C4 Therapeutics, Inc. · NASDAQ:CCCC

C4 Therapeutics — Investor Presentation (November 2023)

24 slides from C4 Therapeutics's investor presentation, November 2023

  1. Slide 1: Protein degraded. Disease targeted. Lives transformed.

    Protein degraded. Disease targeted. Lives transformed. November 2023

  2. Slide 2: Forward-looking Statements and Intellectual Property

    Forward-looking Statements and Intellectual Property Forward-looking Statements The following presentation contains forward-looking statements. All statements other than statements of historical fact are forward- looking statements, which are often indicated by terms such as “anticipate,” “believe,”

  3. Slide 3: C4T is a Leader in Delivering on the Promise of Targeted Protein Degradation

    C4T is a Leader in Delivering on the Promise of Targeted Protein Degradation WORLD-CLASS DEGRADER PLATFORM Demonstrated ability to design orally bioavailable, catalytically efficient degraders that maximize the benefits of degradation Our Mission RIGOROUS TARGET SELECTION To deliver on the promise F

  4. Slide 4: Robust Pipeline of Degrader Medicines Pursuing Multiple Targets in Oncology

    Robust Pipeline of Degrader Medicines Pursuing Multiple Targets in Oncology Early phase Late phase Program Target Indications Discovery Pre-clinical Rights development development Multiple Myeloma & Non- CFT7455 IKZF1/3 Hodgkin’s Lymphoma V600 Mutant Cancers CFT1946 BRAF-V600 Non-Small Cell Lung CFT

  5. Slide 5: Continue to Execute on 2023 Key Milestones

    Continue to Execute on 2023 Key Milestones CFT7455 • Cash runway into 2025 • Present Phase 1 dose escalation data from the Phase 1/2 trial at a IKZF1/3 virtual company sponsored event on December 12, 2023 CFT8634 ✓ Present Phase 1 dose escalation data from the Phase 1/2 trial in a BRD9 poster presen

  6. Slide 6: CFT7455

    CFT7455 Targeting IKZF1/3 Multiple Myeloma (MM) & Non-Hodgkin’s Lymphoma (NHL)

  7. Slide 7: CFT7455 Phase 1/2 Trial Progressing through Dose Escalation

    CFT7455 Phase 1/2 Trial Progressing through Dose Escalation Phase 1 Dose Escalation Phase 2 Expansion Arm B1: R/R Multiple Myeloma R/R Multiple Myeloma Monotherapy Monotherapy Arm B2: N = ~30 N = 22 R/R Multiple Myeloma Combination w/ Schedule: Dexamethasone2 Arm A: R/R Multiple Myeloma w/ 14-days o

  8. Slide 8: Single Agent CFT7455 Arm A Data Demonstrated Potent On Target Degradation

    Single Agent CFT7455 Arm A Data Demonstrated Potent On Target Degradation; Dosing Schedule Modified to Improve Therapeutic Index Deep Degradation of IKZF1/3 Meaningful Reductions in dFLC Grade 4 Neutropenia Modified Dosing Schedule with 14 Days Off Source: C4T data on file; AACR 2022 © 2023 C4 Thera

  9. Slide 9: Multiple Paths to Success for CFT7455 across Evolving Multiple Myeloma Landscape

    Multiple Paths to Success for CFT7455 across Evolving Multiple Myeloma Landscape Potential for CFT7455 to replace other IKFZ1/3 Potential to combine CFT7455 with next- degraders and become a backbone therapy generation therapies IKZF1/3 degrader competitive landscape 1L 2L 3L 4L CAR T-Cell Bi-specif

  10. Slide 10: CFT1946

    CFT1946 Targeting BRAF V600 Melanoma, Colorectal (CRC) & Non-Small Cell Lung Cancer (NSCLC)

  11. Slide 11: Current Standard of Care BRAF Inhibitors Lead to Resistance

    Current Standard of Care BRAF Inhibitors Lead to Resistance Unmet Need Degrader Rationale Resistance to approved BRAF Inhibitor causes paradoxical ~$2B inhibitors results in a median PFS approved activation of wild-type RAF of less than 15 months2 BRAF inhibitor Toxicity associated with market1 inhi

  12. Slide 12: CFT1946 Shows Superior Efficacy Compared to Approved BRAF Inhibitor in Preclinical Models

    CFT1946 Shows Superior Efficacy Compared to Approved BRAF Inhibitor in Preclinical Models Combination Treatment of BRAFi Resistant Xenograft CFT1946 Shows More Durable Efficacy than Encorafenib Model with CFT1946 and MEKi Shows Tumor Growth Inhibition/Regression A375 Xenograft A375 + NRAS-Q61K Xenog

  13. Slide 13: CFT1946 is the First Clinical BRAF V600 Degrader

    CFT1946 is the First Clinical BRAF V600 Degrader Phase 2 Expansion Phase 1 Dose Escalation Monotherapy Arm A: Monotherapy1 V600 Melanoma and RP2D NSCLC V600 solid tumors Post BRAF inhibitor including CRC, N =~30 Melanoma and NSCLC Post BRAF inhibitor CFT1946 + trametinib N=~40 Arm B: V600 Melanoma a

  14. Slide 14: CFT1946 Has the Potential to Address Multiple Tumor Types with BRAF V600 Mutations

    CFT1946 Has the Potential to Address Multiple Tumor Types with BRAF V600 Mutations ~70-90% 1.9M Cancer Diagnoses Each Year in V600 of BRAF mutations the United States1 are V600 BRAF Mutations Occur in ~5% of All 35% 1-2% Cancers2 Late-stage Non-Small Melanoma2 Cell Lung Cancer3 ~100K annual incidenc

  15. Slide 15: CFT8919

    CFT8919 Targeting EGFR L858R EGFR L858R + Non-Small Cell Lung Cancer (NSCLC)

  16. Slide 16: Potential for CFT8919 to Improve Outcomes for NSCLC Patients with L858R Mutations

    Potential for CFT8919 Single Agent CFT8919to Improve Provides Outcomes to Opportunity forImprove NSCLC Patients Outcomeswithfor EGFR L858R NSCLCMutations Patients with L858R Mutations Degrader Rationale Osimertinib and other inhibitors ~$6B provide suboptimal response for approved NSCLC patients wit

  17. Slide 17: EGFR L858R Driven NSCLC has Higher Prevalence in Asia

    EGFR L858R Driven NSCLC has Higher Prevalence in Asia Non-Small Cell Lung Cancer (NSCLC) ~200K ~693K Patients in the US Patients in Asia diagnosed in diagnosed in 2022 2020 ~10 – 15% ~40% of NSCLC patients have mutant EGFR (mEGFR) in the of NSCLC patients have mEGFR in the U.S. population Asian popu

  18. Slide 18: CFT8919 is Selective for EGFR L858R and Active in Osimertinib Resistance in Preclinical Models

    CFT8919 is Selective for EGFR L858R and Active in a Setting of Osimertinib Resistance in Preclinical Models Specific for EGFR Exon 21 Mutants Active in setting of EGFR C797S Vehicle PO BID BaF3 EGFRL858R/T790M/C797S 2000 Osimertinib 25 mpk PO QD Tumor volume (mm3) CFT8919 10 mpk PO BID EGFR-L861Q CF

  19. Slide 19: CFT8634

    CFT8634 Targeting BRD9 Synovial Sarcoma & SMARCB1-Null Tumors

  20. Slide 20: Pharmacokinetics: Plasma Exposure of CFT8634 Increased Proportionally with Dose

    Pharmacokinetics: Plasma Exposure of CFT8634 Increased Proportionally with Dose after Single and Repeat Oral Administration Cycle 1 Day 1 Cycle 1 Day 15 1000 1000 Plasma PK (ng/mL) Plasma PK (ng/mL) 2 mg QD 100 100 4 mg QD 8 mg QD 10 10 15 mg QD 30 mg QD 1 50 mg QD 0 6 12 18 24 1 Time (hrs) 0 6 12 1

  21. Slide 21: Pharmacodynamics: High Levels of BRD9 Degradation Observed on Tumor Tissue

    Pharmacodynamics: High levels of BRD9 Degradation is Observed on Tumor Tissue After 15 Days of Treatment H&E BRD9 expression A B E BRD9 IHC by visit and dose % expression relative to baseline Baseline 25 0 -25 100um -50 C D -75 Cycle 1 Day -100 15 g g g g g g g n 2m 4m 8m m m m ni 15 30 50 e re Cycl

  22. Slide 22: CFT8634 has Shown Preliminary Evidence of Antitumor Activity

    CFT8634 has Shown Preliminary Evidence of Antitumor Activity in Patients with Synovial Sarcoma and SMARCB1-null Solid Tumors A. Water fall Plot B. Swimmers Plot % Best Change from Baseline in 50 Sum of Target Lesions BOR PR 0 SD PD NE -50 15 mg 30 mg 30 mg 15 mg 30 mg 30 mg 15 mg 15 mg 15 mg 30 mg 8

  23. Slide 23: High Levels of BRD9 Degradation Did Not Result in Sufficient Efficacy To Advance CFT8634

    High Levels of BRD9 Degradation Did Not Result in Sufficient Efficacy To Advance CFT8634 Program • 32 patients treated with CFT8634 at escalating dose levels, CFT8634 was generally well-tolerated - Majority of AEs reported were considered mild to moderate in severity • Demonstrated a dose proportion

  24. Slide 24: Thank You!

    Thank You! C4 Therapeutics

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