C4 Therapeutics, Inc. · NASDAQ:CCCC

C4 Therapeutics — Investor Presentation (October 2024)

30 slides from C4 Therapeutics's investor presentation, October 2024

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

    Protein degraded. Disease targeted. Lives transformed. October 2024

  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 Recognized Leader in Delivering on the Promise of Targeted Protein Degradation

    C4T Is a Recognized Leader in Delivering on the Promise of Targeted Protein Degradation WORLD-CLASS DEGRADER PLATFORM Robust patent portfolio of novel cereblon binders; Demonstrated ability to design orally bioavailable, catalytically efficient degraders Our Mission RIGOROUS TARGET SELECTION To deli

  4. Slide 4: Designed and Advanced Degraders Into the Clinic Across a Range of Target Classes

    Designed and Advanced Degraders Into the Clinic Across a Range of Target Classes, Demonstrating Robust Target Degradation Interrogated Diverse Attained IND Achieved Desirable Degraded Target as Target Classes Clearance Drug-like Properties Predicted Discovered degraders and advanced 4 INDs against a

  5. Slide 5: Advancing a Broad Pipeline to Deliver Near-Term Value

    Advancing a Broad Pipeline to Deliver Near-Term Value Early Phase Late Phase Program Target Indications Discovery Preclinical Rights Development Development Multiple Myeloma & Cemsidomide IKZF1/3 Non-Hodgkin’s Lymphoma BRAF V600 CFT1946 V600 Mutant Cancers Mutant Non-Small Cell Lung CFT89191 EGFR L8

  6. Slide 6: C4T is On Track to Achieve All 2024 Goals

    C4T is On Track to Achieve All 2024 Goals, Progressing Multiple Clinical and Preclinical Programs ASH 2024 (Dec.): Present updated data from Phase 1 dose escalation +dex trial in R/R MM Cemsidomide ASH 2024 (Dec.): Present data from Phase 1 dose escalation monotherapy trial in R/R NHL IKZF1/3 By YE

  7. Slide 7: Cemsidomide

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

  8. Slide 8: IKZF1/3 Degradation Drives Three Distinct Areas of Hematopoietic Biology

    IKZF1/3 Degradation Drives Three Distinct Areas of Hematopoietic Biology; Degrading IKZF1/3 Is a Validated Therapeutic Strategy in MM and NHL IKZF1 / IKZF3 Transcription Factors Drive MM and NHL Cell Activate Fully Regulate Hematopoietic Growth and Survival Differentiated T-cells Stem Cell Different

  9. Slide 9: Cemsidomide Has the Potential to Address Multiple Opportunities Across MM and NHL

    Cemsidomide Has the Potential to Address Multiple Opportunities Across MM and NHL Annual Market Size3 U.S. Unmet Needs Incidence 2023 20304 • Additional efficacious and tolerable agents that work well in combination regimens Multiple Myeloma ~36,0001 ~$21B ~$42B • Therapies that increase the durabil

  10. Slide 10: Cemsidomide Phase 1 Dose Escalation Trial Design in R/R MM and R/R NHL

    Cemsidomide Phase 1 Dose Escalation Trial’s Goal Is to Define the Safety Profile and Identify Signs of Anti-Tumor Activity in R/R MM and R/R NHL Phase 1 Dose Escalation Trial Endpoints R/R MM Monotherapy Primary: Dosing: QD 21 days on/7 days off • Safety and tolerability N=5 • Determine the maximum

  11. Slide 11: Prior Data Demonstrated Cemsidomide as a Potential MM Therapy

    Prior Data Demonstrated Cemsidomide as a Potential MM Therapy + Established Safety Profile Demonstrated Promising Responses with and Dosing Schedule Monotherapy Activity Cemsidomide + Dexamethasone Cemsidomide is a potential treatment for multi-refractory MM patients with the ability to move into ea

  12. Slide 12: Clinical Evidence of Immune T-cell Activation With Cemsidomide Monotherapy

    Clinical Evidence of Immune T-cell Activation With Cemsidomide Monotherapy Supports potential of cemsidomide % positive cells (C1D21 vs C1D1) as a maintenance therapy option 100 C1D1 **** C1D21 and in combination with novel MM agents to improve efficacy: 80 ** ✓ Cemsidomide induces CD8+ T- % positiv

  13. Slide 13: Cemsidomide Combined With Novel MM Agents Demonstrated Enhanced Immune Cell Lysis

    Cemsidomide Combined With Novel MM Agents Demonstrated Enhanced Immune Cell Lysis in Non-clinical Translational Models Daratumumab (Anti-CD38) Combo Teclistamab (BCMA BiTE) Combo Antibody-Dependent Cell-Mediated Cytotoxicity Assay T-cell Dependent Cellular Cytotoxicity Assay (ADCC) (TDCC) Daratumuma

  14. Slide 14: Cemsidomide + Dexamethasone Dose Escalation in R/R MM Continues to Progress

    Cemsidomide + Dexamethasone Dose Escalation in R/R MM Continues to Progress KEY INCLUSION CRITERIA • Adults with R/R MM, at Phase 1: Dose Escalation + Dexamethasone Phase 2 least 3 prior lines that 14 Days On/14 Days Off have included lenalidomide, Potential for future dose escalation pomalidomide,

  15. Slide 15: Cemsidomide + Dexamethasone Is Well Tolerated and Shows Best Responses

    Cemsidomide + Dexamethasone Is Well Tolerated and Shows Best Responses in Patients Refractory to BCMA Therapies, Updated Data to be Presented at ASH Anti-myeloma Activity: Prior Dosing EMD # of Prior Cycle Cycle Cycle Cycle Cycle Cycle Cycle Cycle Cycle Cycle Cycle Dose Level CAR-T 1 2 3 4 5 6 7 8 9

  16. Slide 16: Cemsidomide Profile Supports Multiple Opportunities Across MM Landscape

    Cemsidomide Profile Supports Multiple Opportunities Across MM Landscape Potential Data Development Path Potential Opportunity Cemsidomide + Cemsidomide Accelerated Approval in Dexamethasone + Dexamethasone Multi-Refractory MM Registrational Study + PI Studies Approvals in Early Line MM + Anti-CD38 S

  17. Slide 17: Cemsidomide Monotherapy Dose Escalation in R/R NHL Continues to Progress

    Cemsidomide Monotherapy Dose Escalation in R/R NHL Continues to Progress, Initial Data to be Presented at ASH KEY INCLUSION CRITERIA • Adults with R/R NHL, with minimum prior Phase 1: Dose Escalation Monotherapy lines of therapy required for each NHL 14 Days On/14 Days Off sub-type: – PTCL: At least

  18. Slide 18: CFT1946

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

  19. Slide 19: CFT1946 Has the Potential to Overcome Several Shortcomings Seen With BRAF Inhibitors

    CFT1946 Has the Potential to Overcome Several Shortcomings Seen With Inhibitors for BRAF V600X Cancers Key Limitations of Approved BRAF Potential Advantages of CFT1946, a Novel, Inhibitors: Oral, BRAF V600 Mutant BiDAC degrader: • Durable and deep responses are often Despite limitations, ✓ Prevents

  20. Slide 20: Kpu,u Results Demonstrate CFT1946's Ability to Cross the Blood Brain Barrier

    Kpu,u Results Demonstrate CFT1946’s Ability to Cross the Blood Brain Barrier and Supports Activity in Preclinical Intercranial Metastatic Models A375 BRAF V600E-Luc Intracranial Model Survival Luminescence Per Mouse A375 BRAF V600E-Luc Intracranial Model Luminescence Luminescence Per Mouse Per Mouse

  21. Slide 21: CFT1946 Phase 1/2 Dose Escalation Trial Continues to Progress

    CFT1946 Phase 1/2 Dose Escalation Trial Continues to Progress Across BRAF V600 Mutant Driven Solid Tumors KEY INCLUSION MONOTHERAPY DOSE PK, PD, ANTI-TUMOR 2 Exploratory Expansion: CRITERIA1 ESCALATION ACTIVITY EVALUATION CFT1946 monotherapy in melanoma • Evidence of BRAF V600 Potential for further

  22. Slide 22: CFT1946 Monotherapy Phase 1 Data Demonstrate Proof of Mechanism

    CFT1946 Monotherapy Phase 1 Data Demonstrate Proof of Mechanism and Provide Early Evidence of Proof of Degrader Concept Proof of Mechanism Proof of Degrader Concept Well tolerated and highly Early evidence of monotherapy CFT1946 has the selective degrader, results in no anti-tumor activity in patien

  23. Slide 23: Well-Tolerated Monotherapy Safety Profile of CFT1946

    Well-Tolerated Monotherapy Safety Profile, Consistent With BRAF V600 Mutant Selectivity Design of CFT1946 Summary of TEAEs ≥ 10% of 36 patients treated with CFT1946 Grade 1 Grade 2 Grade 3 Grade 4 Grade 5 Total (n=36) Preferred Term n (%) n (%) n (%) n (%) n (%) n (%) • No DLTs Patients with any TEA

  24. Slide 24: Early Signs of Anti-tumor Activity: 59% Patients Demonstrated Tumor Reductions

    Early Signs of Anti-tumor Activity: 59% (16/27) Patients Demonstrated Target Lesion Tumor Reductions With 11 Efficacy Evaluable Patients Continuing Treatment * (As of 7/19/2024) V600R V600K V600K SD SD SD PR SD PD 5 SD PR 4 SD PR # 3 2 PD 1 PR *Other tumor types include cholangiocarcinoma, non-small

  25. Slide 25: CFT1946 Has the Potential to Address Multiple Tumor Types With BRAF V600X Mutations

    CFT1946 Has the Potential to Address Multiple Tumor Types With BRAF V600X Mutations Where BRAF Inhibitors Are Insufficient BRAF V600X 2023 U.S. Incidence of Approved BRAF Inhibitor Mutation Rate BRAF V600X Patients4 BRAF Inhibitors Regimen mPFS5 • Dabrafenib 1 • Encorafenib 11.4 months ~35% ~35,000

  26. Slide 26: CFT8919

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

  27. Slide 27: Potential for CFT8919 to Improve Outcomes for NSCLC Patients With EGFR L858R Mutations

    Potential for CFT8919 to Improve Outcomes for NSCLC Patients With EGFR L858R Mutations Strong Rationale for an EGFR L858R Degrader CFT8919 Key Properties • Orally bioavailable • Potent and selective against L858R, EGFRL858R regardless of secondary mutations 1L • Allosteric binding osimertinib 1st-ge

  28. Slide 28: CFT8919 is a Potent, Oral, Allosteric, Mutant-selective Degrader of EGFR L858R

    CFT8919 is a Potent, Oral, Allosteric, Mutant-selective Degrader of EGFR L858R • CFT8919 exploits allosteric binding site, close CFT8919 to L858R activating mutation • Allosteric binding site avoids known Orthosteric resistance-causing mutations in orthosteric Inhibitor binding site • Allosteric bin

  29. Slide 29: CFT8919 is Selective for EGFR L858R and Active in Osimertinib Resistance

    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

  30. Slide 30: C4T is On Track to Achieve All 2024 Goals

    C4T is On Track to Achieve All 2024 Goals, Progressing Multiple Clinical and Preclinical Programs ASH 2024 (Dec.): Present updated data from Phase 1 dose escalation +dex trial in R/R MM Cemsidomide ASH 2024 (Dec.): Present data from Phase 1 dose escalation monotherapy trial in R/R NHL IKZF1/3 By YE

C4 Therapeutics — Investor Presentation (October 2024) on 6ix