Captor Therapeutics Sa · GPW:CTX

Captor Therapeutics Sa — Q1 2023 Earnings Presentation

30 slides from Captor Therapeutics Sa's earnings presentation, May 30, 2023

  1. Slide 1: A new dawn in drug discovery

    A new dawn in drug discovery Corporate Presentation – Q1 2023 update May 2023

  2. 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

  3. Slide 3: Q1 2023 Executive summary

    Q1 2023 Executive summary Announcement of the next steps in the Strategy - increase of authorised share capital Target announcements in CT-01, CT-02 and CT-05 CT-01 - additional compelling in-vivo efficacy data in preclinical studies - moving towards the clinic as planned Financial results - almost

  4. Slide 4: Development of projects and molecular targets announcement

    DEVELOPMENT OF PROJECTS AND MOLECULAR TARGETS ANNOUNCEMENT 4

  5. Slide 5: Optigrade discovery platform – importance of structure

    OptigradeTM discovery platform – importance of structure OptigradeTM – addressing Molecular Glues, Bifunctional Degraders and novel Ubiquitin E3 Ligases • Industry leading capability in protein engineering and structural biology • Unique structure-guided lead optimization paradigm gives high selecti

  6. Slide 6: Fully owned pipeline

    Fully owned pipeline Target Indications Modality Discovery Preclinical* IND Filing Phase IA / IB Phase II GSPT1, Hepatocellular carcinoma, NEK7, MG SALL4 Autoimmunity, CNS, NEK7 MG MCL-1 Liquid & solid tumours BID PKCӨ Autoimmunity, Oncology, BID Transplantation, Metabolism New target MG projects Au

  7. Slide 7: CT-01: Multi-target GSPT1, NEK7 & SALL4 degrader

    CT-01: Multi-target GSPT1, NEK7 & SALL4 degrader CPT-6281: first-in-class MG degrader of GSPT1, SALL4 & NEK7 Lung cancer 400k patients GSPT1 degradation leads to an Integrated Stress Response and induction of apoptosis in HCC cells SALL4 is expressed foetal liver, silenced in adults, but often re- e

  8. Slide 8: Convincing tumor growth inhibition in HCC PDX models

    Convincing tumor growth inhibition in HCC PDX models Tumor Growth Inhibition Tumor regression 111 97 %Δ Inhibition 75 62 10 randomly selected HCC models, CPT-6281 100mg/kg, BID 42 3 animals per vehicle & treatment groups 35 31 22 Efficacy demonstrated in 8/10 models; TGI>50% in 4 models, LI-1 LI-2 L

  9. Slide 9: Clear synergy of CPT-6281 with an approved drug

    Clear synergy of CPT-6281 with an approved drug HUH-7 Xenograft Model NUDE_HUH-7 LI1097 HCC PDX 2000 1750 1500 1250 Vehicle 1000 Compound A, 5mg/kg, QD CPT-6281, 30mg/kg, BID 750 CPT-6281 + Compound A 500 250 0 0 2 4 6 8 10 12 14 Day of treatment 9 CT-01 – GSPT1 Business Use Only | Do not use withou

  10. Slide 10: Captor compound is structurally different to the clinical ones

    Captor compound is structurally different to the clinical ones Captor’s Captor’s Captor’s Captor’s liberated Liberated prodrug prodrug active drug active drug <0.05 <0.05 <0.05 <0.05 MRT-2359 MRT-2359 CC-90009 CC-90009 „Tails” comparison; Tanimoto comparison; Tanimoto coefficient <0-1>, where 0 mean

  11. Slide 11: CPT-6281 – pro-drug with target tissue activation

    CPT-6281 – pro-drug with target tissue activation 11 CT-01 – GSPT1 Business Use Only | Do not use without written consent of Captor Therapeutics Inc. © 2023

  12. Slide 12: Development timeline – CPT-6281

    Development timeline – CPT-6281 Initial indication: Expected milestones: hepatocellular carcinoma CTA submission for initiation of clinical trials in Q3 2023 Degradation profile Phase Ia/Ib top-line data to be reported by the end of 2024 Molecular GSPT1, SALL4 + NEK7 Combination study data by end 20

  13. Slide 13: CT-02: Vast market potential for inflammasome modulators

    CT-02: Vast market potential for inflammasome modulators Neuroinflammation Allergy (AD, PD, MS, ALS) Asthma >10 M patients Myocardial infarction Diabetic cardiomyopathy Fibrotic Inflammasome Inflammatory Bowel Disease Lupus Caspase 1 nephritis 1.6 M patients Gout Rheumatoid Arthritis Psoriasis >2 M

  14. Slide 14: Therapeutic edge in autoimmunity through NEK7 degradation

    Therapeutic edge in autoimmunity through NEK7 degradation Potent Potent degradation degradation of NEK7 IL-1𝛽 IL-1 IL-18 150 200 150 Target amount [%] DC50=2.5 nM ] % [ Dm a x=94% 150 t n 100 100 u o 100 m a t e 50 50 g r 50 a T 0 0 0 T S 0 MM U LP5 N IG S O 9µµ µM 10 -11 10 -10 10 -9 10 -8 10 -7…

  15. Slide 15: Differentiated intervention in NLRP3 pathway via NEK7 degradation

    Differentiated intervention in NLRP3 pathway via NEK7 degradation Aberrant activation Disease of NLRP3 development Therapeutic response Increased infections via reduced immunity NEK7 NLRP3 inhibition Complete inactivation of IL-1β NLRP3 Therapeutic response Maintained immunity NLRP3 NEK7 degradation

  16. Slide 16: In vivo PoC in peritonitis model & brain penetration

    In vivo PoC in peritonitis model & brain penetration -24h 0h 2h 4h 6h Plasma and brain concentration of CPT-565 Concentration [ng/g] Brain 1000 Single MSU Terminal Plasma dose of induction bleeding & CPT- LPS In-life collection 100 764 challenge bleeding 10 IL-1β levels 1 400 Plasma 4h Plasma 6h Per

  17. Slide 17: NEK7 summary

    NEK7 summary Multiple series of NEK7 molecular glue degraders discovered Lead compounds show low nanomolar potency and excellent PK properties Molecular Glue In-vivo proof-of-efficacy for systemic degraders achieved in initial study Larger optimised efficacy study reporting soon Significant brain pe

  18. Slide 18: CT-03: MCL-1 – a critical pathway of cancer resistance

    CT-03: MCL-1 – a critical pathway of cancer resistance MCL-1 is one of the most amplified proteins in cancer Lung cancer 400k patients A critical resistance mechanism in haematological and solid tumours Ablation of MCL-1 protein directly attenuates tumours in vivo as monotherapy & sensitizes tumors

  19. Slide 19: MCL-1 degraders effective in AML and lung cancer models

    MCL-1 degraders effective in AML and lung cancer models Strong tumor growth inhibition Potent MCL-1 degradation and apoptosis kDa Vehicle CPT-2036 50 37 MCL-1 150 PARP FL 100 PARP CL 75 20 15 CC3 50 Stain Free blot 37 Mice with 150 mm3 MV4-11, IV DMS-114, 75 mpk, IV, single injection 19 CT-03 – MCL1

  20. Slide 20: Ultrapotent compounds active ex vivo and in cancer cell lines

    Ultrapotent compounds active ex vivo and in cancer cell lines ABU-098 is more potent than ABS-994 in most of the ] 150 ABU-098 tested models [% ] 150 e 125 c CPD-1 ABU-098 ABU-098 + ABR-183 10 CTG-3950 CTG-4044 % [ n e 125 c a d 100 ABU-098 + ABR-183 DC50 ~1 nM 9 CPD-1 was tested in the panel of 30

  21. Slide 21: Development timeline – CT-03

    Development timeline – CT-03 Initial indications: Expected milestones: blood cancers, subsequently solid tumours • IND/CTA approval in Q3/4 2024 Bifunctional Degrader • Initiation of Phase I clinical trial Q4 2024 Degradation profile: • Phase Ia/Ib top-line data reported 2025 Selective first-in-clas

  22. Slide 22: CT-05: PKCθ an inadequately drugged high value target

    CT-05: PKCӨ an inadequately drugged high value target Multiple sclerosis TCR Allergy Asthma CD3 CD28 T-cell membrane Cytoplasm Myocarditis Breast cancer PKCθ IL-2 Kidney injury IL-17 Gastrointestinal cancer Nucleus Inflammatory Bowel Disease Psoriasis 1.6 M patients 22 CT-05 – PKCӨ >7 M patients Bus

  23. Slide 23: Unique opportunity tailored for bifunctional degraders

    Unique opportunity tailored for bifunctional degraders Multiple PKCӨ inhibitors were in clinical trials: Inhibitor shows significant effects on non-immune cells 1st generation, e.g. pan-PKC Sotrastaurin – many side effects Degrader has no effect in non-immune cells 2nd generation, e.g. Astellas, Abb

  24. Slide 24: Captor Partnering

    Captor Partnering Existing collaborations: • Sosei Heptares collaboration was extended and continues as planned • Ono partnership is advancing well with positive data confirming our approach Pipeline partnering strategy: • CT-01 + CT-03: Early clinical trials for human POC and partner at point of op

  25. Slide 25: Financials and plans for the future

    FINANCIALS AND PLANS FOR THE FUTURE 25

  26. Slide 26: Strong balance sheet and cash position

    Strong balance sheet and cash position Consolidated statement of financial position (PLN, M) Cash position 101,3 96,3 91,7 83,4 Available funding secured (PLN M; as of 31/03/2023): 146,7 Total : - PLN 146,7 M 64,2 82,5 • PLN 82,5 M 16,1 13,4 10,5 11,7 cash, short-term bonds 2,7 3,3 • PLN 64,2 M Fixe

  27. Slide 27: Next steps

    Next steps 2023 • CT-01: Phase Ia/Ib initiation in liver cancer patients • CT-02 and CT-05: In vivo proof of concept in autoimmunity • In cell degradation of target with novel E3 ligase-based degrader 2024 • CT-03: Phase Ia/Ib initiation in haematological cancer patients • CT-01: Clinical readouts:

  28. Slide 28: Q&A Session

    Poa Captor ° Therapeutics Q&A SESSION Therapeutics

  29. Slide 29: Captor Therapeutics S.A contact details

    Captor Therapeutics S.A ul. Duńska 11 54-427 Wrocław, Poland Captor Therapeutics GmbH Hegenheimermattweg 167A 4123 Allschwil, Switzerland Contact: t.shepherd@captortherapeutics.com

  30. Slide 30: Projects are co-financed by the European Regional Development Fund

    Projects are 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) Dis

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