Captor Therapeutics Sa · GPW:CTX
Captor Therapeutics Sa — Investor Presentation (October 2025)
58 slides from Captor Therapeutics Sa's investor presentation, Oct 6, 2025
Slide 1: Pioneering targeted protein degraders for human health
Pioneering targeted protein degraders for human health H2 2025 Business Use Only | All rights reserved
Slide 2: Legal notice
Legal notice This document and the information contained herein (unless otherwise indicated) have been prepared by Captor Therapeutics S.A. (the “Issuer”) solely for informational purposes. For this notice, the presentation that follows shall mean and include the slides that follow, the oral present
Slide 3: Beyond the Pipeline
Beyond the Pipeline Beyond the Pipeline 3 Business Use Only | All rights reserved
Slide 4: Captor's Research in Print
Captor’s Research in Print Targeted degradation of GSPT1 and NEK7 by a molecular glue prodrug for treatment of HCC A Robust Crystallographic Platform for High-Throughput β-Catenin Ligand Discovery Exploration of chemical probes and conformational flexibility of GID4 - the substrate receptor of human
Slide 5: Captor Express
Captor Express CT 01: An innovative drug for liver cancer Technology Platform Changing the face of cancer treatment with MCL-1 degraders Redefining the future of cancer treatment with MCL-1 degraders 5 Business Use Only | All rights reserved
Slide 6: In the Spotlight
In the Spotlight CT-01 (ABS-752) featured by Drug Hunter as Molecule of the Month, June 2025 European Innovation Council (EIC) Accelerator grant for CT-03 Interview with Politykazdrowotna.com on discovering drug candidates in oncology 6 Business Use Only | All rights reserved
Slide 7: An experienced leadership team
An experienced leadership team Michal Walczak, PhD Anna Pawluk, PhD & MBA Tomáš Drmota, PhD Co-founder Chief Operating Officer Chief Technology Officer CEO and CSO • PhD ETH Zurich • PhD Wroclaw University • PhD Charles University • Post-doc at FMI Basel (Novartis • MBA WSH in Wroclaw • Post-doc at
Slide 8: Targeted Protein Degradation expected to unlock $974 bn by 2030
Targeted Protein Degradation expected to unlock $974* bn by 2030 protein of interest PoI DEGRADER PoI PoI E3 ligase proteasome degraded protein ubiquitin Degraders Inhibitors mAbs siRNA Removing multiple pathological functions 🗶 🗶 Oral bioavailability 🗶 🗶 Uncoupling PK from PD = prolonged…
Slide 9: Optigrade discovery platform – importance of structure
Optigrade discovery platform – importance of structure CRANBERRIES TULIPS OptigradeTM Platform BID discovery & optimization Rational Molecular Glues LILIS Novel E3 Ligases BID – Bifunctional Degraders OptigradeTM – addressing Molecular Glues, Bifunctional Degraders and novel E3 Ubiquitin Ligases 9 B
Slide 10: Fully-owned pipeline
Fully-owned pipeline # Target Indications Modality Discovery Pre-clinical CTA-enabling Phase I HCC, Lung cancer, Rare CT-01 GSPT1 & NEK7 cancers MG Neuroinflammation CT-02B NEK7 (Parkinson's Disease, ALS, MS) MG Systemic autoimmunity CT-02S NEK7 (IBD, Gout, Dermatological MG diseases) CT-03 MCL-1 Li
Slide 11: CT-01: First-in-Class GSPT1 Targeted Degrader for HCC
CT-01: for Hepatocellular First-in-Class Carcinoma GSPT1 Targeted (HCC) Degrader CT-01: First-in-Class GSPT1 Targeted Degrader for Hepatocellular Carcinoma (HCC) 11 Business Use Only | All rights reserved
Slide 12: CT-01: A first-in-class molecular glue prodrug degrader of GSPT1 & NEK7
CT-01: A first-in-class molecular glue prodrug degrader of GSPT1 & NEK7 Lung cancer 496k patients1,2 GSPT1 degradation leads to an Integrated Stress Response (ISR) and induction of apoptosis in HCC cells NEK7 degradation leads to reduction of IL-1𝛽 production – a well- established pro-carcinogenic…
Slide 13: Degradation of GSPT1 halts proliferation of cancer cells
Degradation of GSPT1 halts proliferation of cancer cells Target Biology and Therapeutic Rationale protein G1 to S phase transition 1 protein (GSPT1, eRF3a) is a translation termination factor that regulates mRNA translation1 GSPT1 GSPT1 and eRF1 form a translation termination complex that eRF1 facil
Slide 14: Degradation of GSPT1 induces apoptotic death in cancer
Degradation of GSPT1 induces apoptotic death in cancer NEK7 degradation attenuates tumor-microenvironment via IL-1β depletion protein GSPT1 degradation leads to apoptosis via induction Integrated Stress Response (ISR) An excellent opportunity for targeting of cancer cells that require translational
Slide 15: Dual GSPT1 & NEK7 degrader is in Phase 1 for liver cancer
Dual GSPT1 & NEK7 degrader is in Phase 1 for liver cancer CT-01 due to its mechanism & dual activity could become the-only-in class drug ABS-752 - Phase 1 clinical studies in hepatocellular carcinoma (HCC) Dose escalation initiated in May 2025 High unmet medical need in advanced HCC Est. market size
Slide 16: Standard of care fails to significantly extend lives of HCC patients
Standard of care fails to significantly extend lives of HCC patients Improvement of modest survival of patients offers accelerated path to approval Line of therapy Therapy Survival Benefit vs Sorafenib [months] FDA Approval 1 Tecentriq + Avastin +5.81 uHCC / mHCC 1 Imfinzi + Imjudo +2.72 uHCC 1/2 Ne
Slide 17: CT-01 is highly differentiated among GSPT1 degraders
CT-01 is highly differentiated among GSPT1 degraders Characteristics of CT-01 may provide disease-specific efficacy and high safety Antibody-conjugated Feature CT-01 (Captor) Systemic degraders degraders Targeting Degradation of GSPT1 and NEK7 Degradation of GSPT1 Degradation of GSPT1 Cell cytotoxic
Slide 18: Competitive landscape of GSPT1 degraders is highly attractive for CT-01
Competitive landscape of GSPT1 degraders is highly attractive for CT-01 The-only-in-class status of CT-01 offers strong partnering & commercialization position Tissue-activated degrader; dual selectivity Systemic degrader multiple other multiple other Antibody- conjugated degraders (DAC) Class Disco
Slide 19: CT-01 potently regresses fast growing HCC tumors in mice
CT-01 potently regresses fast growing HCC tumors in mice CT-01 efficiently degrades GSPT1 and NEK7 NSG_Hep3B CPT-5170* CT-01 CPT-6281, PO, BID Vehicle 10 mg/kg 10 mg/kg kDa Tumor volume [mm3] 75 Vehicle GSPT1 37 37 1 mg/kg NEK7 3 mg/kg 150 10 mg/kg Vinculin Day of treatment Regression of large tumor
Slide 20: Convincing tumor growth inhibition in HCC PDX models
Convincing tumor growth inhibition in HCC PDX models Results from Patient Derived Xenografts (PDXs) strongly translate to humans Tumor Growth Inhibition Tumor regression 10 randomly selected HCC patient samples to ensure patient-like responses Tumor growth inhibitions (TGI)of 40% or more observed in
Slide 21: Strong synergy of CT-01 in combination with everolimus
Strong synergy of CT-01 in combination with everolimus (eve) Everolimus and CT-01 display strong synergy via molecular pathway cross-talk HUH-7 Xenograft Model LI1097 HCC PDX Tumor volume [mm3] Tumor volume [mm3] Vehicle Vehicle CT-01, 30 mg/kg, BID CT-01, 100 mg/kg, BID Everolimus, 5 mg/kg, QD Ever
Slide 22: Phase I in HCC patients - study design
Phase I in HCC patients - study design PART 1 – MONOTHERAPY – CT-01 PART 2 – COMBOTHERAPY – CT-01 Part 1a – DOSE ESCALATION Part 1a – DOSE EXPANSION Part 2a – DOSE ESCALATION Part 2a – DOSE EXPANSION DLm+2 + Eve RDc -1 + Eve (12-20 subjects) DL7 RDm -1 (20 subjects) DL6 DLm+1 + Eve DL5 RDc + Eve (12
Slide 23: The-only-in-class potential of highly differentiated CT-01
The-only-in-class potential of highly differentiated CT-01 CT-01 opportunity due to high disease burden, fast growing market & unique activity Strong differentiation from other GSPT1 degraders (BMS, Monte Rosa) Best-in-class degradation profile Active degrader lingers inside cancer cells after activ
Slide 24: CT-03: First-in-Class MCL-1 Degraders for Liquid & Solid Tumors
CT-03: for Liquid First-in-Class Solid Tumors MCL-1 Degraders CT-03: First-in-Class MCL-1 Degraders for Liquid & Solid Tumors 24 Business Use Only | All rights reserved
Slide 25: CT-03: MCL-1 – a critical pathway for cancer resistance
CT-03: MCL-1 – a critical pathway for cancer resistance MCL-1 constitutes a gate to cancer immortality MCL-1 is one of the most amplified proteins in cancer† A critical resistance mechanism in hematological and solid tumors‡, cancer cells Breast Cancer require very high levels to avoid induction of
Slide 26: CT-03: MCL-1 – a critical pathway for cancer resistance
CT-03: MCL-1 – a critical pathway for cancer resistance MCL-1 is over-produced in up to 30% of cancers with acquired resistance MCL-1 MCL-1 biology and clinical relevance MCL-1 degrader MCL-1 is a well-characterized oncogenic protein with a key role in BAX INACTIVE evading apoptosis and promoting th
Slide 27: Targeted Protein Degradation is the only modality to break MCL-1
Targeted Protein Degradation is the only modality to break MCL-1 Classical drugs induce dramatic MCL-1 accumulation in healthy and cancer cells MCL-1 MCL-1 degraders advantage over inhibitors MCL-1 MCL-1 inhibitor degrader MCL-1 inhibitors induce strong accumulation of this MCL-1 protein in cells1.
Slide 28: Over $100billion market potential of MCL-1 targeting agents
Over $100billion market potential of MCL-1 targeting agents Classical drugs failed to address needs of this market due to their poor safety Haematological malignancies Multiple Myeloma Acute Myeloid Leukaemia Non-Hodgkin Lymphoma $53B by 20301 $6B by 20282 $16B by 20323 Selected solid tumors Small c
Slide 29: MCL-1 degraders remain safe to healthy tissues
MCL-1 degraders remain safe to healthy tissues Inhibitors induce MCL-1 accumulation toxic to healthy tissues Compound MCL-1 levels MCL-1 levels addition read-out read-out 0 24 48 Time [h] 24h 48h CT-03 MIK665 CT-03 MIK665 DMSO DMSO 0.01 0.01 0.1 0.1 0.1 0.1 10 10 kD 1 1 1 1 a 3 MCL-1 -100 7 100 PARP
Slide 30: High potency of MCL-1 degraders in an in vivo AML model
High potency of MCL-1 degraders in an in vivo AML model MCL-1 degraders demonstrate strong activity in mono- and combination therapies MONOTHERAPY COMBOTHERAPY Tumor volume [mm3] Vehicle, QD, PO/IV Tumor volume [mm3] Vehicle, QD/IV CT-03p*, 7.5 mpk CT-03p*,15 mpk Venetoclax,7.5 mpk CT-03p*, 25 mpk C
Slide 31: Degradation of MCL-1 in NHP after single IV dose of degraders
Degradation of MCL-1 in NHP after single IV dose of degraders Complete degradation of MCL-1 is safe to non-human primates WB data CT-03p* Internal ctrl Relative MCL-1 abundance Vehicle 0.03 mpk 0.1 mpk 0.3 mpk 1 mpk kDa CT-03p*, 0.03 mg/kg (mean) [%] -24 3 6 -24 3 6 -24 3 6 -24 3 6 CT-03p*, 0.1 mg/k
Slide 32: CT-03p shows great toxicokinetic profile
CT-03p shows great toxicokinetic profile TK and PK profiles demonstrate lasting and complete target coverage At all doses tested, CT-03p* shows plasma concentrations for 20 hours or longer at levels exceeding the estimated effective dose (DC50). Even the highest dose, 36 mg/kg, (70-120x above pHED)
Slide 33: CT-03 candidate drug with unmatched therapeutic window
CT-03 candidate drug with unmatched therapeutic window First-in-class MCL-1 degrader is poised to unlock the cancer resistance market Strong differentiation from MCL-1 inhibitors Pharmacology of MCL-1 degradation vs. pharmacology of accumulation (inhibitors) No accumulation of MCL-1 protein No cardi
Slide 34: Differentiation of MCL-1 degrader vs MCL-1 inhibitors
Differentiation of MCL-1 degrader vs MCL-1 inhibitors Clinical development of MCL-1 inhibitors limited by cardiotoxicity issues • Literature & experimental MOA now demonstrated for inhibitor induced toxicity • MCL-1 inhibitors cause MCL-1 accumulation in healthy tissue and necrosis MCL-1 degraders -
Slide 35: Summary: first-in-class MCL-1 degrader
Summary: first-in-class MCL-1 degrader • MCL-1 a well validated oncology target • Differentiation of degrader vs inhibitor modalities • MCL-1 inhibitors show cardiotoxicity in the clinic • Strong literature & experimental MOA now demonstrated for inhibitor induced toxicity • Protein degradation moda
Slide 36: CT-02: First-in-Class NEK7 Degraders
CT-02: First-in-Class Autoimmune Neuroinflammation (CT-02S), (CT-02B) NEK7 Degraders for CT-02: First-in-Class NEK7 Degraders for Autoimmune (CT-02S), Neuroinflammation (CT-02B) 36 Business Use Only | All rights reserved
Slide 37: NEK7 as a new target of the NLRP3 inflammasome pathway
NEK7 as a new target of the NLRP3 inflammasome pathway NEK7 overview TLR-L IL-1𝛽 PAMPs DAMPs NEK7 is master regulator of the NLRP3 inflammasome complex through its scaffolding function TLR IL-1R NEK7 KO/KD in mouse abrogates production of IL-1 beta in response to stimulating factors. Cell membrane…
Slide 38: NEK7 as a new target of the NLRP3 inflammasome pathway
NEK7 as a new target of the NLRP3 inflammasome pathway IL-1𝛽 inhibitors Differentiation (rilonacept, canakinumab) From anti-IL-1𝛽 antagonists: IL-1𝛽 receptor inhibitors Once daily oral administration instead of injection TLR-L IL-1𝛽 (anakinra) PAMPs DAMPs Uncoupling pharmacokinetics from…
Slide 39: NEK7 degradation as a differentiated intervention in NLRP3 pathway
NEK7 degradation as a differentiated intervention in NLRP3 pathway Degradation of NEK7 provides therapeutic benefit and maintains basal immunity Aberrant activation of NLRP3 INCREASED INFECTIONS, TOXICITY FROM NON-INFLAMMASOME FUNCTIONS OF NLRP3 NLRP3 inhibition COMPLETE INACTIVATION OF NLRP3 PARTIA
Slide 40: Potent degradation of NEK7 in human macrophages in vitro
Potent degradation of NEK7 in human macrophages in vitro CPT-635r CPT-732r 0.003 0.003 Conc. [µM] 0.03 0.03 0.01 0.01 0.1 0.1 10 10 Nigericin [5 µM] 1 1 kDa - - + + + + + + + + + + + + + + + 40 35 NEK7 55 ß-actin 40 180 130 Vinculin CPT-635r (CT-02S) and CPT-732r (CT-02B) degrade NEK7 protein dose-d
Slide 41: High selectivity of NEK7 molecular glue degraders
High selectivity of NEK7 molecular glue degraders CPT-764* CPT-635r CPT-732r CT-02S CT-02B DMSO CPT-635 CPT-732 kDa 10 10 10 Conc. [µM] 1 µM 1 µM 37 NEK7 NEK7 25 NEK7 37 CK1α 25 100 GSPT-1 -Log10(P-value) -Log10(P-value) 75 NEK1 75 NEK6 Ikaros NEK4 50 NEK2 p=0.01 p=0.01 NEK2 NEK9 75 ZFP91 NEK3 NEK6
Slide 42: CPT-635r efficiently covers & degrades NEK7 in NHPs after a single dose
CPT-635r efficiently covers & degrades NEK7 in NHPs after a single dose CT-02S CPT-635r [3 mg/kg] CPT-635r kDa 0h 3h 6h 24h 37 NEK7 25 20 150 Vinculin 100 NEK7 degradation in monkey PBMCs ex vivo at 3, 6, and 24 h after PO administration of CPT-635r [1 & 3 mg/kg] CT-02S (NEK7) CT-02S (NEK7) 42 Busin
Slide 43: High efficacy of CPT-635r with oral dosing in EAE mouse model in vivo
High efficacy of CPT-635r with oral dosing in EAE mouse model in vivo Disease progression in EAE model Clinical CT-02S Score Clinical Sign 0 Normal mouse; no overt signs of disease 0.5 Tail weakness/partial tail weakness (50% of length) 1 Loss of tail tonicity (complete tail paralysis)/ Limp tail Sh
Slide 44: Therapeutic potential of NEK7 degraders in Collagen-Induced Arthritis model
Therapeutic potential of NEK7 degraders in Collagen-Induced Arthritis model Clinical Clinical Sign Score CT-02S 0 No redness or swelling Sham control 1 Slight swelling in ankle and or redness in one toe Progressive swelling from ankle to midfoot and or Disease control 2 involvement of more than two
Slide 45: CPT-732r efficiently covers & degrades NEK7 in NHPs after a single dose
CPT-732r efficiently covers & degrades NEK7 in NHPs after a single dose CPT-732r [3 mg/kg] CT-02B CPT-732r kDa 0h 3h 6h 24h 37 NEK7 25 20 150 Vinculin 100 NEK7 degradation observed in monkey PBMCs isolated at 3, 6, and 24 h after PO administration of CPT-732r [1 & 3 mg/kg] CT-02B (NEK7) CT-02B (NEK7
Slide 46: CT-02S: Transforming the Treatment of Autoimmune Disorders
CT-02S: Transforming the Treatment of Autoimmune Disorders Activity confirmed in vitro in mouse, monkey and human cells and in vivo in mice and monkeys CT-02S CPT-635 Specificity-driven safety demonstrated in in vitro Peripheral autoimmunity analysis, in vivo tolerability studies and confirmed in NE
Slide 47: CT-02B: Breakthrough for Neurodegeneration
CT-02B: Breakthrough for Neurodegeneration Activity confirmed in vitro in mouse, monkey and CT-02B human cells and in vivo in mice and monkeys CPT-732 Neurodegenerative diseases Specificity-driven safety demonstrated in in vitro Growing evidence for role of pathological activation analysis, in vivo
Slide 48: CT-05: First-in-Class PKCӨ Degraders for Autoimmune Disorders
CT-05: for Autoimmune First-in-Class Disorders PKCӨ Degraders CT-05: First-in-Class PKCӨ Degraders for Autoimmune Disorders 48 Business Use Only | All rights reserved
Slide 49: PKCӨ: an undrugged high value target
PKCӨ: an undrugged high value target TCR Multiple sclerosis Allergy Asthma CD3 CD28 T-cell membrane Cytoplasm Myocarditis Breast cancer PKCӨ IL-2 Kidney injury IL-17 Gastrointestinal cancer Nucleus Inflammatory Bowel Psoriasis Disease CT-05 (PKC Ө) CT-05 (PKCӨ) 49 Business Use Only | All rights rese
Slide 50: PKCӨ Biology and target rationale
PKCӨ Biology and target rationale Target Biology and rationale PKCӨ Ser/Thr kinase PKCӨ has a thoroughly established role in regulatory and effector T cell functions1,2 MHCII A PRCKQ locus was shown associated with several immune-related B7 P diseases in multiple GWAS studies (type I diabetes, rheum
Slide 51: First-in-class PKCӨ degrader as an antibody-like activity in a pill
First-in-class PKCӨ degrader as an antibody-like activity in a pill Established a screening workflow that allows for discovery of PKCƟ degraders superior to existing inhibitors Highly selective for PKCƟ with no off-target toxicity Early stage of lead optimisation with 2 compounds has demonstrated: I
Slide 52: Optigrade Targeted Protein Degradation Platform
Optigrade Targeted Protein Degradation Platform Molecular glues Bifunctional Degraders Novel E3 ligases 652 Business Use Only | All rights reserved Business Use Only | Do not use without written consent of Captor Therapeutics Inc. © 2023
Slide 53: LiLis program: developing novel E3 ligases beyond CRBN
LiLis program: developing novel E3 ligases beyond CRBN Expanding the range of targets for effective degradation CRBN down regulation-driven resistance mechanisms in cancer Crowded IP space for CRBN binders Opportunity for cell type or cell compartment specificity In-house developed E3 ligase product
Slide 54: LiLis: new E3 Ligases
LiLisTM: new E3 Ligases N-degron pathway DesCEND pathway GID4 Ligase A* KLHDC2 Ligase B Ligase C Ligands available PROTACability PROTACability Fragments & X-ray Fragments & X-ray Stage & degraders confirmed confirmed structures structures tested SRS of an evolutionarily Expressed in cytosol conserve
Slide 55: Finance Highlights
Finance Highlights Finance Highlights 55 Business Use Only | All rights reserved
Slide 56: Financial and equity summary
Financial and equity summary Source: stooq.pl (Oct 2, 2025), H1 2025 report of Captor Therapeutics Michał Walczak: 16.6% Paweł Holstinghausen Holsten: Shares outstanding: 5,528,709 (October 2, 2025) 10.8% Market: Warsaw Stock Exchange (main market) ISIN: PLCPTRT00014 Non-founders: Sylvain Cottens: T
Slide 57: Captor Therapeutics S.A. ul. Duńska 11 54-427 Wrocław, Poland
ul. Duńska 54-427 Captor Hegenheimermattweg 4123 Contact: Allschwil, Therapeutics Wrocław, investor.relations@captortherapeutics.com 11 Switzerland Poland S.A. GmbH 167A Captor Therapeutics S.A. ul. Duńska 11 54-427 Wrocław, Poland Captor Therapeutics GmbH Hegenheimermattweg 167A 4123 Allschwil, Swi
Slide 58: Projects co-financed by the European Regional Development Fund
Projects co-financed by the European Regional Development Fund: Discovery and development of a new clinical drug candidate for the eradication of cancer stem cell in the treatment of hepatocellular carcinoma, through degradation of oncofetal transcription factor” (POIR.01.01.01-00-0740/19-00) Discov
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