C4 Therapeutics, Inc. · NASDAQ:CCCC
C4 Therapeutics — Investor Presentation (January 2023)
29 slides from C4 Therapeutics's investor presentation, Jan 9, 2023
Slide 1: C4 Therapeutics
C4 Therapeutics Protein degraded. Disease targeted. Lives transformed. January 2023 oe ’ sss. C4 Therapeutics
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 Leader in Delivering on the Promise of Targeted Protein Degradation
| CAT 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 To deliver on the promise of targeted protein degra
Slide 4: Medicines that Transform Patients' Lives
Medicines that Transform Patients’ Lives Progress multiple Advance the next small molecule oral wave of research oncology targets for difficult-to- degraders in the drug and classically clinic undruggable targets Robust internal discovery pipeline including 7 new oncology research 1 Additional progr
Slide 5: Achievements in 2022 Position C4T for Success in 2023
Achievements in 2022 Position C4T for Success in 2023 2022 2023 Progress multiple small molecule oral oncology degraders Progressed lead clinical program, CFI7455 Initiated two new Clinical trials, CFT8634 Present Phase 1 dose escalation data from the Phase 1/2 trials of CFT7455 and CFT8634 Advance
Slide 6: TORPEDO Platform Delivers MonoDAC and BiDAC Degraders against a Diverse Array of Target Types
TORPEDO Platform Delivers MonoDAC and BIDAC Degraders against a Diverse Array of Target Types Projects successfully MENS jong BDAC transitioned to hit Late lead optimization! Projects Initiated " acta 50) @ Targets Cereblon- Programs evaluated mediated with series across diverse degrader hit contain
Slide 7: Robust Pipeline of Wholly Owned Degrader Medicines Pursuing Multiple Targets in Oncology
Robust Pipeline of Wholly Owned Degrader Medicines Pursuing Multiple Targets in Oncology Program Indications Multiple Myeloma & Non- CFI7455 IKZF1/3 Hodgkin's lymphoma CFT8634 BRD9 Synovial Sarcoma & SMARCBI- Null Cancers CFT1946 BRAF V600 Vé00 Mutant Cancers CFT8919 EGFR L858R Non-Small Cell Lung C
Slide 8: CFT7455
CFT7455 Targeting IKZF1/3 Multiple Myeloma (MM) & Non-Hodgkin's Lymphoma (NHL)
Slide 9: Establish CFT7455 as a Standard of Care IKZF1/3 Degrader
Establish CFT7455 as a Standard of Care IKZF1/3 Degrader Currently approved IKZF1/3 CFI7455 has the degraders (lenalidomide, pomalidomide) potential to become a backbone are suboptimal for multiple myeloma: therapy for multiple myeloma: Class-leading catalytic activity to enable potent, rapid, Nev e
Slide 10: 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 0. 10 © IKZFA -20 4m IKZF3 30 — 50 pg dosing ‘% Degradation to baseline 0 5 10 1520 Days Grade 4 Neutropenia Neutrophils (10°1L) = Pationt 1 “©
Slide 11: Phase 1/2 Trial Progressing through Dose Escalation
Phase 1/2 Trial Progressing through Dose Escalation; Safety Data and Enrollment Strategy Supported Opening of Dexamethasone Combination Arm Phase 1 Dose Escalation Phase 2 Expansion eben eeeeanan, osc annnaoam, ee Arm C: Non-Hodgkin's Lymphoma Monotherapy Manile @ ° See feamienenonts N=~20 N=-15 Per
Slide 12: Multiple Paths to Success for CFT7455 across Evolving Multiple Myeloma Landscape
Multiple Paths to Success for CFT7455 across Evolving Multiple Myeloma Landscape Potential to combine CFT7455 with next- Potential for CFT7455 to replace other IKFZ1/3 generation therapies degraders and become a backbone therapy IKZF1/3 degrader competitive landscape IL 2L $l aL Bi-specific T-Cell|
Slide 13: CFT8634
CFT8634 Targeting BRD9 Synovial Sarcoma & SMARCB1-Null Solid Tumors
Slide 14: BRD9 was Previously Considered an Undruggable Target where Inhibitors are Ineffective
BRD9 was Previously Considered an Undruggable Target where Inhibitors are Ineffective for Synovial Sarcoma Unmet Need Degrader Rationale Oncogenicity of BRD? depends on protein . age . function not addressed by traditional inhibitors No approved therapies specifically for synovial sarcoma Current tr
Slide 15: CFT8634 Demonstrated Deep Degradation and Robust Responses in Preclinical Synovial Sarcoma Models
CFT8634 Demonstrated Deep Degradation and Robust Responses in Preclinical Synovial Sarcoma Models PDX 310 PDX SA13412 BRD? urable Tumo ession ms lo (PO OD) © CFTE634 10 mg/kg (PO QD) Vehicle (PO, QD) o 3634 t mg/kg (POQD) —_-@ CFTA634 30malkg (PO QD) + CFT8634 50 mg/kg (PO QD) 2 © CFT8634 3 mglkg (P
Slide 16: CFT8634 Phase 1/2 Trial Progressing through Dose Escalation
CFT8634 Phase 1/2 Trial Progressing through Dose Escalation Phase 2 Expansion Phase 1 Dose Escalation CFTé Mon jerapy Status: Enrolling Solid Tumors Phasel Dose Escalation Data Expected 2H 2023 eee 1 sss CATherAPeUtics — recommended Phase 2 Dove (RP2D) © 2023 C4 Therapeutics, Inc. 16
Slide 17: CFT8634 Pharmacokinetic and Pharmacodynamic Data Supportive of Proof of Mechanism
CFT8634 Pharmacokinetic and Pharmacodynamic Data Supportive of Proof of Mechanism Plasma CFT8634 Concentration Mean (+SD) —e 2mg ——4mg —* 8mg 2 Time (h) 18 24 a—BRD9 immunohistochemistry C4 Therapeutics Effective Degradation of a Previously Undruggable Target © 2023 C4 Therapeutics, Inc.
Slide 18: Recent Publications Support Potential Additional Indications for BRD9
Recent Publications Support Potential Additional Indications for BRD9 C4 Therapeutics Interferonopathies BRD9 is a druggable component of interferon-stimulated gene expression and antiviral activity EMBOpress Interferonopathies BRD9 regulates interferon-stimulated genes during macrophage activation
Slide 19: CFT1946
CFT1946 Targeting BRAF-V600 Melanoma, Colorectal (CRC) & Non-Small Cell Lung Cancer (NSCLC)
Slide 20: 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 ~$2B Inhibitor causes paradoxical inhibitors results in a median PFS activation of wild-type RAF f less than 15 months? approved meNRAS otess than |) months BRAF inhibitor sep cation
Slide 21: CFT1946 Shows Superior Efficacy Compared to Approved BRAF Inhibitor in Preclinical Models
CFT1946 Shows Superior Efficacy Compared to Approved BRAF Inhibitor in Preclinical Models CFT1946 Shows More Durable Efficacy than Encorafenib ith CFT1946 Inhibiti A375 Xenograft A375 + NRAS-Q61K Xenograft 2500; ~ 2500: « _ E - Vehicle (PO BID) © 2000 -® Vehicle, PO BID = 2000 “© MEKi: Trametinib (0
Slide 22: CFT1946 is the First Clinical BRAF-V600 Degrader
CFT1946 is the First Clinical BRAF-V600 Degrader Phase 1 Dose Escalation Arm A: Monotherapy! 600 solid tumors including CRC, Melanoma and NSCLC Post BRAF inhibitor Arm B: CFT946 + netinib V600 solid tumors, including CRC, Melanoma and NSCLC Post BRAF inhibitor N=~25 Phase 2 Expansion CFT1946 + trame
Slide 23: CFT1946 Has the Potential to Address Multiple Tumor Types with BRAF-V600 Mutations
V600 Mutations 1.9M Cancer Diagnoses Each Year in the United States! BRAF Mutations Occur in ~5% of All Cancers? ~100K annual incidence of BRAF mutated cancers! Sources: CFT1946 Has the Potential fo Address Multiple Tumor Types with BRAF- » ~70-90% v600 BY of BRAF mutations are V600 35% 1-2% Late-st
Slide 24: CFT8919
CFT8919 Targeting EGFR L858R EGFR L858R + Non-Small Cell Lung Cancer (NSCLC)
Slide 25: 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 Unmet Need L858R activating D )) 25-45% ~S6B mutation MEGFR NSCLC approved EGFR inhibitor go EGFRUSS8R Degrader Rationale markeft® Osimertinib and other inhibitors provide suboptimal 1L . . i ini 1s-gen EGFR TKls
Slide 26: CFT8919 is Selective for EGFR L858R and Active in a Setting of 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 _. 20007 == Osimertinib 25 mpk PO QD t- CFT8919 10 mpk PO BID —* CFT8919 25 mpk PO BID — CFT8919 50 mpk PO
Slide 27: C4T is a Leader in Delivering on the Promise of Targeted Protein Degradation
| CAT is a Leader in Delivering on the Promise of Targeted Protein Degradation Our Mission To deliver on the promise of targeted protein degradation science to create a new generation of medicines that transform patients’ lives = C4 Therapeutics WORLD-CLASS DEGRADER PLATFORM Demonstrated ability to
Slide 28: 2023 Expected to be a Transformative Year for C4T
2023 Expected to be a Transformative Year for C4T with Two Clinical Readouts and a Fourth Program Entering Development CFT7455 Present Phase 1 dose escalation data from the Phase 1/2 trial 2H IKZF1/3 CFT8634 Present Phase 1 dose escalation data from the Phase 1/2 trial 2H BRD? CFT1946 + Advance the
Slide 29: Thank You
Thank You C4 Therapeutics
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