Sensei Biotherapeutics, Inc. · NASDAQ:SNSE
Sensei Biotherapeutics — Faeth Therapeutics — Investor Day (October 2026)
84 slides from Sensei Biotherapeutics's investor day presentation, Oct 6, 2026
Slide 1: Inaugural Investor/Analyst Day
FAETH THERAPEUTICS Inaugural Investor/ Analyst Day OCTOBER 6, 2026 1
Slide 2: Forward-Looking Statements
— Forward-Looking Statements This Presentation contains forward-looking statements of Faeth Therapeutics, Inc. (the “Company”) within the meaning of the federal securities laws. Words such as “may,” “will,” “should,” “could,” “believe,” “expect,” “anticipate,” “intend,” “plan,” “estimate,” “potentia
Slide 3: PIKTOR - one regimen, multiple high value opportunities
INTRODUCTION — PIKTOR - one regimen, multiple high value opportunities Designed for broad activity across PI3K-mutant and wild-type tumors, with near-term focus on endometrial and breast cancers Co-founded by Dr. Lewis Cantley - discoverer of the PI3K pathway Oral, multi-node PI3K/AKT/mTOR (PAM) inh
Slide 4: Agenda
INTRODUCTION — 10:00 AM Introduction Anand Parikh, Co-founder and CEO 10:15 AM PAM overview and single-node inhibitor escape Dr. Marcus Goncalves, Scientific co-founder 10:30 AM Preclinical and Translational data review Dr. Oliver Maddocks, Co-founder and CSO 10:45 AM Clinical Dr. Debbie Chirnomas,
Slide 5: Focused pipeline of potentially best-in-class product candidates
INTRODUCTION — Focused pipeline of potentially best-in-class product candidates, leveraging Faeth’s unique metabolic insights PIPELINE AND PROGRAM TARGET POPULATION PRECLINICAL PHASE I PHASE II PHASE III Oncology: PIKTOR PIK-201 Endometrial Oncology: PIKTOR PIK-101 Breast Oncology: Ovarian SAPANISER
Slide 6: Faeth scientific co-founders
INTRODUCTION — Built on work by Dr. Lewis Cantley, discoverer of the PI3K pathway. Molecules designed by Kevan Shokat, one of the world’s leading medicinal chemists FAETH SCIENTIFIC CO-FOUNDERS Lew Cantley, PhD Sid Mukherjee, MD PhD Dana Farber Cancer Institute, Asst. Prof., Columbia, Pulitzer Prize
Slide 7: PAM is one of the most frequently altered pathways in cancer
INTRODUCTION — PAM is one of the most frequently altered pathways in cancer 7
Slide 8: PAM is one of the most frequently-altered pathways in cancer
INTRODUCTION — PAM is one of the most frequently-altered pathways in cancer PAM pathway alterations by tumor type % PAM altered cBioPortal (~21,000 patients) 8
Slide 9: Embedded feedback loops create a challenge for single-node inhibitors
INTRODUCTION — Embedded feedback loops create a challenge for single-node inhibitors Feedback Loop 1 PI3K → insulin → PI3K PI3K-alpha inhibitor Feedback Loop 2 mTOR → S6 → AKT mTORC1 inhibitor 9
Slide 10: Multi-node inhibition is the key to unlocking PAM inhibition
INTRODUCTION — We believe that multi-node inhibition is the key to unlocking the promise of PAM inhibition The Problem: The Problem: 1. Feedback reactivation prevents single-node inhibitors from 1. Feedback reactivation prevents single-node inhibitors fully suppressing the pathway, even at high dose
Slide 11: PIKTOR: potent and selective multi-node PI3K/AKT/mTOR inhibition
INTRODUCTION — PIKTOR: Designed for potent and selective multi-node PI3K/AKT/mTOR pathway inhibition PIKTOR combines serabelisib (PI3K-alpha specific inhibitor) with sapanisertib (mTORC1 and mTORC2 inhibitor). serabelisib PI3K-alpha PIKTOR specific inhibitor Targeting the PI3K/AKT/mTOR pathway to sa
Slide 12: Multi-nodal inhibition broadens the treatable landscape
INTRODUCTION — Multi-nodal inhibition broadens the treatable landscape relative to single-node approaches PAM pathway alterations by tumor type PIK3CA mutation only PAM Pathway (+/- PIK3CA) PIK3CA mutation only % PAM altered cBioPortal (~21,000 patients) 12
Slide 13: Company history
INTRODUCTION — Company history Founded 2019 Faeth Therapeutics established around the hypothesis that simultaneously suppressing multiple nodes of a pathway produces deeper, more durable tumor suppression than targeting any single node alone Serabelisib in-licensed 2021 Initial work exploring combin
Slide 14: Takeda has already done much of the legwork for us
INTRODUCTION — Takeda has already done much of the legwork for us… PIKTOR asset history 2020 2021 2022 2023 Now Takeda Petra in-licensed serabelisib Faeth in-licensed serabelisib develops1 serabelisib Takeda Faeth in-licensed sapanisertib develops1 Calithera in-licensed sapanisertib sapanisertib Fir
Slide 15: PIKTOR: Designed to solve the challenges of drugging the PI3K pathway
INTRODUCTION — PIKTOR: Designed to solve the challenges of drugging the PI3K pathway MULTI-NODE SINGLE-NODE PIKTOR GEDATOLISIB MUTANT-SPECIFIC FDA-APPROVED Celcuity (Ph.3, Breast) Relay, Lilly, OnKure, Novartis Alpelisib, Everolimus, (Ph.2, Endometrial, Ph.1b Breast) (Ph.1/2, Breast) Capivasertib, I
Slide 16: PIKTOR has three potential advantages
INTRODUCTION — PIKTOR has three potential advantages: efficacy, tolerability and patient experience Efficacy Tolerability Patient Experience Oral multi-node inhibition designed for longer Patient-centric oral regimen designed to Hyperglycemia AEs 3, 4 duration of target coverage, achieving ~2–3x rep
Slide 17: Oral PIKTOR dosing designed for sustained exposure with reduced Cmax toxicity
INTRODUCTION — Oral PIKTOR dosing is designed for sustained exposure with reduced Cmax-related toxicity risk Plasma protein Peak Time above binding / free exposure IC90 / fraction (Cmax : IC90 week ratio) Bound Free Multiple of IC90 (log scale) Serabelisib 2.2 42 h 69% 31% Higher Stomatitis Risk for
Slide 18: Where we are, Where we're going
INTRODUCTION — Where we are, Where we’re going Our strategy is to prove that PIKTOR’s RP2D in endometrial is clinically active, potentially enabling us to rapidly dose-escalate in breast cancer, and sequentially un-lock the potential of multi-node PAM inhibition in multiple cancers TAM BJC publicati
Slide 19: Marcus Goncalves, MD PhD
INTRODUCTION — Marcus Goncalves, MD PhD Current roles Academic background Weill Cornell Medicine ● Associate Professor of Endocrinology Postdoc / Ass. Professor ● Associate Professor Department of Radiation Oncology Memorial Sloan Kettering ● Director, Holman Division of Endocrinology, Endocrinology
Slide 20: PAM Overview and Single-Node Inhibitor Escape
FAETH THERAPEUTICS PAM Overview and Single-Node Inhibitor Escape OCTOBER 6, 2026 20
Slide 21: Overview
PAM OVERVIEW — Overview Dr. Marcus Goncalves, Scientific co-founder 1 Uncovering the flaws in single-node PI3K inhibition approaches 2 Explaining the origins of PI3K-inhibitor induced hyperglycemia 3 Setting the scene for multi-node PAM inhibition 21
Slide 22: Post-meal Glucose and Insulin
PAM OVERVIEW — Post-meal Glucose and Insulin Adapted from P.D. Home Diabetes, Obesity and Metabolism 17: 1011–1020, 2015 22
Slide 23: Muscle dominates insulin-stimulated glucose disposal
PAM OVERVIEW — Muscle dominates insulin-stimulated glucose disposal Tumor Width of glucose flows proportional to uptake. Rounded Study estimates. Glucose uptake by brain not Ramos et al. JCEM 2020 23 included as not insulin dependent. DeFronzo et al JCI 1985
Slide 24: Identifying the flaws in Single-Node PAM inhibition
PAM OVERVIEW — Identifying the flaws in Single-Node PAM inhibition ↑ Insulin Hyperglycemia ↓Muscle glucose uptake Tumor PI3Ka blockade in PI3K-alpha inhibitor cell peripheral muscle 24
Slide 25: Marcus
01 Normal insulin response TUMOUR CELL There utic targe > m2 1 fal Growth / survival signalling 02 PI3Ka inhibition 03 Reduced glucose uptake 04 Hyperglycaemia SKELETAL MUSCLE Insulin-responsive glucose disposal BLOOD ®@ @ @ Glucose @@ ® @ ® @ e@ Membrane GLUTA J Insulin receptor PI3Ka AKT GLUT4 tra
Slide 26: Influence of hepatic glucose production is outweighed by glucose disposal
PAM OVERVIEW — Influence of hepatic glucose production is outweighed by glucose disposal Insulin dependent (PI3K inhibitor responsive) glucose metabolism Dietary Carbohydrate Intake Hepatic Systemic 4.7 Glucose Production Glucose Rate Pool 1.9 Glucose Liver Muscle Disposal Rate Primarily Muscle Nine
Slide 27: Breaking the glucose/insulin feedback loop improves efficacy
PAM OVERVIEW — Breaking the glucose/insulin feedback loop improves efficacy Insulin Suppressing ↑ Insulin Diet Hyperglycemia ↓Muscle glucose uptake Tumor PI3Ka blockade in PI3K-alpha inhibitor cell peripheral muscle 27
Slide 28: Breaking the glucose/insulin feedback loop improves efficacy
PAM OVERVIEW — Breaking the glucose/insulin feedback loop improves efficacy Control Control Control Control PI3Ki ISD PI3Ki + ISD PI3Ki + ISD + Insulin Tumour Volume (cm3) Tumour Volume (cm3) Tumour Volume (cm3) Tumour Volume (cm3) Drug alone Insulin suppression alone Drug + insulin suppression Drug
Slide 29: Towards Multi-Node: PI3K inh. + ISD converges on mTOR
PAM OVERVIEW — Towards Multi-Node: PI3K inh. + ISD converges on mTOR Insulin Suppressing Vehicle Control Diet PI3Ka inhibitor PI3Ka inh. + Diet Complete pathway Phospho- inhibition associated Insulin Receptor with preclinical efficacy mTORC2 target Phospho-AKT mTORC1 target Phospho-S6 Hopkins et. al
Slide 30: mTORC1 and mTORC2 signaling are vital for PAM activity
PAM OVERVIEW — mTORC1 and mTORC2 signaling are vital for PAM activity mTOR is a vital coordinator of pathway activity and reactivation in the setting of PI3K inhibitors Multi-node inhibition at PI3K and mTOR are associated with strong anti-tumor response Pharmacologic mTOR inhibition may improve the
Slide 31: Single-Node PAM inhibitors have numerous resistance mechanisms
PAM OVERVIEW — Single-Node PAM inhibitors have numerous resistance mechanisms 31 Tyrakis et. al., BJC, 2025, Lero et al JBC, 2026
Slide 32: Multi-Node Inhibition & Hyperglycemia: Part 1
PAM OVERVIEW — Multi-Node Inhibition & Hyperglycemia: Part 1 Why the Multi-Node mechanism reduces hyperglycemia More complete inhibition of the pathway enables lower relative doses versus single-node e.g. serabelisib 4.5x lower dose as multi-node combo Multi-Node ‘spreads’ the hit to mTOR PI3K/AKT a
Slide 33: Multi-Node Inhibition & Hyperglycemia: Part 2
PAM OVERVIEW — Multi-Node Inhibition & Hyperglycemia: Part 2 Why route of administration is unrelated Muscle, not liver, is the primary site of glucose disposal and PI3K inhibition in muscle is what drives hyperglycemia; IV drugs impact muscle as much or more-so than oral drugs Study Regimen Any gra
Slide 34: Multi-node oral PAM inhibition could improve efficacy and tolerability
PAM OVERVIEW — Multi-node oral PAM inhibition has the potential to improve efficacy and tolerability Building on the clinical success of Gedatolisib …With a deep understanding of the biology Blocking multiple nodes at once keeps the feedback PI3Kα mediates insulin signaling in skeletal muscle. loops
Slide 35: Oliver Maddocks
PRECLINICAL AND TRANSLATIONAL — Oliver Maddocks Current roles Academic background University of Glasgow ● Chief Scientific Officer and Co- Professor of Cancer Biology and Metabolism Founder of Faeth ● Honorary Professor of Cancer Beatson Institute Postdoctoral Fellow Biology and Metabolism, Universi
Slide 36: Preclinical → Clinical
FAETH THERAPEUTICS Preclinical → Clinical OCTOBER 6, 2026 36
Slide 37: Overview
PRECLINICAL AND TRANSLATIONAL — Overview Dr. Oliver Maddocks, Co-founder and CSO 1 PIKTOR Mechanism of Action 2 Preclinical Data 3 PK-PD → Dose Selection 37
Slide 38: Towards Multi-Node: PI3K inh. + ISD converges on mTOR
PAM OVERVIEW — Towards Multi-Node: PI3K inh. + ISD converges on mTOR Insulin Suppressing Vehicle Control Diet PI3Ka inhibitor PI3Ka inh. + Diet Complete pathway Phospho- inhibition associated Insulin Receptor with preclinical efficacy mTORC2 target Phospho-AKT mTORC1 target Phospho-S6 Hopkins et. al
Slide 39: Adding sapanisertib - highly potent 2nd gen. mTOR inh
PRECLINICAL AND TRANSLATIONAL — Adding sapanisertib - highly potent 2nd gen. mTOR inh serabelisib PI3K-alpha PIKTOR specific inhibitor sapanisertib mTORC1 and mTORC2 inhibitor 39
Slide 40: Sapanisertib
PRECLINICAL AND TRANSLATIONAL — Sapanisertib First generation (rapalog) Everolimus structure. Rapamycin was derived from Streptomyces inhibitors of mTOR only target hygroscopicus, Easter Island. the mTORC1 complex via drug-FKBP12 complexation, Rapalogs target FKBP12 which they are not ATP competitiv
Slide 41: Serabelisib
PRECLINICAL AND TRANSLATIONAL — Serabelisib Serabelisib is an investigational, orally available, selective small molecule inhibitor of the class I phosphoinositide 3-kinase (PI3K) alpha isoform (PIK3α, encoded by PIK3CA gene). PI3K enzymes rely on ATP to phosphorylate phosphatidylinositol-4,5-bispho
Slide 42: Multi-node pharmacologic inhibition could be a more durable approach
PRECLINICAL AND TRANSLATIONAL — Multi-node pharmacologic inhibition has the potential to be a more durable approach. PIKTOR reduced PI3K-pathway signalling in cancer cell lines more than single-node inhibitors at clinically relevant concentrations¹ AN3CA Endometrial Cancer Cell Line ● PIK3CA Wild-ty
Slide 43: PIKTOR: Consistent pathway inhibition irrespective of genotype
PRECLINICAL AND TRANSLATIONAL — PIKTOR: Consistent pathway inhibition at S6/4E-BP1/AKT in breast and endometrial models irrespective of genotype 43 Figure 2a, b: 1Tyrakis et. al., (2025) British Journal of Cancer, 133: 144-154.
Slide 44: PIKTOR demonstrated preclinical pathway suppression at lower concentrations
PRECLINICAL AND TRANSLATIONAL — PIKTOR demonstrated preclinical pathway suppression at lower concentrations than other PI3K/AKT/mTOR targeted agents Cell Line PI3K-Pathway Status Serabelisib 1 Sapanisertib 1 PIKTOR 1 Gedatolisib 2 Alpelisib 1 Everolimus 1 Capivasertib 1 RLY-2608 1 STX-478 1 Inavolis
Slide 45: PIKTOR achieved effective in vivo tumor growth inhibition
PRECLINICAL AND TRANSLATIONAL — PIKTOR achieved effective in vivo tumor growth inhibition MDA-MB-361 Breast Cancer Model AN3CA Endometrial Cancer Model Vehicle Vehicle + ISD Vehicle Paclitaxel Vehicle + ISD PIKTOR Paclitaxel PIKTOR + ISD PIKTOR PIKTOR + Paclitaxel PIKTOR + ISD PIKTOR + Paclitaxel +
Slide 46: Overview
PRECLINICAL AND TRANSLATIONAL — Overview Dr. Oliver Maddocks, Co-founder and CSO 1 PIKTOR Mechanism of Action 2 Preclinical Data 3 PK-PD → Dose Selection 46
Slide 47: Takeda C32001 trial informed PIKTOR dose and schedule
PRECLINICAL AND TRANSLATIONAL — Takeda C32001 trial informed PIKTOR dose and schedule Typical later-line, treatment-refractory Phase 1 cohort with predominantly metastatic cancer (NCT01899053) ● Heavily pretreated, advanced solid-tumour population that had exhausted standard therapy ● ~62% had Stage
Slide 48: PK-PD Analysis in human subjects (C32001)
PRECLINICAL AND TRANSLATIONAL — PK-PD Analysis in human subjects (C32001) Source: Exposure/Response Analysis of an oral Multi-Node PI3K/AKT/mTOR pathway inhibitor combination of Serabelisib and Sapanisertib. Summit for novel therapeutics in oncology and precision medicine, August 2026 48 (https://in
Slide 49: Dose selection based on human PK-PD (C32001)
PRECLINICAL AND TRANSLATIONAL — Dose selection based on human PK-PD (C32001) Source: Exposure/Response Analysis of an oral Multi-Node PI3K/AKT/mTOR pathway inhibitor combination of Serabelisib and Sapanisertib. Summit for novel therapeutics in oncology and precision medicine, August 2026 49 (https:/
Slide 50: Endometrial RP2D PK versus PD / efficacy thresholds
PRECLINICAL AND TRANSLATIONAL — Endometrial RP2D PK versus PD / efficacy thresholds Source: Exposure/Response Analysis of an oral Multi-Node PI3K/AKT/mTOR pathway inhibitor combination of Serabelisib and Sapanisertib. Summit for novel therapeutics in oncology and precision medicine, August 2026 50 (
Slide 51: Oral PIKTOR dosing designed for sustained exposure with reduced Cmax toxicity
PRECLINICAL AND TRANSLATIONAL — Oral PIKTOR dosing is designed for sustained exposure with reduced Cmax-related toxicity risk Plasma protein Peak Time above binding / free exposure IC90 / fraction (Cmax : IC90 week ratio) Bound Free Multiple of IC90 (log scale) Serabelisib 2.2 42 h 69% 31% Higher St
Slide 52: Dr. Debbie Chirnomas
CLINICAL — Dr. Debbie Chirnomas Current role Background Arvinas ● Chief Medical Officer, Faeth VP, Oncology Clinical Development Gamida Cell VP, Clinical Development Dr. Debbie Chirnomas, Pfizer Medical Director / Medical MD MPH Strategy Head Yale School of Medicine Assistant Professor, Director of
Slide 53: Clinical
FAETH THERAPEUTICS Clinical OCTOBER 6, 2026 53
Slide 54: Overview
CLINICAL — Overview Dr. Debbie Chirnomas, CMO 1 The ‘Why’ Behind Endometrial Endometrioid Cancer 2 How We Got Here 3 PIK-201 Today & Read-Through to Breast 54
Slide 55: Multi-nodal inhibition potentially broadens the treatable landscape
CLINICAL — Multi-nodal inhibition potentially broadens the treatable landscape relative to single-node approaches PAM pathway alterations by tumor type PIK3CA mutation only PAM Pathway (+/- PIK3CA) cBioPortal (~21,000 patients) 55
Slide 56: Endometrial Cancer is a rising and underserved indication
CLINICAL — Endometrial Cancer (EC) is a rising and underserved indication The most common gynecological cancer (+68k new U.S. cases annually) From 2015 - 2025 Unlike many cancers, both new cases and mortality are increasing ↑26% High unmet need Incidence Chemotherapy remains the backbone, with very
Slide 57: How we got here: Han et al, 2023 Study Design
CLINICAL — How we got here: Han et al, 2023 Study Design Randomized phase 2, open-label, four arms (NCT02725268) 241 randomized Randomized 1:1:1:1 Outcomes 234 treated 28 Day Cycles Paclitaxel 80 mg/m² IV Median PFS Advanced, recurrent (primary endpoint) Days 1, 8, 15; n=87 endometrial cancer 3.7 vs
Slide 58: How we got here: Han et al, 2023
CLINICAL — How we got here: Han et al, 2023 Safety population, n (%) Paclitaxel Paclitaxel + Sapanisertib Sapanisertib Sapanisertib + Serabelisib n=87 n=86 n=41 n=20 CR 2 (2.3) 2 (2.3) 0 0 PR 14 (16.1) 19 (22.1) 2 (4.9) 0 SD 34 (39.1) 48 (55.8) 12 (29.3) 7 (35.0) SD ≥16 weeks 16 (18.4) 23 (26.7) 5 (
Slide 59: Taxane resistance activates PI3K/AKT/mTOR signaling, sensitive to PIKTOR
CLINICAL — Taxane resistance activates PI3K/AKT/mTOR pathway signaling in cancer models, sensitive to inhibition by PIKTOR Taxane resistance activates Taxane resistant cells retain sensitivity to PIKTOR PAM Pathway Tyrakis et. al., (2025) British Journal of Cancer, 133: 144-154. 59
Slide 60: Building on the Starks et al Phase 1b
CLINICAL — Building on the Starks et al Phase 1b Advanced Solid Tumors Sapanisertib / Serabelisib Cohort 1: 2mg / 100mg (Pac 60mg/m2) Advanced solid tumors Cohort 2: 2mg / 200mg (Pac 60mg/m2) All-comers (mutation agnostic) Cohort 3: 2mg / 200mg (Pac 80mg/m2) Second line or later3 3mg / 200mg (Pac 80
Slide 61: Ph1b: PIKTOR + paclitaxel drove deep, durable responses
CLINICAL DEVELOPMENT: ENDOMETRIAL — Ph1b: PIKTOR + paclitaxel drove deep, durable responses 80% ORR in endometrial cancer ALL PATIENTS (RECIST EVALUABLE) 47% overall response rate 73% clinical benefit rate 71% ORR in patients with PI3K pathway mutation ● 7 response evaluable patients with PI3K pathw
Slide 62: Ph1b: durable responses in both PIK3CAmut and wt patients
CLINICAL DEVELOPMENT: ENDOMETRIAL — Ph1b: PIKTOR + paclitaxel showed durable responses in both PIK3CAmut and wt patients All RECIST Available Patients MTOR & AKT1 PIK3R1, PTEN, MTOR 47% Overall Response Rate TP53 PIK3R1 71% ORR in patients with PI3k pathway mutation KRAS, RB1, ERRFI1 TP53, NF1, CHEK
Slide 63: Hyperglycemia: PIKTOR compared to other PI3K compounds
CLINICAL DEVELOPMENT: ENDOMETRIAL — Hyperglycemia: PIKTOR compared to other PI3K compounds Hyperglycemia AEs 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 c
Slide 64: Stomatitis: PIKTOR compared to other PI3K compounds
CLINICAL DEVELOPMENT: ENDOMETRIAL — Stomatitis: PIKTOR compared to other PI3K compounds Stomatitis AEs 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-
Slide 65: PIK-201: Ph2 study of PIKTOR + paclitaxel in endometrial cancer
CLINICAL DEVELOPMENT: ENDOMETRIAL — PIK-201: A Ph2 Study with PIKTOR + paclitaxel in advanced endometrial cancer (currently enrolling) Eligibility Criteria Single arm (n≅40) Primary endpoint • ORR • Endometrioid endometrial • Sapanisertib 3 mg cancer • Serabelisib 200 mg Secondary endpoints • 2nd li
Slide 66: Endometrioid and HR+/HER2- BC share ER/PR dependence
CLINICAL DEVELOPMENT: ENDOMETRIAL, BREAST — Endometrioid and HR+/HER2- BC share ER/PR dependence Endometrioid ~80% of cases | hormone-dependent ● Estrogen driven — unopposed estrogen from obesity, anovulation, PCOS, and other causes ● ER/PR high ● PAM alterations in >80% of cases Non-endometrioid (s
Slide 67: Breast: Ongoing Phase 1b/2 trial design
CLINICAL DEVELOPMENT: BREAST — Breast: Ongoing Phase 1b/2 trial designed to rapidly identify recommended dose and initiate expansion cohorts Cohort A Cohort B Planned Cohort C PIKTOR + Fulvestrant PIKTOR + Fulvestrant + PIKTOR + Oral SERD ± Palbociclib Palbociclib B4 (optional): Sap 4 mg + Ser 300 m
Slide 68: Brian Stephenson
MARKET — Brian Stephenson Current roles Background BridgeBio Pharma ● Chief Financial Officer, Faeth CFO and Co-founder Capital IP Investment Partners Partner and Head of Life Sciences Leerink Partners Brian Stephenson, Director and Vice President PhD, CFA McKinsey & Company Manager Massachusetts In
Slide 69: Market Opportunity
FAETH THERAPEUTICS Market Opportunity OCTOBER 6, 2026 69
Slide 70: Overview
MARKET — Overview Brian Stephenson, CFO 1 Endometrial Cancer: Market opportunity 2 PIK-201 Benchmarks for success 3 HR+ Breast Cancer: Market opportunity 70
Slide 71: 2L+ endometrial market, rising unmet need, one PAM-pathway option
MARKET: ENDOMETRIAL — 2L+ endometrial market, rising unmet need, one PAM- pathway option Expanding market Endometrial cancer is a growing market and ADC PAM recently overtook ovarian as the most deadly 6+ sponsors · Ph2/33 1 oral multi-node program gynecological cancer (per SEER statistics) High unm
Slide 72: Relevant benchmarks for 2L+ Endometrial Cancer
MARKET: ENDOMETRIAL — Relevant benchmarks for 2L+ Endometrial Cancer ● Patients lack a consensus 2L+ standard-of-care once surgery with curative intent is no longer an option ● Re-challenge with taxane-based chemotherapies (paclitaxel or docetaxel) is the most common approach ● Patients with endomet
Slide 73: KEYNOTE-775 in more detail
MARKET: ENDOMETRIAL — KEYNOTE-775 in more detail ● KEYNOTE-775 readout in 2022 and at the time was the largest ever randomized trial in 2L endometrial cancer ● It tested pembrolizumab + lenvatinib vs. chemotherapy rechallenge. ● Chemotherapy rechallenge had 15% ORR (95% CI between 11–18%) and median
Slide 74: TroFuse-005: first large readout in post-chemo + I/O setting
MARKET: ENDOMETRIAL — TroFuse-005: The first large readout in a post-chemo + I/O setting ● Chemo I/O has since replaced platinum chemotherapy as the frontline treatment of choice in endometrial cancer ● KEYNOTE-775 is no longer the most contemporaneous bar. All patients in PIK-201 require prior trea
Slide 75: Potential changes to frontline could favorably impact PIKTOR
MARKET: ENDOMETRIAL — Potential changes to frontline could favorably impact PIKTOR ● Merck is currently exploring Sac-TmT in the frontline maintenance setting (TroFuse-033) ● Given the inability to sequence TOPO1-based ADCs, we would expect other developers to follow-suit U.S. New Uterine Cancer Cas
Slide 76: Estimated PIKTOR addressable U.S. population (2L+)
MARKET: ENDOMETRIAL — Estimated PIKTOR addressable U.S. population (2L+) U.S. Incident Therapeutic Build (Annual) Anticipated FDA Label Population U.S. New Uterine Cancer Cases1 ~68,000 Post-1L advanced/recurrent endometrioid EC • Endometrioid histology Endometrioid Histology (~80%)2 ~54,000 • Advan
Slide 77: Breast Cancer: PAM blockade more than doubles addressable market
MARKET: BREAST — Breast Cancer: PAM blockade more than doubles addressable market relative to mutant-selective inhibitors High unmet need HR+/HER2- patients comprise ~70% of all PI3K MUT PI3K WT + PI3K MUT metastatic breast cancer patients1 ~40% of HR+/HER2- breast cancer have 100% of HR+/HER2- PIK3
Slide 78: HR+/HER2- Advanced Breast Cancer potential
MARKET: BREAST HR+ / HER2- Advanced Breast Cancer HR+/HER2- PI3K WT PI3K MT Advanced Breast aBC endocrine sensitive BRCA Cancer potential future state PIKTOR + AI/SERD + CDK 4/6 PARP PARP 1L Gedatolisib + AI + CDK 4/6 inhibitor inhibitor We believe PIKTOR has the potential to become CDK4 inhibitor o
Slide 79: PIKTOR's reach potentially extends to virtually all 2L patients
MARKET: BREAST — PIKTOR’s reach potentially extends to virtually all 2L patients Multi-nodal inhibitors (PIKTOR and gedatolisib) are the only PAM treatments that are designed to work agnostic to mutational status PIK3CA mutant PIK3CA wild-type 18% 27% ESR1 SERD SERD 45% mutant Mutant-selective PI3Kα
Slide 80: PIKTOR could expand the reach of oral SERDs
MARKET: BREAST — We believe PIKTOR could expand the reach of oral SERDs To date, oral SERDs have only been approved in ESR1-mutant patients. Combining with PIKTOR could enhance activity in wild-type patients because endocrine resistance often runs through PAM. PIK3CA mutant PI3KCA wild-type ESR1 45%
Slide 81: HR+/HER2- breast cancer: Large unmet need
MARKET: BREAST — HR+/HER2- breast cancer: Large unmet need Three addressable patient populations from the ~48k advanced pool U.S. Incident Therapeutic Build (Annual) U.S. New Breast Cancer Cases1 ~48,000 ~$10B ~316,000 1L patients receiving U.S. TAM4 aromatase inhibitor + CDK4/6 HR+/HER2− Subtype (~
Slide 82: Closing Remarks
FAETH THERAPEUTICS Closing Remarks OCTOBER 6, 2026 82
Slide 83: $186.4M in cash expected to fund PIKTOR through anticipated readouts
KEY MILESTONES — $186.4M1 in cash expected to fund PIKTOR through anticipated readouts in endometrial cancer and breast cancer PROGRAM Achieved in 2026 2H 2026 2272027 2028+ Topline data readout; Last patient dosed + 6 ENDOMETRIAL Fast Track Designation Ph2 enrollment months data ongoing Trial initi
Slide 84: Thank you
faeth Thank you