Immunocore Holdings Plc · NASDAQ:IMCR
Immunocore — Q2 2025 Earnings Presentation
52 slides from Immunocore's earnings presentation, August 2025
Slide 1: Transformative immunomodulating medicines for patients
Transformative immunomodulating medicines for patients August 2025 1
Slide 2: Forward Looking Statements
Forward Looking Statements This presentation contains “forward-looking statements” within the meaning of the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. Words such as “may”, “will”, “believe”, “expect”, “plan”, “anticipate”, “estimate”, “continue” and similar expr
Slide 3: Harnessing the immune system with bispecific soluble TCRs
Harnessing the immune system to fight disease with targeted, off-the-shelf, bispecific, soluble T cell receptors (TCRs) Targeting >90% ImmTAX Proteome TCR therapeutics can target >90% of the human proteome 3
Slide 4: Platform candidates and capabilities across therapeutic areas
Platform candidates and capabilities across 3 therapeutic areas Oncology Infectious diseases Autoimmune diseases ImmTACs ImmTAVs ImmTAAIs Activation Downmodulation of the immune system of the immune system 4
Slide 5: Leading bispecific TCR pipeline
Leading bispecific TCR pipeline Candidate Target (HLA type) Indication IND-enabling Phase 1 Phase 2 Phase 3 Approved Uveal (ocular) melanoma On Market gp100-A02 Adjuvant uveal (ocular) melanoma ATOM sponsored by Phase 3 ongoing Phase 3 complete 2L+ advanced cutaneous melanoma TEBE-AM randomization |
Slide 6: Maximizing potential of KIMMTRAK in HLA-A02+ melanoma
Maximizing potential of KIMMTRAK ® in HLA-A02+ melanoma 6
Slide 7: KIMMTRAK is the global standard of care
KIMMTRAK is the global standard of care+ 4th year of launch; expecting continued moderate growth in 2025 2025 Drivers of growth: $192M1H 2025 net sales • U.S. community expansion • New launches $98.0M Q1’22 Q2’22 Q3'22 Q4'22 Q1’23 Q2’23 Q3'23 Q4'23 Q1'24 Q2'24 Q3'24 Q4'24 Q1'25 Q2'25 2022 2023 2024
Slide 8: KIMMTRAK active in cutaneous melanoma (CM)
KIMMTRAK active in cutaneous melanoma (CM) Phase 1/2 study of KIMMTRAK + checkpoints in CM patients who progressed on prior anti-PD1 Dosing frequency Weekly Monthly Time from prior 1-yr OS 2-yr OS anti-PD(L)1 Remained weekly Remote 75% 22% Immediately prior 75% 23% Durable Benchmark 55% N/A disease
Slide 9: TEBE-AM: Phase 3 trial in 2L+ cutaneous melanoma
TEBE-AM: Phase 3 trial in 2L+ cutaneous melanoma 1:1:1 Randomization Phase 3 Endpoint KIMMTRAK ~180 per arm Overall Survival R KIMMTRAK + anti-PD-1 ~180 per arm Straight to follow up (active control) ~180 per arm 1H 2026: expected enrollment completion 2L+ cutaneous melanoma market opportunity up to
Slide 10: Opportunity in 2L+ CM for off-the-shelf therapy with OS benefit
Opportunity in 2L+ CM for off-the-shelf therapy with OS benefit tebentafusp+/- Other Lifileucel2 pembrolizumab1 Status Ph 3 Accelerated approval Commonly used Supporting data Randomized Ph 3 Single arm Ph 2 — SoC re-treatment Autologous cell Therapy Biologic, off-the-shelf Chemotherapy therapy Clini
Slide 11: Rationale for KIMMTRAK in adjuvant uveal melanoma
Rationale for KIMMTRAK in adjuvant uveal melanoma Clinical activity expected to be highest in adjuvant setting with minimal disease burden In Phase 3 trial, highest clinical activity in tumors with ctDNA reduction in 1st line > 2nd+ line mUM minimal disease burden1 Largest metastatic lesion PFS Haza
Slide 12: ATOM – Phase 3 KIMMTRAK adjuvant UM trial design
ATOM – Phase 3 KIMMTRAK adjuvant UM trial design Global trial led by European Organisation for Research and Treatment of Cancer (EORTC) 1:1 Randomization Treatment phase Follow-up KIMMTRAK (tebentafusp) Key endpoints ~290 HLA-A*02:01 patients N ~145 (Q1W IV) Primary: Relapse-Free Survival (RFS) • Wi
Slide 13: KIMMTRAK has the potential to help up to 6K patients per year
KIMMTRAK has the potential to help up to 6K patients per year Rare gp100+ tumors <100* Investigator led up to Adjuvant uveal ATOM Phase 3 6,000* >1K* melanoma 2028+ patients 2L+ advanced Up to TEBE-AM Phase 3 cutaneous melanoma 4K* 2026 ~1K* APPROVED in 2022 Metastatic UM patients FY 2024 net sales
Slide 14: PRAME portfolio
PRAME portfolio IMMUNOCORE
Slide 15: Disease control is hallmark of ImmTAC
Based on data to date, disease control is hallmark of ImmTAC KIMMTRAK Brenetafusp late line mUM (IMCgp100-102) late line mCM1 (IMCgp100-201) late line mCM (IMCF106C-101) late line PROC2 (IMCF106C-101) OS benefit in Ongoing Ph3 study Ongoing Ph3 study Evaluating combos in PROC metastatic uveal melano
Slide 16: Maximizing PRAME portfolio over next 12-18 months
Maximizing PRAME portfolio over next 12-18 months 12 to 18 months Cutaneous Melanoma Phase 3 PRISM-MEL Randomizing Brenetafusp Ovarian Phase 1 combo Building on initial signals • Non-platinum chemo (PROC) • Platinum chemo (earlier line PSOC) • Bevacizumab (earlier line PSOC) Translatability between
Slide 17: Brenetafusp in cutaneous melanoma
Brenetafusp in cutaneous melanoma 17
Slide 18: CM demographics and baseline characteristics
CM Demographics and baseline characteristics Brenetafusp monotherapy and in combination with pembrolizumab Monotherapy + Pembro Patients were heavily pre-treated Characteristic N = 47 N=9 • All received prior checkpoint inhibitors (CPI) Age, yr – median (range) 64 (31-79) 65 (24-78) – Median 2 prior
Slide 19: Brenetafusp CM monotherapy was well-tolerated
Brenetafusp CM monotherapy was well-tolerated TRAE in ≥ 15% of patients (N = 47) Incidence of selected TRAEs Preferred Term (%) Any grade Grade 3/4 Any 43 (92%) 19 (40%) Cytokine release syndrome1 24 (51%) - Rash (composite)2 23 (49%) 1 (2%) Pyrexia 17 (36%) 1 (2%) Chills 13 (28%) - Lymphocyte decre
Slide 20: Clinical benefit characterized by durable disease control
Clinical benefit characterized by durable disease control Brenetafusp CM monotherapy (N = 36 evaluable*) PRAME positive group for efficacy analysis includes H-score ≥1 and pts with unknown PRAME IHC results. * 36/47 patients had baseline and at least one tumor assessment on treatment; 10 patients ha
Slide 21: Promising DCR for brenetafusp rationale for 1L Ph3
Promising DCR for brenetafusp rationale for 1L Ph3 (nivo + brene) Comparison to nivolumab and relatlimab + nivolumab 2L+ 1L mPFS 3.7m 3.1m 3.2m 3.3m 4.2m 4.6m 10.2m ? 56% 58% 60% 47% 11% 13% 13% 49% 38% 40% 43% 27% 9% 10% 8% 33% DCR 44% 45% 45% PR/CR 31% 28% SD 20% 16% 17% Chemo Nivo Rela + Nivo All
Slide 22: PRISM-MEL-301: Phase 3 trial in first-line advanced cutaneous melanoma
PRISM-MEL-301: Phase 3 trial in first-line advanced cutaneous melanoma Registrational trial currently enrolling patients Randomization Treatment phase Follow-up Key inclusion criteria • Previously untreated, advanced melanoma IMC-F106C + nivolumab (q4w) N ~325 • HLA-A*02:01 Key endpoints • No prospe
Slide 23: Brenetafusp in ovarian
Brenetafusp in ovarian IMMUNOCORE
Slide 24: Phase 1 ovarian demographics and baseline characteristics
Phase 1 ovarian demographics and baseline characteristics1 Mono Chemo Combo Patients were heavily pre-treated N = 37 N = 16 • Median 4-5 prior lines General • All platinum resistant, majority prior bevacizumab Age, median yr (range) 63 (40-80) 65 (47-72) (81%, 75%) and PARPi (59%, 75%) ECOG PS 0, n
Slide 25: Brenetafusp monotherapy & chemo combo well-tolerated
Brenetafusp, Phase 1 monotherapy & chemo combo, well-tolerated Treatment related adverse events (TRAE) frequency and severity attenuated over time Mono Chemo combo No TRAE leading to treatment discontinuation N = 37 N = 16 or death Preferred Term TRAE G3/4 TRAE† TRAE G3/4 TRAE† Monotherapy: ANY 36 (
Slide 26: Monotherapy benefit characterized by durable disease control
Monotherapy benefit characterized by durable disease control Monotherapy (N = 31 evaluable*) DCR mPFS, mo Treated beyond N ORR (PR+SD) (95% CI)† 6-mo OS rate† progression‡ All mono* 31 58% 6% 3.3 (2.1-4.0) 73% 64%, median 2 mo On therapy at Month 18 New lesion Month 12 but still on therapy thru Mont
Slide 27: Chemotherapy combination may enhance clinical benefit
Chemotherapy combination may enhance clinical benefit Chemo increases antigen presenting machinery Chemo increases antigen presenting machinery BOR, best overall response by RECISTv1.1; DCR, disease control rate; NE, non evaluable; ORR, overall response rate; PD, progressive disease; PR, partial res
Slide 28: Evaluating brenetafusp in ovarian cancer
Evaluating brenetafusp in ovarian cancer Multiple cohorts in ongoing Phase 1 trial Newly diagnosed Recurrent disease 1L 2L 3L 4L 5L+ Platinum doublet Platinum resistant & refractory (PROC) ± maintenance 2-4L: ~9,000 pts1 ~16,000 pts1 Non-platinum chemo PROC: ORR ~10 – 15% ORR ~<10% DCR ~50 – 60% DCR
Slide 29: Advancing PRAME candidates through a proven framework
Advancing PRAME candidates through a proven framework KIMMTRAK Brenetafusp Development Steps Uveal Cutaneous Cutaneous Serous melanoma melanoma melanoma ovarian Robust monotherapy activity? ctDNA reduction ✓ ✓ ✓ ✓ PR/CR/DCR ✓ ✓ ✓ ✓ OS rate ✓ ✓ ✓ ✓ Combinability with standard of care? – ✓ ✓ ✓ Ongoing
Slide 30: T Cell Fitness (TCF)
tness (TCF) T Cell Fi wW w 12) oO [@) Zz =) = 2
Slide 31: Phenotype of peripheral blood T cells may be important
Phenotype of peripheral blood T cells, which are recruited by brenetafusp, may be important for clinical activity Blood Hypothesis: Brenetafusp recruits Specific T cell subsets in the blood may peripheral blood T cells be associated with brenetafusp benefit into the tumor Baseline (CD3 T cell) Metho
Slide 32: Novel T cell fitness signature associated with ImmTAC benefit
Novel T cell fitness (TCF) signature associated with ImmTAC benefit TCF higher in earlier lines of therapy and highly correlated with naïve/Tscm cells Brenetafusp benefit in CM by TCF signature TCF signature in CM, by line of therapy High1 Low N = 483 N = 412 N = 21 N = 20 mPFS 6 mo 2 mo Higher ORR
Slide 33: Novel ImmTAC candidate for GI cancers from our discovery engine
Novel ImmTAC candidate for GI cancers from our discovery engine 33
Slide 34: IMC-R117C: First-in-class target PIWIL1 for colorectal & GI cancers
IMC-R117C: First-in-class target PIWIL1 for colorectal & GI cancers First patient randomized Q4 2024 PIWIL1 RNA in situ hybridization Negative prognostic marker in multiple cancers, role in tumor Normal colon Colon adenocarcinoma progression Expressed in CRC1, historically insensitive to IO, and acr
Slide 35: Pursuing a functional cure in infectious diseases
Pursuing a functional cure in infectious diseases 35
Slide 36: A cure is key to ending the HIV pandemic
A cure is key to ending the HIV pandemic Lifelong antiretroviral therapy (ART) globally is not a Goal of functional cure: sustainable solution • Reduce or eliminate rebound-competent reservoir • Benefits depend on lifelong adherence • Target viral levels < 200 copies/mL and enable stopping • Does no
Slide 37: Vast majority of HIV reservoir will not produce infectious virus
Vast majority of HIV reservoir will not produce infectious virus Depth of reservoir reduction that can enable PTC is not currently known HIV reservoir Cell-associated HIV RNA is very stable Integrated DNA Therapeutic antibodies e.g. vedolizumab minimally impact active reservoir 90% defective vs. 10%
Slide 38: After ART is stopped, HIV rebounds rapidly
After ART is stopped, HIV rebounds rapidly (median ~2 weeks) Vast majority have virus above transmission level (>200 c/mL) by Week 8 Individual viral rebound (382 PLWH / 24 trials) Time to first rebound 108 Plasma HIV RNA level (copies/mL) 107 >95% >200 copies/mL 106 105 104 103 Median ~2 weeks >50
Slide 39: HIV STRIVE Phase 1 multiple ascending dose enrolling
HIV STRIVE Phase 1 multiple ascending dose enrolling Goal is to determine safety and anti-viral activity of IMC-M113V Anti-Retroviral Therapy (ART) interrupted Key eligibility • PLWH on ART ART ART interruption ART • Initiated ART >3 mo Week 1 2 3 4 5 6 7 8 9 10 11 12 Weekly monitoring 24 after HIV
Slide 40: IMC-M113V is well tolerated, with only low grade CRS
IMC-M113V is well tolerated, with only low grade cytokine release syndrome Target dose (mcg) 15 / 30 / 60 20 / 40 / 120 20 / 40 / 300 Participants (n) 5 5 6 Cytokine release syndrome*: Grade 1 (Fever ≥ 38 oC) 0 0 5 Grade ≥ 2 (Fever + hypoxia or 0 0 0 hypotension) Other treatment related AEs: Headach
Slide 41: Significant reduction in cell-associated HIV Gag RNA
Significant reduction in cell-associated HIV Gag RNA and trend of reduction in intact HIV DNA after completion of multiple dose schedule Cell-associated HIV Gag RNA Intact HIV DNA 15 / 30 / 60 mcg 20 / 40 / 120 mcg 20 / 40 / 300 mcg 150 8000 4000 CA-RNA copies / 106 TBP 10000 n=6 n=5 n=5 n=3 copies/
Slide 42: Delayed viral rebound and/or control of viremia at target doses ≥120 mcg
Delayed viral rebound and / or control of viremia at target doses ≥120 mcg 15 / 30 / 60 mcg 20 / 40 / 120 mcg 20 / 40 / 300 mcg Plasma viremia (copies/ml) 10 8 Plasma viremia (copies/ml) 10 8 ATI extended Plasma viremia (copies/ml) 10 8 5 evaluable 10 7 10 7 10 7 10 6 10 6 10 6 10 5 105 c/ml 10 5 10
Slide 43: Pioneering tissue-specific immune downmodulation for autoimmune diseases
Pioneering tissue- specific immune downmodulation for treatment of autoimmune diseases 44
Slide 44: Our vision for autoimmunity and inflammation
Our vision for autoimmunity and inflammation: tissue‐specific down modulation of the immune system Vision for autoimmunity and ImmTAAI ImmTAAI Mechanism inflammation landscape Tissue-tethered targeting of Current HLA-family of molecules Systemic immune Suppresses T cell activity only when suppressio
Slide 45: Inhibition of T cell activity only when tethered to target cell
Inhibition of T cell activity only when tethered to target cell 120 NFAT activity (% of stim cont) Non-tethered, soluble PD1 agonist 100 T cell activity (%) Target cell 80 CR2113-H5 PD-1 agonist Raji CD1a- 60 CR2113-H5 PD-1 agonist Raji CD1a+ 40 ImmTAAI (red fluorescent) Tethered ImmTAAI Raji PD-L1
Slide 46: IMC-S118AI (PPI x PD1) for delay or prevention of T1D
IMC-S118AI (PPI x PD1) for delay or prevention of T1D ~50K newly diagnosed, HLA-A02+ type 1 diabetes (T1D) patients per year* 160 cell number in cell culture cells alone, no T cells 140 T1D: β cells killed by T cells cells + T cells 120 IMC-S118AI binds to pre-pro- IMC-S118AI insulin (PPI) pep
Slide 47: Ex vivo proof of confidence for IMC-S118AI
Ex vivo proof of confidence for IMC-S118AI Experiment in pancreatic slices from deceased donor with recent onset T1D IMC-S118AI binds to β-cells located Rate of T cell migration within and around pancreatic islets in pancreatic islet ns ns ns Significantly slower migration as Perfused IMC-S118AI T c
Slide 48: CD1a and Langerhans cell key roles in allergic inflammation
CD1a and Langerhans cell key roles in allergic inflammation1-4 CD1a expressed on Langerhans cell Langerhans cells Antigen presenting cell in skin and mucosa Healthy skin Monitor skin & trigger inflammation Present lipid and peptide antigens to activate T cells Antigens Presentation Polymorphism in h
Slide 49: IMC-U120AI: Universal candidate for dermatology
IMC-U120AI : Universal (non-HLA restricted) candidate for dermatology CD1a-tethered PD1 agonist ImmTAAI that blocks T cell activation by lipid and peptides PD1 agonist CD1a targeting effector domain CD1a reactive T cells Any PD1+ T cell CD1a+ Langerhans cell CD1a blockade on LC suppresses (LC) PD1 a
Slide 50: Leading TCR pipeline
Leading TCR pipeline IMMUNOCORE
Slide 51: Pioneering & delivering transformative immunomodulating medicines
Pioneering & delivering transformative immunomodulating medicines Priorities over the next year KIMMTRAK PRAME portfolio Infectious diseases HIV MAD data Expand leadership PRISM-MEL-301 position in mUM Phase 3 trial HBV SAD data TEBE-AM Phase 3 trial – Ovarian and NSCLC complete randomization Phase
Slide 52: Thank you
IMMUNOCORE Thank you