (n=1926 patients) • In preclinical breast and colon models, inhibiting ENPP1 enhanced the antitumor immune response 26

AN2 Boron Heterocycles – Opportunity for Best-In-Class Molecules AN2 Boron Heterocycles Liabilities of Other Binding Groups AN2 potential compounds Ideal TPP (preclinical observations) Sulfamide • hERG inhibition liability Sulfonamide • Poor physicochemical properties/PK Sulfoximine • pH dependent activity Sub nM potency • Poor permeability Phosphonic Highly selective • Poor pharmacokinetics Acid • SC/IV administration or prodrug Excellent drug-like properties Ortho- • Metabolic stability functionalized Oral PK • Orthoquinone toxicity considerations phenol • Poor physicochemical properties/PK methoxyphenyl Potent in vivo activity • Metabolic stability Phenylboronic • Poor permeability/low oral bioavail. acid • CMC development challenges Strong IP with broad FTO through boron chemistry designs 27

Oncology PI3Kα 28

PI3Kα – Developing Potential Next Generation Compound Potential 3rd generation First Generation Second Generation - 2 FDA-approved drugs; - Allosteric-site inhibitors❑ Allosteric-site inhibitors validates mechanism - Early clinical stage❑ Covalent boron binding - ATP-site inhibitors - Some selectivity ❑ Robust selectivity between - No selectivity between wild- between wild type and wild type and mutants with type and mutants mutants and potentially potentially lower lower hyperglycemia hyperglycemia risk than - Significant levels of GR3+ second generation hyperglycemia compounds ❑ Boron affords differentiated IP in competitive market 29

PI3Kα Signaling Pathway Has High Potential Phosphoinositide 3-kinases (PI3Ks) are lipid kinases that mediate signaling cascades involved in cell proliferation, survival, metabolism, and migration Class IA PI3 Kinases are a heterodimer of p110 catalytic subunit and p85 regulatory subunit Stimulation by RTKs, GPCRs, GTPases (RAS or RAF) recruit PI3K to the plasma membrane p85 binds to the phosphorylated tyrosines and loses its inhibitory effect on p110, which then phosphorylates PIP2 to produce PIP3 PIP3 then interacts with AKT, which is then phosphorylated by PDK1 and mTORC2 Garcia-Echeverria, C., Sellers, Oncogene 2008, Sun, P., Meng, Lh. Acta Pharmacol Sin 2020 30

st 1 Generation Inhibitors Provide Breakthrough Efficacy But Hyperglycemia Limits Use Major Opportunity for Best-in-Class Pan-Mutant WT-Sparing PI3Kα Tissues affected by PI3Ka mutations Targetable PI3Ka driver mutations are highly prevalent in cancer patients occur in 14% of all cancers (~35% in breast cancer) • PI3Kα is the second most frequently mutated gene in cancer • Mutant selective PI3Kα inhibitors can be used in patients with PI3Ka hotspot mutations, including breast, lung, ovary, and colon cancers • Mutant selective PI3Kα inhibitors could be more efficacious than current non-selective PI3Kα inhibitors and have the potential to be best-in-class Castel et al., Nature Cancer 2021 31

AN2 Boron-based Mutant-Selective Inhibitors Designed to Bind Covalently to an Allosteric Site of PI3Kα ATP-site inhibitors (non-WT sparing) Genentech and Novartis Kinase-domain inhibitors Kinase Allosteric Site 1 Synnovation Kinase Allosteric Site 2 Relay and Scorpion 32

Boron Chemistry Enables Selective Targeting PI3Kα Potential Third Generation PI3Kα AN2 potential Covalent Mutant-Specific Borophore compounds (preclinical observations) Targeted profile • Novel covalent binding to PI3Kα allosteric site nM potency • Pan-mutant potency with 10-100 fold selectivity Highly selective over WT over WT in vitro • Potentially differentiated on/off rate and kinetics Differentiated binding • Accumulation in tumors in vivo Oral PK • Tumor regression observed in vitro without hyperglycemia or hyperinsulinemia Potent in vivo activity • Strong IP from differentiated boron structures Strong IP with broad FTO through boron chemistry designs 33

NTM M. abscessus 34

Epetraborole Potential Path Forward in M. abscessus Lung Disease • Phase 3 study in treatment-refractory MAC lung disease enrolled patients with severe, advanced disease, and provides robust enabling clinical data to support potential development in M. abscessus • Supportive EBO preclinical M. abscessus data – >256-fold lower MIC90 vs Phase 3 MIC90 EBO-301 – Cidal activity in mouse models of infection: comparable to the gold standard IV drug, imipenem – Novel MOA and oral dosing • Large potential market opportunity ﹣50,000 patients in U.S., Japan, and Europe • Evaluating multiple cost-efficient paths forward including option to use non-dilutive funding to advance program 35

Epetraborole Exhibited Potent MICs for M. abscessus Mycobacterium abscessus sensitivity to epetraborole Large collection of contemporary, international M. abscessus isolates MIC range of 0.03 – 0.25 mg/L, MIC50 of 0.06 mg/L and MIC90 of 0.12 mg/L Activity was not affected by subspecies, resistance to amikacin or clarithromycin, or by colony morphology Epetraborole holds promise as a novel antimycobacterial against M. abscessus and warrants further investigation into its therapeutic potential in patients J. Antimicrob Chemother 2025; 80: 713–716 C. Daley et. al. 36

Enabling Data in M. abscessus Paves Way for Phase 2 Development SOC agent, Imipenem, is No FDA-approved treatments Off-label treatments have a parenteral only. EBO had cidal for NTM lung disease caused high rate of drug resistance or activity similar to imipenem in by M. abscessus tolerability limitations mouse efficacy model Antimicrobial Agents and Chemotherapy July 2024 M. abscessus burden in lungs of mice infected with isolates ATCC 19977 (A), M9501 (B), and M9530 (C). Time point -1 represented 24 h after infection with M. abscessus via the aerosol route. Time point 0 represents 1 week infection and the day of treatment initiation. Time points weeks 1,2, and 4 represent the end of 1, 2, and 4 weeks of treatment with once-daily 1x PBS (PBS), twice daily 100 mg/kg subcutaneous imipenem (IMI), once-daily k after 25 mg/kg oral EBO (EBO25), or once-daily 50 mg/kg oral EBO (EBO50). Mean Mab burden in the lungs and standard error are shown (per group per time point, n = 5 at weeks -1, 0, +1, and +2, 37 n=1- at week +4)

M. abscessus Lung Disease: Global Opportunity and Unmet Need 1 United States ~$1B Opportunity 2 Europe ~$350M Opportunity 3 Asia (ex China) ~$1B Opportunity 1. Assumes 2028 NTM prevalence of 115k (Strollo, The Burden of Pulmonary NTM in the U.S. , AnnalsATS Vol 12:10, 2015). Est. 10% due to M. abscessus species (Prevots, Epidemiology of Human Pulmonary Infection with NTM: A Review , Clin Chest Med, 2015). Est. 75% do not currently have optimal therapy (ATS/IDSA Guidelines on Dx, Tx, and prevention of NTM Diseases. Am J Respir Crit Care Med Vol 175. pp 367–416, 2007: no antibiotic regimens based on in vitro susceptibilities has been shown to produce long-term sputum conversion for patients with M. abscessus lung disease. The goal of 12 months of negative sputum cultures while on therapy may be reasonable, but there is no medication strategy to reliably achieve this goal ). $433 per Day of Oral Therapy and 75% compliance. 2. Schildkraut, et al annual prevalence range of 6.0-6.6/100,000 in EU5 with RGM accounting for 10-44% of cases. Estimated M. abscessus prevalence for all Europe at ~3,000/yr. Rest of Europe estimated at same NTM prevalence with ~10% M. abscessus. Same price/compliance estimates as U.S. 3. Korea: Simon et al establishing not only high incidence/prevalence rates, but 18-39% coming from M. abscessus. Prevalence >5,000 (~$600M market opportunity). High rates 38 of NTM in Japan, but low % from M. abscessus. However, high rates of M. abscessus projected in Thailand and other countries with significant coastlines. Projection that Rest of Asia accounts for 1/3 of total. Same price/compliance estimates as U.S.

Leadership 39

Team With Significant Experience in Bringing Medicines to Market SENIOR MANAGEMENT ADVISORS Eric Easom, MBA, MEng Sanjay Chanda, PhD Lucy Day Chris LeMasters Co-Founder, President & CEO Chief Development Officer Chief Financial Officer Oncology Advisor Josh Eizen Steve Prior, PhD Vincent Hernandez George Talbot, M.D. Chief Legal & Operating Officer Chief Strategy Officer SVP, Head of Research & Co-Founder & Sr. Clinical Advisor Chemistry Dickon Alley, PhD Co-Founder, SVP Biology BOARD OF DIRECTORS Eric Easom Stephanie Wong Rob Readnour, PhD Kabeer Aziz Mel Spigelman, MD Board Chair Calithera Biosciences Mountain Group Partners Adjuvant Capital Global Alliance For TB Patricia Martin Maggie FitzPatrick Joseph Zakrzewski Lynn Marks, MD Co-founder FitzPatrick & Co. Presidential Advisory Council Antibiotic-Resistant Bacteria 40