Celcuity : Corporate Presentation (Celcuity Investor Presentation V.6.12 Final)

Published: 2025-06-30 13:47:07 ET CELC

Published on 06/30/2025 at 13:47

June 2025

The Celcuity Opportunity

1 • Gedatolisib's differentiated MOA and PK profile result in a highly potent, cytotoxic, and well tolerated PAM inhibitor

2

Very compelling data in 1L (mPFS 48 months) and 2L (mPFS 12.9 months) patients with HR+/HER2- ABC

A Phase 3 study in 2L patients is enrolling and a Phase 3 study in 1L patients is expected to begin enrolling in Q2 2025

3

Strong scientific rationale to develop gedatolisib for prostate cancer indications

Parallels between breast and prostate cancer - interdependent activity between PAM pathway and hormonal pathways

4

Uniquely positioned to advance multiple potential blockbuster indications in breast and prostate cancer

Cash, cash equivalents and short-term investments of $205M as of Q1 2025 expected to fund operations through 2026

3

One of the most important oncogenic pathways

Most highly altered of all signaling pathways1

Largest untapped drug development opportunity in solid tumors

Breast and prostate cancers involve PAM pathway

>500,000 addressable patient population in US, 5EU, and Japan

Nominal penetration of PAM drugs in these markets

PI3K/AKT/mTOR (PAM)

regulates key metabolic functions

Plays a key role promoting tumor cell proliferation

Cross-regulates other oncogenic pathways

Affects immune response by regulating tumor microenvironment

Proportion of alterations correlates to pathway's role as a cancer driver

PAM

38%

RAS

15%

HER2

8%

EGFR

5%

(1) cBioPortal References:Cerami et al., Cancer Discov. 2012, and Gao et al., Sci. Signal, 2013;

4

1st Gen

Oral pan-PI3K/mTOR inhibitors

Toxicity high, poor PK properties Failed in Phase 1/2

2nd Gen

Pan-PI3K inhibitors

Significant toxicity Failed in Phase 3

3rd Gen

Single-target inhibitors

Limited PFS benefit Four drugs approved

Today

Need safe, potent pan-PI3K/mTORi

If only a single target is inhibited, redundancy ensures pathway function is maintained1-9

Feedforward and feedback loops between PI3K isoforms, AKT, and mTOR cross-activates uninhibited targets1-9

Explains why 1st generation of PAM inhibitors were pan-PI3K/mTOR inhibitors

Difficult to optimize pathway inhibition without inducing undue toxicity

Early generations of orally administrated pan-PI3K or pan-PI3K/mTOR inhibitors induced unacceptable toxicity10

Led to focus on development of single-node

PAM inhibitors (e.g. PI3Kα, mTORC1, AKT)

Sources: (1) Juric 2015 Nature. 518:240-244; (2) Castel 2021 Nat Cancer. 2:587-597; (3) Mao 2021 Nat Commun. 12:5053; (4) Schwartz 2015 Cancer Cell. 27:109-122. (5) Chandarlapaty

2011, Cancer Cell. 19:58-71; (6) Bago 2016, EMBO J. 35:1902-1922; (7) Manning 2017, Cell. 169:381-405.; (8) Mukherjee 2021, Mol Cell. 81:708-723 e705 (9) Elkabets 2013, Sci Transl

Med; 5(196); (10) Alves 2023, Int. J. Mol. Sci., 24, 4522 5

Disclaimer

Celcuity Inc. published this content on June 30, 2025, and is solely responsible for the information contained herein. Distributed via Public Technologies (PUBT), unedited and unaltered, on June 30, 2025 at 17:46 UTC.