C4 Therapeutics, Inc. · NASDAQ:CCCC
C4 Therapeutics — Investor Presentation (October 2024)
29 slides from C4 Therapeutics's investor presentation, October 2024
Slide 1: Protein degraded. Disease targeted. Lives transformed.
Protein degraded. Disease targeted. Lives transformed. October 2024
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,”
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
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
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
Slide 6: C4T is On Track to Execute Across All 2024 Goals
C4T is On Track to Execute Across 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/
Slide 7: Cemsidomide
Cemsidomide Targeting IKZF1/3 Multiple Myeloma (MM) & Non-Hodgkin’s Lymphoma (NHL)
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
Slide 9: Differentiated PK and Class-leading Catalytic Activity of Cemsidomide
Normalized to GAPDH in NCI-H929 Tumors Differentiated PK and Class-leading Catalytic Activity of Cemsidomide Percent of IKZF3 Remaining/ Normalized to GAPDH in NCI-H929 Tumors Leads to Sustained Degradation Compared to Other Agents in this Class 100 Percent of IKZF3 Remaining/ 100 50 Extended Plasma
Slide 10: Cemsidomide Phase 1 Dose Escalation Trial Design and Endpoints
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
Slide 11: Schedule Adjustment Yielding Expected Results for Cemsidomide as a Potential MM Therapy
Schedule Adjustment Yielding Expected Results for Cemsidomide as a Potential MM Therapy + Cemsidomide is a potential treatment for multi-refractory MM patients with the Established Safety Profile Demonstrated Promising Responses with ability to move into and Dosing Schedule Monotherapy Activity Cems
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
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
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, Cemsidomide: DL5 QD pomalidomide, a +dex: 40 mg QW*
Slide 15: Cemsidomide + Dexamethasone is Well Tolerated with Best Responses in BCMA-Refractory Patients
Cemsidomide + Dexamethasone is Well Tolerated and Best Responses in Patients Refractory to BCMA Therapies 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 10 11 Schedule Status Lines or TCE No No 6
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
Slide 17: CFT1946
CFT1946 Targeting BRAF V600 Mutant Melanoma, Colorectal (CRC) & Non-Small Cell Lung Cancer (NSCLC)
Slide 18: CFT1946 Potential to Overcome Shortcomings of BRAF V600X 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
Slide 19: 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
Slide 20: 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
Slide 21: No Discontinuations, Dose Interruptions or Reductions Due to CFT1946 Treatment-related Adverse Events
No Discontinuations, Dose Interruptions or Reductions Due to CFT1946 Treatment-related Adverse Events 20 mg BID 80 mg BID 160 mg BID 320 mg BID 640 mg BID Total (n=5) (n=5) (n=9) (n=12) (n=5) (n=36) n (%) n (%) n (%) n (%) n (%) n (%) Patients with any TEAEs 4 (80) 4 (80) 7 (78) 11 (92) 5 (100) 31 (
Slide 22: 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
Slide 23: Early Signs of Anti-tumor Activity: 59% Patients Demonstrated Target Lesion 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
Slide 24: CFT1946 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
Slide 25: On Track for Multiple CFT1946 Milestones in 2025
On Track for Multiple CFT1946 Milestones in 2025 ✓ Initiated monotherapy • Complete CFT1946 melanoma expansion monotherapy dose cohort at 640 mg escalation portion of ongoing Phase 1 trial and present full • Continue dose data in 2025 Initiate escalation beyond 640 registrational 2024 mg if 2025 • D
Slide 26: CFT8919
CFT8919 Targeting EGFR L858R Non-Small Cell Lung Cancer (NSCLC)
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
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
Slide 29: C4T is On Track to Execute Across All 2024 Goals
C4T is On Track to Execute Across 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/
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