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1© 2026 Faeth Therapeutics. 1 Break through the PAM barrier.FAETH THERAPEUTICS COMPANY OVERVIEW OCTOBER 2026Oral inhibition of the PI3K/AKT/mTOR pathway, one of the most frequently altered pathways in cancer.
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2© 2026 Faeth Therapeutics. — Forward-Looking StatementsCertain matters discussed in this Presentation may contain forward-looking statements made by Faeth Therapeutics, Inc. (the “Company”) that are, by their nature, subject to significant risks and uncertainties. Forward-looking statements can be identified by words such as "may," "will," "should," "would," "could," "believe," "expect," "anticipate," "intend," "plan," "continue," "seek," "estimate," "potential" or the negative of these terms or other similar terms. Forward-looking statements in this Presentation include, but are not limited to, statements about: the use of proceeds from the February 2026 financing and cash runway expectations therefrom, including such proceeds funding the Company through key clinical milestones; the Company's product candidates and the potential benefits thereof; planned and ongoing pre-clinical and clinical studies, including the timing for data readouts and future development milestones; the potential peak sales and estimated total addressable markets, currently and in the future, for the Company's product candidates; the Company's CMC infrastructure plans and positioning for growth, including expectations regarding DS/DP supply for ongoing and proposed clinical trials; and expectations regarding patent protection for the Company's product candidates, including plans to file patent applications and the timing thereof. Such forward-looking statements reflect the current views of the Company's management regarding future events; they are not guarantees of future performance.These forward-looking statements involve significant risks and uncertainties that could cause actual results to differ materially and adversely from results expressed or implied by this Presentation, including, amongst others: the ability of the Company to obtain sufficient additional capital to further advance its clinical programs; the ability of the Company's clinical trials to demonstrate acceptable safety and efficacy of its product candidates and other positive results; the progress of the Company's preclinical studies and clinical trials; risks related to clinical development and regulatory approval of the Company's product candidates, including potential delays in the commencement, enrollment and completion of clinical trials; the size of the market opportunities for the Company's product candidates; competition in the Company's industry; changes in applicable laws or regulations and other risks and uncertainties from time to time described in the Company’s Annual Report on Form 10-K for the fiscal year ended December 31, 2025, and any subsequent Quarterly Reports on Form 10-Q, including those under the "Risk Factors" section therein, and in the Company’s other filings with the U.S. Securities and Exchange Commission. The Company assumes no obligation to update any forward-looking information contained in this Presentation. Certain information contained in this Presentation related to or are based on studies, publications and other data obtained from third party sources as well as our own internal estimates and research. While the Company believes that such third-party sources are reliable, there can be no assurance as to the accuracy or completeness of the indicated information. The Company has not independently verified the information provided by such third-party sources.This Presentation may contain trademarks, service marks, trade names and copyrights of other companies, which are the property of their respective owners. Solely for convenience, some of the trademarks, service marks, trade names and copyrights referred to in this Presentation may be listed without the TM, SM or © or ® symbols, but the Company will assert, to the fullest extent under applicable law, the rights of the owners to these trademarks, service marks, trade names and copyrights.
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3© 2026 Faeth Therapeutics. INVESTMENT HIGHLIGHTSCOMPLETE PAM BLOCKADEOral multi-node blockade that hits PAM at the three nodes that we believe matter. PK EDGE (TOLERABILITY AND EFFICACY)Intermittent dosing schedule that has been observed to flatten the peaks, providing~2-3x more time above IC90 than other PAM inhibitors with a low rate of stomatitisVALIDATED PATHWAY WITH LARGE MARKET OPPORTUNITIES~$1.5B market opportunity in endometrial cancer3~$5-10B market opportunity in breast cancer4CAPITALIZED THROUGH CATALYSTSExpected to be fully funded through 2 major catalysts•Phase 2 endometrial topline data expected by year-end 2026•Interim Phase 1b/2 breast data expected 2H 2027Top-tier investors including Montanova, Avoro, Baker Brothers, Cormorant, Fairmount, RA Capital Management, and Vivo Capital2 Oral PAM1regimen, built for longer target coverage without class-defining toxicities PIKTORserabelisib (PI3Kα) + sapanisertib (mTORC1/2)1PAM: PI3K/AKT/mTOR, a pathway that regulates cell metabolism, growth, and survival and is altered in up to half of solid tumors; 2as of February 2026 private placement3For Endometrial TAM estimates, refer to slide 12; 4For Breast TAM estimates, refer to slide 17.
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4© 2026 Faeth Therapeutics. — Built on work by Dr. Lewis Cantley, discoverer of the PI3K pathway. Molecules designed by Kevan Shokat, one of the world’s leading medicinal chemistsINTRODUCTION Lew Cantley, PhDDana Farber Cancer Institute, Harvard. Founder: Agios (NASDAQ), Petra, VolastraCo-founder: Faeth (NASDAQ) Kevan Shokat, PhDProfessor of Cellular & Molecular Pharmacology, UCSF; Professor of Chemistry, UC Berkeley; Howard Hughes Investigator FAETH SCIENTIFIC CO-FOUNDERSSid Mukherjee, MD PhDAsst. Prof., Columbia, Pulitzer Prize Winner, Time 100 Most Influential PeopleOliver Maddocks, MPharm, PhDCSO & Co-Founder, Honorary Professor of Cancer Biology & Metabolism, University of GlasgowKaren Vousden, PhDGroup Leader, Crick Institute, Former Chief Scientist of CRUK, Director, Bristol Myers SquibbScott Lowe, PhDChair of Cancer Biology & Genetics at Memorial Sloan Kettering, Founder: ORIC (NASDAQ)Greg Hannon, PhDFormer Director of CRUK Cambridge Institute
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5© 2026 Faeth Therapeutics. — PIKTOR: Designed for potent and selective multi-node PI3K/AKT/mTOR pathway inhibition PIKTORcombines serabelisib (PI3K-alpha specific inhibitor) with sapanisertib (mTORC1 and mTORC2 inhibitor). Targeting the PI3K/AKT/mTOR pathway to address one of the most-frequent genomic drivers in solid tumors1.1cBioPortal References: Cerami et al., Cancer Discov. 2012, and Gao et al., Sci. Signal, 2013 serabelisibsapanisertib PIKTORPI3K-alpha specific inhibitormTORC1 and mTORC2 inhibitor PIKTOR OVERVIEW
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6© 2026 Faeth Therapeutics. — Multi-node synergy designed to allow each agent to run using multiple-fold lower doses than monotherapy RP2DPIKTOR OVERVIEW MONOTHERAPY RP2D DOSE IN PIKTOR + PACLITAXEL³ REDUCTION900 mg QD×3dQW ¹ 200 mg QD×3dQW9 mg QD×3dQW ² 3 mg QD×3dQW ¹Juric et. al., Clin. Cancer Res. 23 (17) 2017. ²Voss et. al., Br. J. Cancer 123 (11) 2020. ³Starks et. al., Gyn. Onc. 166, 2022. ⁴Tyrakis et. al., Br. J. Cancer 133, 2025. ⁵Maddocks et al., STOP Cancer 2026; RP2D – Recommended Phase 2 Dose; QD×3dQW – once daily, 3 days per week; FIH – first-in-human. Deep clinical experience underpins the dose:serabelisib and sapanisertib have been studied in ~1,000 patients across Takeda-era and subsequent trials, including ~150 patients treated with the PIKTOR combination (sapanisertib 2–8 mg / serabelisib 100–400 mg).⁵ Why the combination runs lower• Vertical blockade — PI3Kαupstream + mTORC1/2 downstream — designed to hit the pathway at three nodes and close feedback escape routes⁴• Deep inhibition at lower exposure of each agent designed to widen the therapeutic window — e.g., hyperglycemia rates less than half those reported in single-node inhibitor trials⁴ 4.5× lower3× lowerSerabelisbSapanisertibPIKTOR
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7© 2026 Faeth Therapeutics. — Multi-node inhibition with PIKTOR achieved robust preclinical PI3K-pathway inhibition in cancer cell lines Western blot data shown is from AN3CA endometrial cancer cells (mutations in PTEN, PIK3R1, mTOR ) and is replicated in multiple PI3K-mutated endometrial and breast-cancer cell lines 1.1 Tyrakis et. al., (2025) British Journal of Cancer, 133: 144-154; 2Exposure/Response Analysis of an Oral Multi-Node PI3K/AKT/mTOR Pathway Inhibitor Combination of Serabelisib and Sapanisertib. Maddocks et. al., STOP Cancer Conference, 2026 PIKTOR OVERVIEWPIKTOR reduced PI3K-pathway signaling in cancer cell linesmore than single-node inhibitors at clinically relevant concentrations¹Preclinical data have been recapitulated in human skin biopsy datafrom clinical studies2 Tumor GrowthAN3CA Endometrial Cancer Cell Line, PIK3CA Wild-type (PTENdel, PIK3R1mut, MTORmut)
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8© 2026 Faeth Therapeutics. — Oral PIKTOR dosing is designed for sustained exposure with reduced Cmax-related toxicity riskPIKTOR OVERVIEW Plasma protein binding / free fractionTime above IC90 / weekPeak exposure(Cmax : IC90 ratio)FreeBound31%69%42 h2.2Serabelisib30%70%44 h2.9Sapanisertib2%98%15 h~65Gedatolisib 1 Exposure/Response Analysis of an Oral Multi-Node PI3K/AKT/mTOR Pathway Inhibitor Combination of Serabelisib and Sapanisertib. Maddocks et. al., STOP Cancer Conference, 20262 First-In-Human Study of PF-05212384 (PKI-587), a Small-Molecule, Intravenous, Dual Inhibitor of PI3K and mTOR In Patients With Advanced Cancer. Clin Cancer Res. 2015 April 15; 21(8): 1888–1895. doi:10.1158/1078-0432.CCR-14-1306. 3 Multi-node inhibition targeting mTORC1, mTORC2 and PI3Ka potently inhibits the PI3K/AKT/mTOR pathway in endometrial and breast cancer models. British Journal of Cancer, 133: 144-154. https://doi.org/10.1038/s41416-025-03035-z The ratio of plasma drug concentration to cellular IC90 from 0 - 120 hours was calculated for serabelisib, sapanisertib, and gedatolisib. Sapanisertib (3 mg) with serabelisib (200mg), with food, QDx3dQW plasma drug concentration was obtained from Maddocks et. al.,20261. Gedatolisib (180 mg QW) drug concentration data was derived from Shapiro et. al.,20152by scaling 89 / 154 / 222 / 266 mg single dose data to 180 mg, assuming linearity. Mean gedatolisib plasma concentration at 180 mg was computed with a geometric mean per time-point across the scaled concentrations. The estimated time above IC90 was computed as the time a stepwise linear interpolation crossed the threshold. IC90 values for all drugs were calculated using IC50 values presented in Tyrakis et. al.,20253and Slide 26 in this corporate deck. The cellular IC50 values for all three drugs were derived from an average of six cell lines representing clinically relevant models i.e. HR+/HER2- breast cancer cell lines and endometrial cancer cell lines: MCF7, T47D, AN3CA, HEC1B, MFE-280, MFE-296. Dashed red line denotes the sapanisertib Cmax/IC90 ratio for the combined dose of sapanisertib and serabelisib (4 mg / 200 mg, QDx3dQW, fasted) resulting in Grade 3 stomatitis in a Phase 1b dose escalation study (NCT01899053, described in Maddocks et. al.,20261). Multiple of IC90 (log scale) Higher Stomatitis Risk for Sapanisertib 1 Hours
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9© 2026 Faeth Therapeutics. — PIKTOR had low rates of both stomatitis and hyperglycemia in ongoing Phase 2 endo trial vs. other PAM agentsPIKTOR OVERVIEW The results are presented from different clinical trials at different points in time with differences in trial design. No head-to-head trials have been conducted among the results shown and cross-trial comparisons must be interpreted with caution. As a result, conclusive cross-trial comparisons cannot be made.Hyperglycemia: Turner NEJM 2024 (inavolisib); Hurvitz ASCO 2026 (alpelisib, VIKTORIA-1); Varkaris ESMO TAT 2026 (zovegalisib/RLY-2608); Jhaveri ASCO 2026 (STX-478, PIKALO-1); Celcuity VIKTORIA-1 Wild-type data; ESMO 2025 (gedatolisib); cross-refs. PIKTOR: PIK-201 PIKTOR+paclitaxel snapshot 01-2026, n=22, ongoing Faeth Phase 2. Gedatolisib FDA-approved as Revtorpyk®, 14-Jul-2026.0025255050 75 75 100 100 Stomatitis, any grade (% of patients) Hyperglycemia, any grade (% of patients)Inavolisib90% / 70%Alpelisib34% / 58%Zovegalisib8% / 43%STX-4787% / 39%Gedatolisib63% / 10%PIKTOR14% / 14% PIK-201 (n=22): patients are not required to use steroid mouthwash prophylaxis. Trial eligibility requires HbA1c ≤8% and fasting glucose ≤160 mg/dL at enrollment.Eligibility criteria vary by trial. PIKTORComparatorsPoint labels: stomatitis% / hyperglycemia%
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10© 2026 Faeth Therapeutics. — MULTI-NODE SINGLE-NODE PIKTOR(Ph.2, Endometrial, Ph.1b Breast)GEDATOLISIBCelcuity (Approved))MUTANT-SPECIFICRelay, Lilly, OnKure, Novartis (Investigational)FDA-APPROVEDAlpelisib, Everolimus, Capivasertib, InavolisibMechanism of actionTarget profilePI3K-alphamTORC1mTORC2PI3K-alpha, PI3K-beta, PI3K-gamma, PI3K-delta,mTORC1 and mTORC2Mutant PI3K-alphaAKT ormTORC1 orPI3K-alphaMulti-node inhibition Potentially Immune Sparing (PI3K-alpha specific) Broad pathway mutation coverage Prevents wt-PI3K escape Oral administration PIKTOR OVERVIEWPIKTOR:Designed to solve the challenges of drugging the PI3K pathway
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11© 2026 Faeth Therapeutics. — 2L+ endometrial market, rising unmet need, one PAM-pathway optionExpanding marketHigh unmet needOnly PAM-Pathway optionPaclitaxel rechallenge: 15% ORR, 3–4 mo PFS2. ADCs are moving up in the treatment order, creating challenges for TOPO1 sequencingPAM alterations occur in ~80% of all EC patients3No PI3K inhibitor ever approved in EC41. ACS 2026 / SEER 2025. 2. Single-agent chemotherapy control arm, KEYNOTE-775 (Makker et al., NEJM 2022). 3. TCGA 201. 4. FDA approvals database. 5. Per publicly registered Phase 3 eligibility criteria (clinicaltrials.gov). Endometrial cancer is a growing market and recently overtook ovarian as the deadliest gynecological cancer1. CLINICAL DEVELOPMENT: ENDOMETRIAL ADC6+ sponsors5· Ph2/3PAM1 program · oral
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12© 2026 Faeth Therapeutics. — Estimated PIKTOR addressable U.S. population (2L+)U.S. Incident Therapeutic Build (Annual) U.S. New Uterine Cancer Cases1 ~68,000Endometrioid Histology (~80%)2~54,000Advanced / Recurrent Req. Systemic Tx3~12,300Post-1L Anti-PD-(L)1; 2L+ Eligible4~9,000 Anticipated FDA Label Population Post-1L advanced/recurrent endometrioid EC•Endometrioid histology•Advanced or recurrent, not amenable to curative surgery/radiation•Progressed on/after prior anti-PD-1/PD-L1-containing regimen and TOPO1-based ADC (if available) ~9,000U.S. incident patients per yearpost-anti-PD-(L)1, endometrioid EC ~$1.5B US TAM51. ACS 2026 / SEER 2025: ~68,000–69,000 new uterine corpus cases/yr. 2. Endometrioid histology ~80% ((SEER-based series, 80–85%; Clarke, JAMA Oncol 2019)).3. Advanced/recurrent requiring systemic Tx (~12,300/yr): de novo advanced ~9,700 (54K × 18% FIGO III/IV; SEER ~11% distant + ~half of 18% regional; conservatively 18%) + steady-state early-stage recurrence ~2,550/yr (44K early-stage entrants/yr × ~8% cumulative recurrence, 27% vaginal-only excluded (Åkesson, Gynecol Oncol 2023; all-stage endometrioid cohort); 73% require systemic Tx).4. ~9,000 addressable 2L+ patients/yr at steady state: 12,300 × ~95% (company assumption; IO+chemo NCCN-preferred post NRG-GY018/RUBY) × ~77% progression (company estimate) ≈ 9,000/yr addressable .5. Total Addressable Market (TAM): ~$20K/28-day supply (TRUQAP WAC) ×231 days (median duration of treatment, lenvatinib + pembrolizumab arm, KEYNOTE-775; Makker et al., NEJM 2022) ×~9,000 patients ≈ $1.5B.Market size estimates reflect the stated assumptions on patient numbers, price and duration of therapy. They estimate the size of the treatment setting and are not forecasts of PIKTOR revenue or market share. MARKET: ENDOMETRIAL
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13© 2026 Faeth Therapeutics. — Ph1b: PIKTOR + paclitaxel drove deep responsesin endometrial cancerCLINICAL DEVELOPMENT: ENDOMETRIAL 47%overall response rate73%clinical benefit rate ENDOMETRIAL PATIENTS ONLY80% overall response rate (4/5)3 complete responses11 mo median PFSRange 0–26.9 mo · avg 3 prior lines (range 1–6)n=19 enrolled (15 response evaluable, 13 RECIST evaluable); endometrial subgroup n=5. Data cutoff per publication 10/1/21. Starks DC, Rojas-Espaillat L, Meissner T, Williams CB. Phase I dose escalation study of dual PI3K/mTOR inhibition by sapanisertib and serabelisib in combination with paclitaxel in patients with advanced solid tumors. Gynecologic Oncology. 2022 Jul 15. Abbreviations: ORR – Overall Response Rate; CBR – Clinical Benefit Rate; CR – Complete Response; PFS – Progression-Free Survival; Ov – Ovarian; En – Endometrial; Br –Breast. ALL PATIENTS (RESPONSE EVALUABLE)
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14© 2026 Faeth Therapeutics. — PIK-201: PIKTOR + paclitaxel in advanced endometrial cancer (currently enrolling) Eligibility Criteria• Endometrioid endometrial cancer• 2nd line or later• Post ICI and Carbo• Must have PI3K/AKT/mTOR pathway mutation Primaryendpoint •ORR Secondaryendpoints•PFS•CBR•Safety/tolerability Exploratoryendpoints•PK•Efficacy endpoints vs. specific mutations NCT06463028Study is being conducted in partnership with: GOG-3111 CLINICAL DEVELOPMENT: ENDOMETRIAL Phase 2Single arm (n≅40)Optional sub-study; diet to suppress glucose / insulin• Sapanisertib 3 mg • Serabelisib 200 mg • Paclitaxel 80 mg/m2•DOR•OS
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15© 2026 Faeth Therapeutics. — We believe regulatory positioning supports accelerated path to registrational trial 1Hurvitz, S. et. al., (2025) ESMO PresentationAbbreviations: PK/BA - Pharmacokinetics / Bioavailability, EC - endometrial cancer, CoC - contribution of componentsSubject to feedback from FDA REGULATORY Combination Dosing Precedent Contribution of Components Precedent supports a PI3K/mTOR multi-node strategy•Recent gedatolisib Ph3 success reinforces the class and mechanism1 Strong safety foundation•More than 240 subjects exposed; no Hy’s Law cases, minimal bilirubin elevations, well-characterized toxicity on intermittent dosing to dateClin Pharm Gaps and Requirements Defined Safety Database Supports Advancement CMC Program on Track Path to Registrational Trial Contribution of Components•Independent monotherapy activity observed for each component •Contribution of components to be established prior to PIKTOR approval
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16© 2026 Faeth Therapeutics. — High unmet needMost patients lack PI3K mutation Oral conveniencePIKTORis designed to work in all patients; not just the ~40% that have an activating PIK3CAmutation.PIKTORis taken with food on a 3 days on/4 days off schedule1. Howlader 2014; SEER subtype rates 91.3/130.8 per 100K) = ~221K/yr2. Tao JJ, et al. JCO Precis Oncol2025 · 3. Zhang Y, et al. Cancer Cell2017;31:820–832.e3 · 4. Breast Cancer Res Treat2025, PMID 40931235 · 5. Krishnamurthy N, et al. Front Oncol2020;10:1475. HR+/HER2- patients comprise ~70% of all metastatic breast cancer patients1 CLINICAL DEVELOPMENT: BREAST PI3K WT + PI3K MUT 100% of HR+/HER2-Breast Cancer PI3K MUT + multiple others ~40% of HR+/HER2- breast cancer with activatingPIK3CAmutation2-5Breast Cancer: Multi-node PAM blockade more than doubles addressable market relative to mutant-selective inhibitors
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17© 2026 Faeth Therapeutics. — HR+/HER2- breast cancer: Large unmet needU.S. Incident Therapeutic Build (Annual) U.S. New Breast Cancer Cases1 ~316,000HR+/HER2− Subtype (~70%)2~221,000Advanced / Metastatic Requiring Systemic Tx3~48,000 ~18,000 ~$3BSEER 2025: ~317K new U.S. female BC cases; ~42K BC deaths/yr (baseline for all three markets shown). 2. HR+/HER2− subtype ~70% of all BC (Howlader 2014; SEER subtype rates 91.3/130.8 per 100K) = ~221K/yr. 3. Advanced/metastatic requiring systemic Tx ~48K/yr: de novo stage IV ~13K (221K × ~6% stage IV at diagnosis (SEER)) + steady-state distant recurrence ~35K (208K early-stage entrants/yr × ~17% cumulative distant recurrence (company blend; Pan, NEJM 2017: 13–41% by stage)). 4.1L TAM: ~48,000 incident 1L patients × ~$17K/month (CDK4/6 inhibitor list price) × 12 months ≈ $10B. PIKTOR is not currently being studied in the first-line setting; 5. [2L post-AI+CDK4/6i] Assume 42K annual deaths in US, of which ~70% are HR+HER2- (per SEER statistics; ACS Facts and Figures 2026) as conservative estimate for the number of patients who progress post AI+CDK4/6. Of these, 40% are PI3K mutant, and 60% are PI3K wild-type. 6. 2L TAM for PI3K mutant patients: ~$20K/28 days (Truqap WAC, conservative) × 11 mo (median PFS, VIKTORIA-1 PIK3CA-mutant triplet arm) × 12,000 = $2.6B, rounded to ~$2B; 7. 2L TAM for PI3K wild-type patients: ~$20K/28 days (as fn 6) × 9 mo (median PFS, VIKTORIA-1 PIK3CA wild-type triplet arm) × 18,000 = $3.2B, rounded to ~$3B.Market size estimates reflect the stated assumptions on patient numbers, price and duration of therapy. They estimate the size of the treatment setting and are not forecasts of PIKTOR revenue or market share. ~48,0001L patients receiving aromatase inhibitor + CDK4/6 ~$10BU.S. TAM4 ~12,0002L patients receiving SERD+/-CDK4/6PI3K Mutant5 ~$2BThree addressable patient populations from the ~48k advanced poolMARKET: BREAST 2L patients receiving SERD+/-CDK4/6PI3K WT5 U.S. TAM6U.S. TAM7
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18© 2026 Faeth Therapeutics. — Serabelisib and Sapanisertib have each independently shown activity in HR+/HER2- breast cancer; Phase 1b/2 underway The results are presented from different clinical trials at different points in time with differences in trial design. No head-to-head trials have been conducted among the results shown and cross-trial comparisons must be interpreted with caution. As a result, conclusive cross-trial comparisons cannot be made. 1Garcia-Saenz et. al., (2022) J. Clinical Cancer Research (2022) 28 (6): 1107–11162Hurvitz, S. et. al., (2025) ESMO Presentation 3Juric et. al., (2017) Clin. Cancer Res. 23 (17)4Juric et. al., (2018) Journal of Clinical Oncology 36 (13),1291-1299 CLINICAL DEVELOPMENT: BREAST HR+/HER2-(Phase 2) VIKTORIA-1 (Phase 3) Sapanisertib Control Arm GedatolisibSTUDY DRUG / COMBINATION ORR DCR mPFS CRGarcia-Saenz et. al., 2022 1 Sapanisertib + Fulvestrant (n=47 arm B)21.3% 75% PR+CR+SD7.2 m2/47 Breast Cancer Subjects from Phase 1 Serabelisib Comparator Drug Data Garcia-Saenz et. al., 2022 1Fulvestrant (n=46 arm A)10.9% 61% PR+CR+SD3.5 m0/46Hurvitz, S. et. al., 2025 2Gedatolisib + Fulvestrant (n=130)28.3% 77% PR+CR+SD7.4 mNASTUDY DRUG / COMBINATION ORR DCR mPFS CRJuric et. al., 2017 3Serabelisib (n=21)14% 76% PR+CR+SDNR0/21Juric et. al., 2018 4Alpelisib (n=23) 4% 61% PR+CR+SDNR0/23
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19© 2026 Faeth Therapeutics. — Breast: First patient dosed in Phase 1b trial in April 2026KEY MILESTONES 227Trial initiated; Ph1b dose escalation underwayInterim safety data from dose escalationExpansion data Achieved in 202620272028 Interim efficacy data; expansion cohorts initiated First patient dosed Apr 2026
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— Breast: Ongoing Phase 1b/2 trial designed to rapidly identify recommended dose and initiate expansion cohortsCLINICAL DEVELOPMENT: BREAST Key eligibility: HR+/HER2− breast cancer · ≥1 prior therapyTreatment: Until disease progression, unacceptable toxicity, withdrawal of consent, or death Cohort APIKTOR + FulvestrantCohort BPIKTOR + Fulvestrant + Palbociclib Planned Cohort CPIKTOR + Oral SERD ± Palbociclib A1:Sap 2 mg + Ser 200 mgA2: Sap 4 mg + Ser 200 mgA2 opens parallel with A1 B1:Sap 2 mg + Ser 100 mgB2: Sap 3 mg + Ser 200 mgB3: Sap 4 mg + Ser 200 mgB4 (optional):Sap 4 mg + Ser 300 mg Currently enrolling for Cohort BC1: Sap 4 mg + Ser 200 mg(+ Oral SERD only)C2: Sap 2 mg + Ser 200 mg(+ Oral SERD + Palbo)C3: Sap 4 mg + Ser 200 mg(+ Oral SERD + Palbo)
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21© 2026 Faeth Therapeutics. — Two clinically de-risked indications outside of endometrial cancer and breast cancer add optionality to pipelinePIPELINE OPTIONALITY Platinum-resistant ovarian cancer (PROC)HR 0.66PFS benefit in randomized Phase 2 DICE trial (90% CI: 0.45–0.96)•Phase 2 complete (n=134): sapanisertib + paclitaxel vs. paclitaxel alone; late-breaking oral presentation at ESMO 2025•Mean PFS 5.8 vs. 4.0 months with no meaningful added toxicity (Grade 3/4 AEs: 7.0% vs. 6.6%)•Supported by ovarian responses in Phase 1b PIKTOR triplet (2 PRs, 4 SDs ≥6 months) NFE2L2/KEAP1-mutated advanced NSCLC25% ORRSingle-agent sapanisertib; mPFS 8.9 months (squamous NSCLC)•Genotype-directed monotherapy activity — potentially the first genotype-directed therapy for squamous NSCLC•FDA Fast Track designation granted based on these results•PIKTOR adds PI3Kαblockade to the validated mTORC1/2 backbone — potential to deepen and extend responsesKrell J et al., ESMO 2025; Paik PK et al., J Thorac Oncol 2023;18(4):516–526; Starks DC et al., Gynecol Oncol 2022. TAM per Deallus report (Feb 2024) and company analysis. Abbreviations: PFS – progression-free survival; HR –hazard ratio; CI – confidence interval; ORR – overall response rate; AE – adverse event; IIT – investigator-initiated trial; TAM – total addressable market. Phase 2 protocol in process • TAM ~$0.75-1.25B FDA interaction planned 2026 • TAM ~$1.5–2B OvarianLung
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22© 2026 Faeth Therapeutics. — $186.4M1in cash expected to fund PIKTOR through anticipated readouts in endometrial cancer and breast cancer KEY MILESTONES 1$186.4M cash and cash equivalents as of June 30, 2026,Abbreviations: EC - endometrial cancer, BC - breast cancer 227Received Fast Track DesignationTopline data readoutLast patient dosed + 6 months dataTrial initiated; Ph1b dose escalation underway (first patient dosed Apr 2026)- Interim safety data from dose escalation- Interim efficacy data; expansion cohorts initiatedExpansion data Achieved in 202620272028+ 2H 2026PROGRAMENDOMETRIALBREASTINDICATION EXPANSION (sapanisertib)Preclinical data on rare disease
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23© 2026 Faeth Therapeutics. — Robust IP portfolio and registration-ready CMCIP & CMCIntellectual propertyCMC & supplyMay 2037 — Composition of matterIssued COM patents for both APIs; serabelisib expiry includes PTA and expected 5 years of PTEISSUEDMay 2039 — Combination MoTIssued patent covering PIKTOR + ISD method of treatment across a range of tumor types~2048 — Pending FilingsPending MoT filings (endometrial/breast; ovarian) plus novel formulation COM filing targeted 2027 Mature DS/DP materialsBoth drug substances highly stable; batches with 36–60 months of stability data and proven manufacturing historyScale-up on trackDS/DP process optimization being completed; demo batches planned for 2026; registrational readiness on trackSupply securedAmple DS/DP supply expected for ongoing and proposed Phase 1b / Phase 2 studiesGlobal exclusive licenses from Takeda for serabelisib and sapanisertib across all oncology indications ISSUEDPENDING
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24© 2026 Faeth Therapeutics. — Faeth team has deep drug development experience Management team Christopher Gerry, JDGeneral Counsel Anand Parikh, JDChief Executive Officer Oliver Maddocks, MPharm PhDChief Scientific Officer Debbie Chirnomas, MD MPHChief Medical Officer Board Bob Holmen, JDBoard MemberSaira RamasastryBrian Stephenson, PhD, CFAChief Financial Officer TEAM Anand Parikh, JDBoard Chair Phil DonenbergBoard Member Board MemberStephen Hahn, MD Board Member
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25© 2026 Faeth Therapeutics. 25Appendix
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26© 2026 Faeth Therapeutics. — PIKTORdemonstrated preclinical pathway suppression at lower concentrations than other PI3K/AKT/mTOR targeted agentsPIKTOR OVERVIEWPaclitaxel 1Inavolisib 1STX-478 1RLY-2608 1Capivasertib 1Everolimus 1Alpelisib 1Gedatolisib 2PIKTOR 1Sapanisertib 1Serabelisib 1PI3K-Pathway StatusCell Line 0.00880.6485.923.860.1115.40.2860.01580.00670.00705.17PIK3CA-P539R, PTEN-R130Q, MTOR-R1482CMFE-2960.00071.446.974.850.3415.01.6530.00400.00500.01083.377PTEN-del, PIK3R1-del, MTOR-R1201QAN3CA 0.00421.3510.58.410.5715.20.4380.05000.00540.01532.346PIK3CA-G1049R, RICTOR-D939GHEC1B 0.0140.1131.062.15>10014.81.7790.05200.00470.01872.19PIK3CA-H1047MFE-2800.035NDNDND0.0646.10.438ND0.00450.00583.521PIK3CA-P539R, PTEN-R130Q, MTOR-R1482CMFE-296 Paclitaxel Resistant 2 0.015NDNDND0.1415.20.494ND0.00380.00722.671PTEN-del, PIK3R1-del, MTOR-R1201QAN3CA Paclitaxel Resistant 2 0.01300.88786.1134.81816.8720.280.84800.03050.00500.01083.213Endometrial Cancer Average IC50:Paclitaxel 1Inavolisib 1STX-478 1RLY-2608 1Capivasertib 1Everolimus 1Alpelisib 1Gedatolisib 2PIKTOR 1Sapanisertib 1Serabelisib 1HR/HER2 StatusPI3K-Pathway StatusCell Line 0.2370.1622.935.940.879>1001.340.0230.00750.0103.82HR+/HER2+PIK3CA-E545K, MTOR-E1427QMDA-MB-361 0.0090.0560.130.610.25528.80.200.0470.00330.0121.34HR+/HER2-PIK3CA-H1047RT47D 0.0260.0630.631.570.455>1000.4070.0140.00210.0051.33HR+/HER2-PIK3CA-E545KMCF-7 0.011>100>10031.687.514.819.890.0240.01110.0246.01TNBC (HR-/HER2-)Wild-type PI3K pathwayMDA-MB-2310.07125.125.929.9322.360.95.460.0270.0060.0133.13Breast Cancer Average IC50: 1Tyrakis et. al., 2025, British Journal of Cancer 2Faeth Internal DataAbbreviations: ND - not done
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27© 2026 Faeth Therapeutics. — Ph1b: PIKTOR + paclitaxel showed durable responses in both PIK3CAmut and wt patients CLINICAL DEVELOPMENT: ENDOMETRIAL 47%Overall Response Rate71%ORR in patients with PI3k pathway mutation73% Clinical Benefit Rate in evaluated patients PIKTOR AND PACLITAXEL (all RECIST evaluable) n=19 enrolled (15 response evaluable, 13 RECIST evaluable). Data cutoff per publication 10/1/21.Starks DC, Rojas-Espaillat L, Meissner T, Williams CB. Phase I dose escalation study of dual PI3K/mTOR inhibition by Sapanisertib and Serabelisib in combination with paclitaxel in patients with advanced solid tumors. Gynecologic Oncology. 2022 Jul 15. Abbreviations: PI3KCAmt - with mutation in PI3KA, wt - wild type, LOT - Lines of Therapy, ORR - Overall Response Rate, CBR - Clinical Benefit Rate, PFS - Progression Free Survival 80%Overall Response Rate80%Clinical Benefit Rate11 moMedian PFS (Range 0 - 26.9 mo)Avg 3 prior lines of therapy (range 1 - 6)Endometrial patients only
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28© 2026 Faeth Therapeutics. — Taxane resistance activates PI3K/AKT/mTOR pathway signaling in cancer models, sensitive to inhibition by PIKTOR Taxane resistance activates PAM Pathway Taxane resistant cells retain sensitivity to PIKTOR Tyrakis et. al., (2025) British Journal of Cancer, 133: 144-154. CLINICAL DEVELOPMENT: ENDOMETRIAL
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29© 2026 Faeth Therapeutics. — All Comers (n= 71)5.2%40.3%Juric et. al., 2017REFERENCEZovegalisibSerabelisb GedatolisibThe results are presented from different clinical trials at different points in time with differences in trial design. No head-to-head trials have been conducted among the results shown and cross-trial comparisons must be interpreted with caution. As a result, conclusive cross-trial comparisons cannot be made. Phase 1 Clinical Data Comparisons (all monotherapy)COHORT ORR DCR (PR+CR+SD) PIKTORBreast Cancer (n=21)All Comers (n= 198)Breast Cancer (n=16)All Comers (n= 19)Breast Cancer (n=2)All Comers (n= 77)Breast Cancer (n=4) 14%76%5.0%42.4%NA NA5.0% NA50% (n=1) 100% (n=2)3.9%39%0% NAVoss et. al., 2020 Varkaris et. al., 2023Shapiro et. al. 2015 Comparison of First in human Phase 1 Clinical Trials including BC sub-groupsNote that patient populations and drug doses are naturally highly variable across trials and not directly comparableData shown to illustrate that early clinical data for PIKTOR agents (used separately) is similar to the related drugs zovegalisib and gedatolisib Sapanisertib MONOTHERAPY ACTIVITY ANALYSIS
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30© 2026 Faeth Therapeutics. — Ovarian cancer: estimated PIKTOR addressable U.S. populationU.S. Incident Therapeutic Build (Annual) U.S. New Ovarian Cancer Cases~21,000Advanced disease requiring systemic therapy~17,000Platinum-resistant or refractory ovarian cancer (PROC)~11,600Anticipated FDA Label Population Advanced platinum resistant ovarian cancer (PROC) ~11,600U.S. incident patients per yearadvanced, platinum-resistant or refractory, PI3K/AKT/mTOR pathway altered ~12,000U.S. prevalent eligible patients TAM1. ACS/SEER 2025: ~20,890 new OC cases/yr; ~12,730 deaths/yr. 2. ~17,000 patients/yr requiring 1L systemic Tx: de novo advanced ~15,750 (21K × 75% FIGO III/IV; Torre et al. CA Cancer J Clin 2018) + early-stage recurrence ~1,050.3. PROC ~11,600/yr at steady state: (a) Primary platinum-resistant/refractory ~3,060 (18% of 17K; Lheureux Lancet 2019: ~20% are primary resistant, conservatively 18% after excluding refractory-who-die-early). (b) Acquired platinum resistance ~8,570/yr: ~12,240 platinum-sensitive patients enter follow-up/yr; at steady state, 70% lifetime cumulative conversion to PROC yields 12,240 × 70% = ~8,570 new PROC patients/yr across all overlapping cohorts. Total: 3,060 + 8,570 = ~11,630, rounded to ~11,600.4. Prevalent ~12,000: 11,600 incident/yr × ~1.0yr ≈ mOS. PROC median OS ~12mo across contemporary trials: AURELIA control mOS 13.3mo, bev+chemo mOS 16.6mo (Pujade-Lauraine JCO 2014); single-agent chemo (PLD, topotecan, weekly paclitaxel) mOS ~9–12mo; blended real-world mOS ~12mo. When mOS ≈ 1yr, prevalent pool ≈ annual incidence. Mortality cross-check: ~12,730 OC deaths/yr (SEER 2025) × ~91% pass through PROC = ~11,600 PROC deaths/yr ≈ incident flow. Converges.Abbreviations: TAM - Total Addressable Market •Epithelial ovarian, fallopian tube, and peritoneal cancers•Platinum-resistant or refractory (progression during or within 6mo of last platinum)•All-comers (no biomarker selection required)•SoC mPFS ~3–4mo; mOS ~12mo; significant unmet need CLINICAL DEVELOPMENT: OVARIAN
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31© 2026 Faeth Therapeutics. — Phase 2 DICE Trial: Sapanisertib + Paclitaxel in PROCPlatinum Resistant Ovarian Cancer Eligibility Criteria• Epithelial ovarian / fallopian tube / peritoneal• Platinum-resistant or refractory• ≥1 prior line; measurable disease (RECIST 1.1) Arm A: Control (n=66)Paclitaxel 80 mg/m² IVDays 1, 8, 15 (q28d) Arm B: Experimental (n=68) Paclitaxel 80 mg/m² IV +Sapanisertib 4 mg PO 3d/w Endpoints• Primary endpoint: PFS• Secondary endpoints: ORR, OS, DoR, CBR, QoL, Safety• Experimental endpoint: Genetic biomarkers in tissue / blood Krell, J. et. al., ESMO 2025. Abbreviations: ORR - Overall Response Rate, OS - Overall Survival, DoR - Duration of Response, CBR - Clinical Benefit Rate, QoL - Quality of Life, PFS - progression free survival, HR - Hazard Ratio, CI - Confidence Interval CLINICAL DEVELOPMENT: OVARIAN R 1:1(N=134)
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32© 2026 Faeth Therapeutics. — Phase 2 DICE Trial: Sapanisertib + Paclitaxel demonstrated benefits in PROCLate breaking oral pres at ESMO Mean PFSArm A: 4.0 months Arm B: 5.8 monthsHR=0.66; 90% CI: 0.45–0.96 (P=0.0776) Grade 3/4 AEsArm A: 6.6% Arm B: 7.0%Gastrointestinal AEs (0% vs. 11.4%) and Rash (0% vs. 2.9%) more common in Arm B but were manageable Next steps• OS, ORR and detailed safety data to come• Potential FDA interaction in 2026 regarding future development, including potential registrational trialKrell, J. et. al., ESMO 2025. Abbreviations: ORR - Overall Response Rate, OS - Overall Survival, DoR - Duration of Response, CBR - Clinical Benefit Rate, QoL - Quality of Life, PFS - progression free survival, HR - Hazard Ratio, CI - Confidence Interval CLINICAL DEVELOPMENT: OVARIAN
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33© 2026 Faeth Therapeutics. Phase 2 DICE Trial PFSSapanisertib(aka TAK 228) and Paclitaxel showed PFS benefit in PROC Krell, J. et. al., ESMO 2025Abbreviations: PFS - progression free survival, CI - Confidence Interval CLINICAL DEVELOPMENT: OVARIAN
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34© 2026 Faeth Therapeutics. — Lung cancer: estimated PIKTOR addressable U.S. populationU.S. Incident Therapeutic Build (Annual) U.S. New Lung Cancer Cases~227,000Non-small cell lung cancer (NSCLC) (~85% of lung cancers)~195,000Advanced / metastatic or recurrent NSCLC (Stage IIIB/IV at dx + early-stage recurrence)~130,000Progressed after first-line systemic therapy (post-platinum +/-immunotherapy)~50,000 Anticipated FDA Label Population Advanced or metastatic non-small cell lung cancer (NSCLC) ~9,500U.S. incident patients per yearadvanced or metastatic NSCLC, KEAP1, NFE2L2 or PIK3CA pathway gene alteration ~7,000U.S. prevalent patients TAMKEAP1, NFE2L2 or PIK3CA mutated (~18%)~9,5001. ACS/SEER 2025: 226,650 new LC cases; ~124,730 deaths. 2. NSCLC ~85% (ACS 2024; Molina et al. Mayo Clin Proc 2008). 3. ~130,000 advanced/recurrent requiring systemic Tx: de novo advanced ~125K (195K × 65% Stage IIIB/IV; SEER stage distribution) + steady-state early-stage recurrence ~12K (68K early-stage entrants/yr × 20% 5yr CIR = ~13,600 at steady state; NLST, Ann Thorac Surg 2023). CIR already incorporates competing mortality. Total ~137K; presented as ~130K (conservative round). De novo advanced dominates (≥91%).4. Post-1L treatment-eligible (~50,000): ~130K × 80–85% receive 1L systemic → ~40% initiate 2L (clinical aūrition: rapid progression, declining PS, death on 1L; ESMO 2023 review 30–46%; SEER-Medicare 47%). Unlike BC/EC where most patients survive to 2L, NSCLC 1L mOS ~12–15mo and many patients deteriorate before 2L is feasible.5. KEAP1, NFE2L2 or PIK3CA mutated (~9,500, ~18%): KEAP1/NFE2L2 ~15% (Frank et al. CCR 2018: KEAP1 11.3%, NFE2L2 3.5%, largely mutually exclusive; Jeong et al. CCR 2020: 17%). PIK3CA adds ~4% of NSCLC (Frank et al. Oncotarget 2014, n=1,144: 3.7%; range 2–4%; squamous ~9% vs. adeno ~3%; TCGA LUSC). PIK3CA co-occurrence with KEAP1/NFE2L2 not significantly enriched (Frank et al. CCR 2018, n.s.), so overlap ~0.6% (15%×4%); union ≈ 15%+4%−0.6% ≈ ~18%. Reflects proposed LUNG-MAP expansion adding PIK3CA to the NFE2L2/KEAP1 (NRF2) subset; PI3K/AKT signaling is mechanistically linked to NRF2. Applied to 2L pool as a stable tumor genotype.6. Prevalent (~7,000): 9,500 incident/yr × ~0.75yr mean post-2L survival. Post-2L NSCLC mOS ~7–9mo (SEER-Medicare 7.3mo); KEAP1/NFE2L2 mutants have HR ~2.0 for death vs. WT (POPLAR/OAK, Front Oncol 2021), mOS ~5–7mo from 2L start, while PIK3CA mutants do not carry an independent adverse prognosis (Frank et al. Oncotarget 2014), so the blended pool survival is slightly more favorable than KEAP1/NFE2L2 alone. Mortality cross-check: ~106K NSCLC deaths × ~8.4% biomarker-positive 2L-eligible = ~8,900 deaths/yr; at mOS ~8mo, prevalent ≈ 8,900 × (8/12) ≈ 5,900. Both methods bracket ~6,000–7,500; point estimate ~7,000.Abbreviations: TAM - Total Addressable Market •Progressed on prior systemic therapy (platinum-based chemo +/-anti-PD-1/PD-L1)•KEAP1, NFE2L2 or PIK3CA pathway gene alteration•All histologies (adenocarcinoma and squamous)Label population may be broader than biomarker-selected subsets CLINICAL DEVELOPMENT: LUNG
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35© 2026 Faeth Therapeutics. Paik PK et al. J Thorac Oncol.2023;18(4):516–526 Vehicle Control Sapanisertib Tumor Volume (mm3) Everolimus Days Post Implantation LK-2 Squamous cell lung cancer xenograft tumor model (NFE2L2 E79K mutant) Sapanisertib showed benefit versus everolimusSapanisertib 3 mg/kg PO QDEverolimus 3 mg/kg PO QD Sapanisertibshows preclinical efficacy in lung cancer models CLINICAL DEVELOPMENT: LUNG
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36© 2026 Faeth Therapeutics. — Phase 2 NSCLC Trial: Sapanisertib demonstrated benefits Paik PK et al. J Thorac Oncol.2023;18(4):516–526. Abbreviations: ORR - Overall Response Rate, OS - Overall Survival, DoR - Duration of Response, CBR - Clinical Benefit Rate, QoL - Quality of Life, PFS - progression free survival, HR - Hazard Ratio, CI - Confidence Interval Key results Sapanisertib monotherapy:25% ORR and mPFS of 8.9 months in patients with NFE2L2-altered squamous NSCLC First successful metabolic targeting of NSCLCand potentially the first genotype-directed therapy for LUSCPIKTOR implications Established single-agent proof of conceptfor mTORC1/2 inhibition in this biomarker-defined population. PIKTOR adds PI3K-alpha inhibition (serabelisib) on top of sapanisertib —multi-node blockade may further enhance depth and durability of response FDA granted Fast Track designation to sapanisertib for NRF2-mutated squamous lung cancer based on these results KRAS mutNFE2L2 mutKEAP1 mutTime from C1D1 (months)% Change Target Lesion Size CLINICAL DEVELOPMENT: LUNG
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37© 2026 Faeth Therapeutics. — Key patentsComposition of Matter• Serabelisib API• Sapanisertib APIMay 2037•Issued COM patents for each API•COM expiry date includes patent term adjustment (PTA) and expected 5 years of patent term extension (PTE) added to serabelisib COM patentPIKTOR + ISD Method of Treatment for CancerMay 2039•Issued Patent•Covers use of PIKTOR + ISD in a range of tumor typesPIKTOR Method of Treatment for CancerPending(March 2046 = 20-year)•Patent Filed March 2025•Endometrial and Breast cancerSapanisertib Method of Treatment for CancerPending(Oct. 2046 = 20-year)•Patent Filed Oct. 2025•Ovarian CancerOpportunity for novel composition of matter IPFormulation development ongoingTarget patent filing = 2027(20-year expiry ~2048)•Development work ongoingGlobal exclusive licenses for Serabelisib and Sapanisertib, from Takeda for all oncology indications SUBJECT MATTER PATENT EXPIRATION DATE NOTESIP
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38© 2026 Faeth Therapeutics. — Focused pipeline of potentially best-in-class product candidates, leveraging Faeth’s unique metabolic insightsPIPELINE AND PROGRAM TARGET POPULATION PRECLINICAL PHASE I PHASE II PHASE III PIKTOR PIK-201Oncology:Endometrial PIKTOR PIK-101Oncology: Breast OTHERNEAAR: Formulated amino acids (+ Chemo / Radiation) Oncology: Rectal (IIT) OTHERIEM: Small molecule targeting amino acid metabolismPediatric: Rare Disease/NeuroSAPANISERTIB Other IndicationsOncology:Ovarian INTRODUCTION Oncology:Lung Abbreviations: NEAAR - non-essential amino acid restriction, IEM - inborn error of metabolism
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39© 2026 Faeth Therapeutics. 39Thank you