C4 Therapeutics : Our Corporate Presentation (41bc83)

Published: 2026-05-12 07:24:08 ET CCCC

Published on 05/12/2026 at 07:24 am EDT

Protein degraded. Disease targeted.

Lives transformed.

May 2026

Advancing Differentiated TPD Medicines and Building a Sustainable Pipeline of High-value Degraders To Achieve Our Vision

Cash runway expected to end of 2028, beyond key value inflection points across the portfolio

Financial Strength to Execute

Leveraging discovery collaborations to generate non-dilutive capital and expand TPD beyond our core focus areas

Platform Collaborations Expand TPD Reach

Progressing potential first-in-class degraders focused on INN diseases to build a sustainable pipeline

Discovery Strategy Focused on INN

(Inflammation, Neuroinflammation, and Neurodegeneration)

Establishing cemsidomide as a potential foundational therapy for the potential treatment of MM across multiple lines of therapy

Potential Best-in-Class IKZF1/3 Degrader for MM

To become a fully integrated biopharmaceutical company

Multiple myeloma (MM); Non-small cell lung cancer (NSCLC); Targeted Protein Degradation (TPD)

C4T is Focused on Advancing Potential Best-in-Class And First-in-Class Degraders Across Clinical Oncology Portfolio and INN Discovery Strategy

Q1 2026 Key

Accomplishments:

First patient dosed in cemsidomide Phase 2 MOMENTUM trial

First patient dosed in cemsidomide Phase 1b trial in combination with elranatamab

Expanded long-term partnership with Roche through new collaboration agreement focused on discovering and developing DACs

Received a $2 million milestone payment for designing and delivering a second degrader to Biogen for clinical development

Shared plan to initiate a Phase 1b trial evaluating cemsidomide with approved multiple myeloma therapies

Advance potential best-in-class and first-in-class degraders

Enroll 2 clinical trials with cemsidomide to address 2L+ and 4L+ opportunities in MM

Establish combinability profile with cemsidomide + elranatamab1

Optimize indication selection for multiple targets across discovery portfolio

Position for regulatory success and pipeline build

Complete enrollment for Phase 2 MOMENTUM trial

Initiate additional Phase 1b trial

Present two cemsidomide data readouts:

Initial ORR data from Phase 2 MOMENTUM trial

Phase 1b data w/ elranatamab1 to support advancement to Phase 3 trial

Start up activities for Phase 3 cemsidomide + BCMAxCD3 Bispecific

Advance internal discovery pipeline to enable INDs

Unlock value

across portfolio

Initiate and enroll Phase 3 trial of cemsidomide + BCMAxCD3 Bispecific

Present efficacy and safety data from the Phase 2 MOMENTUM trial

Potentially submit NDA for cemsidomide

Deliver 3 potential INDs from discovery pipeline in INN indications

Pfizer supplying elranatamab (ELREXFIO®), a B-cell maturation antigen CD3 targeted bispecific antibody, to C4T for the Phase 1b trial

Dexamethasone (dex); Inflammation, Investigational new drug (IND); New Drug Application (NDA); Overall response rate (ORR); Inflammation, Neuroinflammation, Neurodegeneration (INN); Accelerated approval (AA); Multiple myeloma; Degrader antibody conjugates (DACs)

Focused Pipeline Advancing Clinical Oncology Degraders and a New Discovery Strategy in Inflammation, Neuroinflammation & Neurodegeneration (INN) Diseases

RESEARCH &

PROGRAM

TARGET

INDICATIONS

PRECLINICAL

PHASE 1

PHASE 2

PHASE 3

NEXT MILESTONE

CLINICAL

ONCOLOGY

PORTFOLIO

Cemsidomide

IKZF1/3

4L+ Multiple Myeloma

Phase 2 MOMENTUM tria

w/ dex

Q1 2027: Complete

enrollment

2H 2027: Present initial ORR data

2L+ Multiple Myeloma

Phase 1b trial w/ elranatam

ab2

2026: Provide incremental updates

Mid-2027: Present Phase 1b data from all cohorts

CFT89191

EGFR L858R

Non-Small Cell Lung Cancer

INN

DISCOVERY

Discovery

Novel targets in pathways of:

-IL-23/IL-17

-Type 1 IFN

-MAPK, PI3K/AKT, NF-kB

INN

Inflammation, Neuroinflammation & Neurodegeneration

By year-end 2026: Optimize indication selection for multiple targets

License and collaboration agreement with Betta Pharmaceuticals for development and commercialization in Greater China

Pfizer supplying elranatamab (ELREXFIO®), a B-cell maturation antigen CD3 targeted bispecific antibody, to C4T for the Phase 1b trial Dexamethasone (dex)

Strategic Platform Collaborations Expand Potential Reach of C4T TPD Medicines

Ongoing Collaborations

Evaluating targets in autoimmune diseases & oncology

Advanced two programs to preclinical milestones1

By year-end 2026: Deliver at least one development candidate to collaboration partner

Discovering and developing DACs for two programs against oncology targets

Discovering targeted protein degraders against critical oncogenic proteins

Achieved preclinical milestone from a project within the KRAS family

Delivered two development candidates (IRAK4 and BTK) for non-oncology targets2

Both development candidates are now in Phase 1 clinical development

Earned and received preclinical milestones in Q1 2025

Delivered development candidates to Biogen in Q1 2025 and Q3 2024. In Q3 2025, the IRAK4 degrader, BIIB142, entered Phase 1 clinical development and in Q1 2025, the BTK degrader, entered Phase 1 clinical development Targeted Protein Degradation (TPD); Degrader antibody conjugates (DACs)

Cemsidomide

IKZF1/3 Degrader

Multiple Myeloma

Cemsidomide is Positioned for Success in Multiple Myeloma

Despite recent approval for immune-based therapies in the MM landscape, IKZF1/3 are central drivers of MM development and progression, thus IKZF1/3 degraders will remain relevant across multiple lines and in combinations

Cemsidomide has a potential best-in-class profile among other IKZF1/3 degraders, including CELMoDs®, in a large and growing multiple myeloma market with a clinically and commercially de-risked MOA

Two ongoing trials with a third trial expected to start next year to support

cemsidomide's potential to become a foundational MM treatment

Multiple myeloma (MM)

CELMoDs® is a registered trademarks of BMS

IKZF1/3 are Transcription Factors That are Central Drivers of Multiple Myeloma Development and Progression

), CELMoDs® ( Iberdomide

Mezigdomide

Hematopoietic Stem Cell

IKZF1/3

Common Myeloid Progenitor Cell

Common Lymphoid Progenitor Cell

IRF4

Neutrophil

Platelets

B-Cell

Plasma Cell

Oncogenic Mutations/Aberrations

Multiple Myeloma IKZF1/3 and IRF4

T-cell Activation

Adapted from Chen and Gooding, 2022

IKZF1/3

Degrader

Key Roles of IKZF1/3

Physiological Functions:

IKZF1/3 directly regulate the activity of IRF4, another transcription factor that regulates downstream immune cell differentiation

Oncogenic Functions:

Multiple myeloma cells rely on

IKZF1/3 and IRF4 for survival

IKZF1/3 Degradation Leads to:

Downregulation of IRF4 promoting myeloma cell death

T-cell activation

On-target neutropenia

Multiple myeloma (MM)

IMiDs® and CELMoDs® are registered trademarks of BMS

First-generation IKZF1/3 Degraders (IMiDs®) Have Limitations Supporting the Need for Next-generation IKZF1/3 Degraders

First-generation IKZF1/3 degraders limitations:

High to moderate renal clearance

decreasing tolerability

~50% of MM patients suffer from renal impairment1

Limited selectivity resulting in off-target non hematology toxicities

Potency not optimized resulting in modest on-target degradation thereby limiting anti-myeloma activity

First-gen IKZF1/3 degraders' potency

vs. Next-gen IKZF1/3 degraders

(illustrative graphic)

Next-gen IKZF1/3 Degraders:

(Iberdomide, Mezigdomide, Cemsidomide)

Least to Most Potent IKZF1/3 Degraders

Rana 2020 Blood Advances.

Multiple myeloma (MM); First-generation (First-gen); Next-gen (Next generation) IMiDs® are registered trademarks of BMS

Data from Phase 1 Trial Support Cemsidomide as a Potential Best-in-Class Next-generation IKZF1/3 Degrader for Use Across Multiple Lines of Treatment Data cutoff as of 9/10/2025

Heavily Pre-treated Patient Population Representative of current multi-refractory patients

~75% of cemsidomide treated patients received prior BCMA therapy vs. 12% of mezi treated patients and N/A for iber5 treated patients

100% triple-class exposed

100% prior anti CD-38 mAb

3-22 prior lines of therapy

Differentiated safety profile

No dose discontinuations related to cemsidomide4

Grade 3/4 neutropenia: 59% (43/73)

Only 6% dose reductions due to TEAEs

Mezi: 25% dose reductions due to AEs

Iber: 24% dose reductions due to TEAEs

Phase 1 trial of cemsidomide + dex

One patient achieved an MRD negative CR3

10%

Cemsi N=72*

Cemsi N=19

Mezi N=11

0%

Mezi N=77

Iber N=13

ORR Across all Doses

ORR at Highest Dose Level

Cemsi Dose Escalation Mezi Dose Escalation1 Iber Dose Escalation2

20%

25%

30%

31%

32%

36%

40%

50%

53% 55%

60%

Cemsidomide demonstrated compelling anti-myeloma activity with a wide therapeutic index in the Phase 1 dose escalation trial

Iber N=90

Cross-trial comparisons should be used with caution and only as benchmarks for relative comparison; no head-to-head studies have been conducted

Sources: 1.Richardson 2023 NEJM. 2. Phase I dose escalation (Lonial 2022 Lancet Haematology) 3. Unable to determine MRD negativity for one additional patient as the patient did not consent to a biopsy 4. Patient at 75 µg discontinued due to grade 5 AE of septic shock, deemed unrelated to cemsidomide 5. Dose escalation trial was conducted from 2016 - 2020 and BCMA therapies were not approved until 2021

*1 patient in the 62.5µg cohort did not have a post-baseline assessment

Mezigdomide (Mezi); Iberdomide (Iber); Adverse events (AEs); Treatment emergent adverse events (TEAEs); Overall response rate (ORR); Cemsidomide (Cemsi); Minimal residual disease (MRD); Complete response (CR);

Dexamethasone (Dex)

Based on the Mechanism of Action, IKZF1/3 Degraders Are Foundational Therapies Across Multiple Lines of Treatment and Combinations

~11K

MM patient deaths expected in the U.S. in 20264

~40%

of MM patients are not surviving beyond five years, despite recent treatment advance5

~$25.5B

Is the expected revenue for RRMM in U.S., Japan, EU4+UK by 20342

~$59B

Total projected MM market in U.S., Japan, EU4+UK by 20342

Treatment Landscape of Approved MM Agents1

= IKZF1/3 degrader regimens

present across multiple lines of therapy

IKZF1/3 degraders remain relevant across multiple lines of therapy

Unmet need for an IKZF1/3 degrader that is well-tolerated with compelling anti-myeloma activity

2/3 Line

4/5+ Line

GPRC5D bispecific

BCMA bispecific3

Anti-CD38 regimen rechallenge

Selinexor based regimen

BCMA bispecific

PI + IKZF1/3

degrader doublets for frail patients

Anti-CD38 + PI +

dex

PI + IKZF1/3

degrader doublets for frail patients

Anti-CD38 + PI +

IKZF1/3 degrader

+ dex

Anti-CD38 mAB +

IKZF1/3 degrader

+ dex

Anti-SLAMF7

based regimens

Anti-CD38 mAB + IKZF1/3 degrader

+ dex

PI + IKZF1/3

degrader

+ dex

Anti-CD38 + PI +

IKZF1/3 degrader

+ dex

CAR-T

1.NCCN guidelines 2. Datamonitor (accessed 5/1/2026) 3. Linovesltamab is only approved in 5L 4. American Cancer Society; 5. Myeloma Patients Europe. Myeloma A Patients Guide; Updated May 2022. Available from: https://www.mpeurope.org/wp-content/uploads/2023/01/Myeloma-Patients-Guide.pdf ; Mikhael, J, Ismaila N, Cheung M, et al. Treatment of multiple myeloma: ASCO and CCO joint clinical practice guideline. J Clin Oncol. 2019;37(14):1228-1263.

Multiple myeloma (MM); dexamethasone (dex)

Cemsidomide Has the Potential to Be a Foundational Treatment Across Multiple Lines of Multiple Myeloma

Three strategic paths to capture multi-billion dollar opportunities

Late-line Opportunity

Combination with dexamethasone

R A T I O N A L E

No other next-generation IKZF1/3 degrader being developed for this line of treatment

Unmet need for an all-oral treatment regimen that is both well-tolerated and efficacious for patients who have exhausted all options

Near-term value

S T A T U S

Novel Combination

Combination with BCMAxCD3 Bispecific

R A T I O N A L E

For use in earlier lines

Cemsidomide to be established as the IKZF1/3 degrader of choice for novel combinations

Complementary MOA via T-cell activation

while maintaining potent anti-myeloma effect

S T A T U S

IMiD® Replacement Across Lines

Combination with a PI or CD38 antibody

R A T I O N A L E

Opportunity to improve upon first-generation IKZF1/3 degraders

Establish dose of cemsidomide for potential standard of care combination approaches

S T A T U S

Enrolling Phase 2 MOMENTUM Trial

Cemsidomide + dexamethasone

Enrolling Phase 1b Trial

Cemsidomide + dexamethasone + elranatamab3

Initiation of Phase 1b Trial w/ Two Arms Expected in 1H 2027

Cemsidomide + dexamethasone + PI

Cemsidomide + dexamethasone + CD38 antibody

S U P P O R T I V E P R O O F - OF - C O N C E P T

Data from the Phase 1 trial of cemsidomide + dexamethasone presented in September 2025, demonstrated a potential best-in-class profile

S U P P O R T I V E P R O O F - OF - C O N C E P T

Data from MagnetisMM-30 trial1 demonstrates proof-of-concept for combination with opportunity to improve depth of response

S U P P O R T I V E P R O O F - OF - C O N C E P T

Upcoming data from the EXCALIBER RRMM trial2 and SUCCESSOR-1 trial4

GOAL: Develop a potential best-in-class IKZF1/3 degrader to become partner of choice for MM treatment

1. Clinical trial evaluating elranatamab in combination with iberdomide in RRMM; 2.EXCALIBER RRMM trial is a Phase 3 trial comparing iberdomide, daratumumab and dexamethasone versus daratumumab, bortezomib, and dexamethasone 3 . Pfizer supplying elranatamab (ELREXFIO®), a B-cell maturation antigen CD3 targeted bispecific antibody, to C4T for the Phase 1b trial. 4. SUCCESSOR-1 is a Phase 3 trial evaluating mezigdomide, bortezomib, dexamethasone versus pomalyst, bortezomib, dexamethasone

Cemsidomide is an oral IKZF1/3 degrader, advancing through clinical development, with a potential best-in-class profile:

Demonstrated t-cell activation across clinically relevant doses as a monotherapy and in combination w/ dexamethasone

Elranatamab is a BCMAxCD3 Bispecific approved as a monotherapy for patients with RRMM who have received

≥1 IMiD®, ≥1 PI, and ≥1 anti-CD38 mAb1-2

Based on Complementary Mechanisms of Action, Cemsidomide in Combination with Elranatamab Has Potential to Provide Additional Benefit to Patients

Myeloma cell

Elranatamab

BCMA-binding arm

BCMA

Cemsidomide

Cytokines, perforin, granzymes

CD3

CD3-binding arm

T cells, activated by CD3 binding, release cytokines and perforin/granzymes, resulting in myeloma cell lysis

T cell

Ubiquitin

↓myeloma cell survival

↓myeloma cell proliferation

Enhanced myeloma cell killing with elranatamab + cemsidomide

IKZF1/3

↑immunomodulation

Elranatamab + cemsidomide + dexamethasone may provide additional benefit to patients with RRMM based on the complementary mechanisms of action

1. Elrexfio (elranatamab-bcmm). Prescribing information. Pfizer Inc; 2025. 2. Elrexfio (elranatamab-bcmm). Summary of product characteristics. Pfizer Europe MA EEIG; 2024

B-cell maturation antigen (BCMA); Immunomodulatory drug (IMiD); Monoclonal antibody (mAb); Proteasome inhibitor (PI); Relapsed or refractory multiple myeloma (RRMM); Cereblon (CRBN)

Early IKZF1/3 Degrader + BiTE Data Provide Proof of Concept for Cemsidomide with Opportunity For Improvement

Currently CAR-Ts demonstrate higher ORR and >CR than BiTEs alone1

Early data from IKZF1/3 degrader + BiTE combo support POC for similar anti-myeloma activity to CAR-Ts with better overall profile, but opportunity to improve depth of response

Combination is safe

Early evidence of anti-myeloma activity

100%

80%

60%

40%

20%

0%

BiTE

CAR-T

BiTE + IKZF1/3

BiTE

CAR-T

CEMSIDOMIDE DEVELOPMENT RATIONALE IN 2L+ IN COMBO WITH A BITE

Differentiated safety profile

Compelling anti-myeloma activity

across the highest 3 doses

T-cell activation observed across all cemsidomide dose levels

Phase 1b trial with elranatamab3 will evaluate MRD negative responses

Opportunity to improve BiTE response rate including depth of response

BiTE + IKZF1/3

~58%

- 70%

~44%

~26%

- 45%

~74%

~85%

>90%

Cemsidomide is well-positioned to provide further differentiation to BiTE combination

ORR Range >CR Range

Sources: 1. Packaging Insert for each product (carvykti - accessed 8/26/25 and, tecvayli; elrexflo; lynozyfic - accessed 2/27/26) - the data is not a head-to-head trial; 2. 2025 ASH ORR data at each dose level from Phase 1b MagnetismMM-30 trial evaluating iberdomide + elranatamab 3. Pfizer supplying elranatamab (ELREXFIO®), a B-cell maturation antigen CD3 targeted bispecific antibody, to C4T for the Phase 1b trial

Bispecifc T-cell engager (BiTE); Overall response rate (ORR); Complete response (CR); Combination (combo); Minimal residual disease (MRD)

Phase 2 MOMENTUM Trial of Cemsidomide + Dex in 4L+ MM Now Enrolling Patients

2H 2027: Phase 2 initial ORR data

Potential for accelerated approval

Phase 2 MOMENTUM

Cemsidomide + dex (single arm) 4L+

N = ~100

Dose: 100 µg QD

Enrollment Expected to Complete in Q1 2027

PHASE 2 MOMENTUM TRIAL DESIGN:

Endpoints:

ORR per IMWG response criteria assessed by independent review committee

20% increase over a

background rate of 20%

RP2D: 100 µg

Schedule: QD 14/14

Dexamethasone (dex); Overall response rate (ORR); Fourth line (4L); Recommended Phase 2 dose (RP2D); Overall response (ORR); International Myeloma Working Group (IMWG); Once daily (QD)

Phase 1b Trial is Evaluating Safety and Tolerability of Cemsidomide in Combination With Elranatamab, With Data From All Cohorts Expected in Mid-2027

PHASE 1b TRIAL DESIGN:

Primary Objectives:

Characterize the safety and tolerability of cemsidomide in combination with elranatamab

Dosing Regimen:

Cemsidomide: QD 14/14

Dexamethasone: QW through cycle 4

Elranatamab1

Key Differentiators:

Evaluated with dex, which may help manage neutropenic complications

Focused on evaluating MRD negativity rates to demonstrate depth of response

Trial Initiated in Q1 2026; Enrollment Ongoing

Potential to expand at each dose level once combination is declared safe

Cemsidomide

Dose Level: 100 µg

+ Elranatamab

Elranatamab step-up dosing without cemsidomide

Cemsidomide

Dose Level: 75 µg

+ Elranatamab

If 75 µg is declared safe, potential to simultaneously evaluate 50 µg and 100 µg

Cemsidomide

Dose Level: 50 µg

+ Elranatamab

1. Pfizer will supply elranatamab (ELREXFIO®), a B-cell maturation antigen CD3 targeted bispecific antibody, to C4T for its upcoming Phase 1b trial Dexamethasone (dex); Once daily (QD); Once weekly (QW)

Discovery

Inflammation, Neuroinflammation, & Neurodegeneration (INN)

i[;j, C4 Therapeutics

New Discovery Strategy Focused on Inflammation, Neuroinflammation & Neurodegeneration (INN) with First-in-Class Potential in Clinically Validated Pathways Uniquely Suited for TPD

Leveraging C4T's

success

C4T HAS CONSISTENTLY DEVELOPED ORALLY BIOAVAILABLE HIGHLY CATALYTIC HETEROBIVALENT DEGRADERS THAT…

Penetrate the blood brain barrier to achieve high central nervous system exposures and compelling efficacy in central nervous system models

Control target protein levels through finely-tuned degrader kinetics

Maximizing value through target selection

TARGET-TO-DISEASE LINK:

Selecting targets that modulate clinically validated pathways in inflammation, neuroinflammation, and neurodegeneration (INN) to enhance efficacy

Focusing on early clinical validation with opportunity to grow value through indication expansion

STRONG DEGRADER RATIONALE:

Strong competitive positioning

Clear and compelling advantage for a degrader over an inhibitor

EXPANDED CAPABILITIES:

Extended capabilities to identify molecular glue degraders for targets with

and without G- and RT-loops by utilizing DNA-encoded library

(DEL) technology

Targeted Protein Degradation (TPD); Central nervous system (CNS)

Focused on Inflammation, Neuroinflammation & Neurodegeneration (INN) to Address High Unmet Needs in a Large Patient Population with a Clear TPD Advantage

Degraders have the

Fast path to clinical

Normalize elevated

Large market

potential to

proof-of-concept,

protein levels without

opportunities with

outperform inhibitors

including early

the need for

high unmet

in efficacy and safety

in CNS diseases1

validation based on PD markers in healthy volunteers

complete elimination of the target

medical needs

Deploying TPD where the MOA is uniquely positioned to have an advantage over inhibitors to help benefit patients in a large market

Central nervous system (CNS), Pharmacodynamic (PD); Targeted Protein Degradation (TPD); Mechanism of action (MOA)

1. Based on preclinical evidence and working hypothesis

Disclaimer

C4 Therapeutics Inc. published this content on May 12, 2026, and is solely responsible for the information contained herein. Distributed via Public Technologies (PUBT), unedited and unaltered, on May 12, 2026 at 11:23 UTC.