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Science

Anti-PROX1 Retinal Regeneration Platform Technology

Unlocking retinal regeneration by targeting PROX1,
the key suppressor of Müller glia reprogramming.

Anti-PROX1 Retinal Regeneration Platform Technology

Unlocking retinal regeneration
by targeting PROX1, the key suppressor of Müller glia  eprogramming.

A Critical Barrier to
Regeneration

PROX1 is a transcription factor that suppresses the regenerative potential of Müller glia following retinal injury.
In damaged mammalian retina, PROX1 is transferred to Müller glia and prevents the natural reprogramming process required for tissue repair.

Suppression

Suppresses Regenerative
Gene Expression

Müller Glia

Fails cellular reprogramming

Vision Loss

Limits functional recovery

Suppression

Suppresses Regenerative
Gene Expression

Müller Glia

Fails cellular reprogramming

Vision Loss

Limits functional recovery

One Platform,
Multiple Opportunities

Celliaz’s Anti-PROX1 regenerative platform is designed
to address multiple retinal diseases exhibiting a common
Müller glial PROX1 transfer.

Expanding the Future of Regenerative Medicine

From retinal regeneration to broader therapeutic opportunities.

Expanding the Future of Regenerative Medicine

From retinal regeneration to broader therapeutic opportunities.

Discover the Next Stage of
Our Pipeline

Discover the Next Stage
of Our Pipeline

CREATING A NEW THERAPEUTIC
PARADIGM FOR DEGENERATIVE DISEASES

Tissue Regeneration
By Homeoprotein Targeting Therapies.

Contact

Celliaz Co., Ltd.
205 Jinri Hall, KAIST Munji Campus
193 Munji-ro, Yuseong-gu
Daejeon 34051, Republic of Korea

Phone

+82-42-716-4061

E-mail

 info@celliaz.com

© 2026 Celliaz Co., Ltd. All Rights Reserved.

Retinal Regeneration
Through Homeoprotein Science

Advancing retinal regeneration
through homeoprotein-based
therapeutics.

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Contact

Celliaz Co., Ltd.
205 Jinri Hall, KAIST Munji Campus
193 Munji-ro, Yuseong-gu
Daejeon 34051, Republic of Korea

Phone

+82-42-716-4061

E-mail

 info@celliaz.com

© 2026 Celliaz Co., Ltd. All Rights Reserved.