Captor Therapeutics Sa · GPW:CTX
Captor Therapeutics Sa — Investor Presentation (May 2026)
72 slides from Captor Therapeutics Sa's investor presentation, May 5, 2026
Slide 1: Pioneering targeted protein degraders for human health
Pioneering targeted protein degraders for human health 2026 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: Captor Therapeutics: a clinical stage TPD company
Captor Therapeutics: a clinical stage TPD company • biotechnology company based in Wroclaw (Poland) and Basel (Switzerland) • all projects developed in Captor’s own drug discovery platform • develops first-in-class drugs • one of pioneers of targeted protein degradation (TPD) • viadrudomide (CT-01)
Slide 4: An experienced leadership team
An experienced leadership team Michal Walczak, PhD Anna Pawluk, PhD & MBA Adam Łukojć, PhD, CFA Co-founder Chief Operating Officer Chief Financial Officer Chief Executive Officer Cheif Scientific Officer • PhD Kozminski University • PhD ETH Zurich • PhD Wroclaw University • Certificates and licences
Slide 5: Pipeline
Pipeline Project name Target Indications Modality Discovery Pre-clinical IND-enabling Phase I Hepatocellular Viadrudomide GSPT1 & NEK7 carcinoma, lung cancer, MG (CT-01) rare cancers Vratitoclax MCL-1 Liquid & solid tumors BID (CT-03) Neuroinflammation CT-02B NEK7 (Parkinson's disease, MG ALS, MS) S
Slide 6: Mechanism of action of TPD-based drugs
Mechanism of action of TPD-based drugs ubiquitin polyubiquitinated MCL-1 proteasome CT-03 MCL-1 residues from degradation of MCL-1 E3 ligase degrader capable of binding (ubiquitinating molecule) to another MCL-1 molecule Very low doses due to catalytic action (shown for CT-01, CT-02 or MonteRosa GSP
Slide 7: Targeted Protein Degradation expected to unlock $974 bn by 2030
Targeted Protein Degradation expected to unlock $974* bn by 2030 Degraders Inhibitors mAbs siRNA Removing multiple pathological functions 🗶 🗶 Oral bioavailability 🗶 🗶 Uncoupling PK from PD = prolonged efficacy 🗶 🗶 Overcoming mutational resistance Targeting scaffolding function 🗶…
Slide 8: 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 8 B
Slide 9: Viadrudomide (CT-01): First-in-Class GSPT1 Targeted Degrader for HCC
Viadrudomide (CT-01): First-in-Class GSPT1 Targeted Degrader for Hepatocellular Carcinoma (HCC) Viadrudomide (CT-01): First-in-Class GSPT1 Targeted Degrader for Hepatocellular Carcinoma (HCC) 9 Business Use Only | All rights reserved
Slide 10: A first-in-class molecular glue prodrug degrader of GSPT1 & NEK7
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 factor.
Slide 11: Degradation of GSPT1 halts proliferation of cancer cells
Degradation of GSPT1 halts proliferation of cancer cells Target Biology and Therapeutic Rationale G1 to S phase transition 1 protein (GSPT1, eRF3a) protein is a translation termination factor that regulates mRNA translation1 GSPT1 and eRF1 form a translation termination complex that GSPT1 eRF1 facil
Slide 12: 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 of Integrated Stress Response (ISR) An excellent opportunity for targeting of cancer cells that require translation
Slide 13: Dual GSPT1 & NEK7 degrader is in Phase 1 for liver cancer
Dual GSPT1 & NEK7 degrader is in Phase 1 for liver cancer Viadrudomide due to its mechanism & dual activity could become the only-in-class drug Phase 1 clinical studies in hepatocellular carcinoma (HCC) Dose escalation initiated in May 2025 High unmet medical need in advanced HCC Est. market size of
Slide 14: Standard of care fails to significantly extend lives of HCC patients
Standard of care fails to significantly extend lives of HCC patients Improving modest survival: a path to accelerated 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 Nexavar 0.03 uHCC 2 Opd
Slide 15: Viadrudomide is highly differentiated among GSPT1 degraders
Viadrudomide is highly differentiated among GSPT1 degraders Characteristics of viadrudomide may provide disease-specific efficacy and high safety Antibody-conjugated Feature Viadrudomide Systemic degraders degraders Targeting Degradation of GSPT1 and NEK7 Degradation of GSPT1 Degradation of GSPT1 Ce
Slide 16: Competitive landscape of GSPT1 degraders is highly attractive
Competitive landscape of GSPT1 degraders is highly attractive The only-in-class status of viadrudomide offers strong partnering & commercialization position Tissue-activated degrader; dual selectivity Systemic degrader multiple other multiple other Antibody- conjugated degraders (DAC) Class Discover
Slide 17: Viadrudomide potently regresses fast growing HCC tumors in mice
Viadrudomide potently regresses fast growing HCC tumors in mice Viadrudomide efficiently degrades GSPT1 and NEK7 NSG_Hep3B CPT-5170* Viadrudomide 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 Regr
Slide 18: 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 i
Slide 19: Strong synergy of viadrudomide in combination with everolimus
Strong synergy of viadrudomide in combination with everolimus Everolimus (EVE) and viadrudomide 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
Slide 20: Phase I in HCC patients - study design
Phase I in HCC patients - study design PART 1 – MONOTHERAPY PART 2 – COMBOTHERAPY 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 (12-20 subjects) RD
Slide 21: Progress in the treatment of terminally ill HCC patients
Progress in the treatment of terminally ill HCC patients Increased levels of ATF3 & DDIT3 – biomarkers indicating cell death Viadrudomide (CT-01) Prodrug released in liver Increased active drug concentration expected in liver Cohort 1 Cohort 2 Cohort 3 Liver biopsy possible from Cohort 3 onwards Cur
Slide 22: Progress in the treatment of terminally ill HCC patients
Progress in the treatment of terminally ill HCC patients In one of the patients from cohort 2 disease inhibition is seen Viadrudomide (CT-01) Cohort 1 Cohort 2 Cohort 3 FRA-004-002 „Stable disease”; treatment continues No significant adverse effects have been observed to date Information accurate at
Slide 23: What we expect in 2026
What we expect in 2026 Readouts in the coming months will determine project’s value Completing escalation and expansion studies in monotherapy – Value Growth Point Escalation dose study in combination therapy Potential expansion to new indications, e.g. CCA or other cancers without treatment options
Slide 24: The only-in-class potential of highly differentiated viadrudomide
The only-in-class potential of highly differentiated viadrudomide 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 acti
Slide 25: Possible further development
Possible further development Other indications: • cholangiocarcinoma, • lung cancer, • breast cancer, • neuroendocrine cancer. Combotherapies – viadrudomide could possibly be combined with: • everolimus – synergy has been proven in animal models, • anti-PD-1 antibodies, • anti-PD-L1 antibodies. ADC
Slide 26: Vratitoclax (CT-03): First-in-Class MCL-1 Degrader for Liquid & Solid Tumors
Vratitoclax for Liquid Solid (CT-03): Tumors First-in-Class MCL-1 Degrader Vratitoclax (CT-03): First-in-Class MCL-1 Degrader for Liquid & Solid Tumors 26 Business Use Only | All rights reserved
Slide 27: MCL-1 – a critical pathway for cancer resistance
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 apoptos
Slide 28: MCL-1 – a critical pathway for cancer resistance
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 evading apoptosis and promoting the survival of ca
Slide 29: 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 protein in cells1. MCL-1
Slide 30: Over $100 billion market potential of MCL-1 targeting agents
Over $100 billion 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
Slide 31: MCL-1 degraders remain safe to healthy tissues
MCL-1 degraders remain safe to healthy tissues Inhibitors induce MCL-1 accumulation that is 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
Slide 32: 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 33: 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 34: Vratitoclax shows great toxicokinetic profile
Vratitoclax 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 p
Slide 35: Vratitoclax: unmatched therapeutic window
Vratitoclax: 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 cardiotoxicity obs
Slide 36: Differentiating MCL-1 degrader vs. MCL-1 inhibitors
Differentiating MCL-1 degrader vs. MCL-1 inhibitors Clinical development of MCL-1 inhibitors limited by cardiotoxicity issues • Literature & experimental data now demonstrate a MOA for inhibitor-induced toxicity • MCL-1 inhibitors cause MCL-1 accumulation in healthy tissue and necrosis MCL-1 degrade
Slide 37: Investigator-Initiated Trial
Investigator-Initiated Trial Press release dated November 27th, 2025: Captor Therapeutics S.A. (WSE: CTX), an innovative biopharmaceutical company, today announced it has entered into a Memorandum of Understanding with The University of Texas MD Anderson Cancer Center to support an Investigator-Init
Slide 38: Summary: vratitoclax – a first-in-class MCL-1 degrader
Summary: vratitoclax – a 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 data now demonstrate a MOA for inhibitor-induced toxicity •
Slide 39: Possible further development
Possible further development Other indications: • triple negative breast cancer (TNBC), • non-small cell lung cancer (NSCLC), • colon cancer, • venetoclax-resistant cancers. Combotherapies – vratitoclax could possibly be combined with: • venetoclax – synergy has been proven in animal models, • venet
Slide 40: CT-02: First-in-Class NEK7 Degraders for Autoimmune Disorders, Neuroinflammation
CT-02: First-in-Class Autoimmune Neuroinflammation Disorders (CT-02B) NEK7 (CT-02S), Degraders for CT-02: First-in-Class NEK7 Degraders for Autoimmune Disorders (CT-02S), Neuroinflammation (CT-02B) 40 Business Use Only | All rights reserved
Slide 41: 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 42: NEK7 as a new target of the NLRP3 inflammasome pathway
NEK7 as a new target of the NLRP3 inflammasome pathway IL-1𝛽 inhibitors (rilonacept, canakinumab) Differentiation 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 43: 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 44: 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 45: 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 46: 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) 46 Busin
Slide 47: 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 48: 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 49: 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 50: 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 51: 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 52: Research Collaboration and License Option Agreement
Research Collaboration and License Option Agreement Captor (CTX) signed agreement with a U.S. public pharmaceutical company CTX granted a paid, time-limited exclusivity to conduct research on the Captor’s proprietary NEK7 degraders in Partner’s animal models Granting satisfactory reaserch results, t
Slide 53: CT-05: First-in-Class PKCΘ Degraders for Autoimmune Disorders
CT-05: for Autoimmune First-in-Class Disorders PKCӨ Degraders CT-05: First-in-Class PKCӨ Degraders for Autoimmune Disorders 53 Business Use Only | All rights reserved
Slide 54: PKCΘ: 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) 54 Business Use Only | All rights rese
Slide 55: PKCΘ 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 56: First-in-class PKCΘ 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 57: Optigrade Targeted Protein Degradation Platform
Optigrade Targeted Protein Degradation Platform: Molecular glues Bifunctional Degraders Novel E3 ligases 657 Business Use Only | All rights reserved Business Use Only | Do not use without written consent of Captor Therapeutics Inc. © 2023
Slide 58: 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 59: 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 60: Finance Highlights
Finance Highlights Finance Highlights 60 Business Use Only | All rights reserved
Slide 61: Equity summary
Equity summary Ticker: CTX PW Market: Warsaw Stock Exchange (main market) Shares outstanding: 6,353,397 (April 29, 2025) ISIN: PLCPTRT00014 Analyst coverage: Ipopema, mBank, Noble Securities, PKO BP, Trigon Top shareholders Michał Walczak Founder, CEO & CSO 14.4% Paweł Holstinghausen Holsten Early i
Slide 62: Financial summary
Financial summary Highlights: Income Statement and Balance Sheet, PLN mln 2025 2024 • Captor has so far been financed primarily Revenues: through equity, secondarily through grants, Collaboration revenue 4.7 15.8 and thirdly through revenues from research Grant revenue 7.1 5.8 collaborations. Other
Slide 63: Recent corporate developments
Recent corporate developments Recent corporate developments 63 Business Use Only | All rights reserved
Slide 64: EIC Accelerator grant
EIC Accelerator grant The most recent grant agreement: 2.5 mln EUR in an EU programme EIC Accelerator, one of 71 companies chosen from 1,211 applicants from across Europe, one of 12 biotechnology companies, financing the clinical trial of vratitoclax in combination with venetoclax, in R/R AML. 64 Bu
Slide 65: New employee share option programme
New employee share option programme Participants in the program will receive share options: for 220,000 new shares, exercisable at a price of PLN 172 per share (closing price on the announcement date: PLN 36.10), exercisable in early October 2028, exercisable only by individuals who will work at Cap
Slide 66: Share issue
Share issue Recent share issue: 800,000 shares were issued in March 2026 (dilution of 14.5%). PLN 65.6 mln raised extends cash runway until Q3 2027. Share issue was oversubscribed and sold at less than 1% discount to market price. EIC Fund, an investment arm of European Commission, invested alongsid
Slide 67: Beyond the Pipeline
Beyond the Pipeline Beyond the Pipeline 67 Business Use Only | All rights reserved
Slide 68: Captor's Research in Print
Captor’s Research in Print Ligand-Induced Conformational Plasticity of the CTLH E3 Ligase Receptor GID4 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 Ligand-Induced Conformatio
Slide 69: 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 Beta Catenin A Key, Yet Elusive Target in Oncology The Master Switch Resetting Autoimmunity with PKC
Slide 70: 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 70 Business Use Only | All rights reserved
Slide 71: 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 72: Projects co-financed by the European Union
Projects co-financed by the European Union: 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) Discovery and development
Captor Therapeutics — Investor Presentation (May 2026) on 6ix