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Therapeutics

IBIO-101

Solid Tumors and Unmet Needs

Advances in the field of immuno-oncology have led to new and better treatment outcomes for a range of cancers, and particularly, blood cancers. However, even with the advent of checkpoint inhibitors as immunotherapies for solid tumors, significant challenges remain. This is in part due to dynamics in the tumor microenvironment, wherein regulatory T cells [Tregs] proliferate and suppress the immune responses to tumor cells.

The Treg is a type of T cell that is important in preventing autoimmunity by keeping effector T cells [Teffs] “in-check” to prevent destruction of healthy tissues. However, around tumors, Tregs create an immunosuppressive environment and block the work of Teffs to do what they do well – kill cancer cells. So, targeting depletion of Tregs to control tumors has emerged as an area of interest in oncology over the past several years.

Fortunately, Tregs express a protein, CD25, that allows them to be killed with an anti-CD25 antibody. Unfortunately, that protein is part of the interleukin-2 [IL-2] signaling, which also activates Teffs. This is what has presented a challenge; anti-CD25 antibodies can deplete Tregs, but unless they have certain characteristics, those antibodies also prevent Teffs from cancer cell killing, thereby resulting in a failure as a therapeutic to control tumor growth and metastasis.

iBio’s Approach

IBIO-101 has a novel mechanism of action that in preclinical studies has been shown to enable it to effectively bind CD25 on Tregs, but does so without blocking the IL-2 signaling pathway to Teffs. This has been the key challenge with most, but not all, other anti-CD25 mAbs.

IBIO-101 stimulates anti-tumor immunity by depleting immunosuppressive Treg cells via engagement with Natural Killer [NK] Cells

RTX-003 preferential depletion of T-reg, described in text

IL-2 signaling in Teff cells is preserved by targeting of a privileged epitope on the CD25 molecule, allowing Teffs to proliferate and control tumor growth

Development Status

Anti-tumor responses have been observed in pre-clinical models of disease using IBIO-101 as a monotherapy, as well as in combination with checkpoint inhibitors.
Line graph of Tumor Size to Days Post Engraftment. The control, line shows exponential tumor growth over 25 days. Where IBIO-101 was administered, tumor growth rate decreases.

In a colon cancer xenograft model, IBIO-101 alone dose-dependently inhibited tumor growth

Line graph of Tumor volume to Days Post Grouping. Minimal tumor growth observed when treated with IBIO-101 combined with PD1 antibody. Tumor volume increased when treated with either IBIO-101 or PD1 antibody alone, but were still lower than PBS samples.

In combination with a PD1 antibody, IBIO-101 reduced tumor growth in a humanized adenocarcinoma model

IBIO-101 was originally developed with a traditional mammalian-cell expression system. Using our proprietary Glycaneering℠ Technologies, we’re seeking to enhance antibody-dependent cellular cytotoxicity effects. We expect to then produce the molecule using the FastPharming System and initiate IND-enabling studies.

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Changing the Paradigm of Cancer Drug Discovery and Development with Plants

iBio’s Chief Scientific Officer, Martin Brenner, DVM, Ph.D.; Chief Operating Officer, Randy Maddux; and oncology pipeline advisor, Steven King, discuss how the FastPharming System® and iBio’s Drug Discovery Center are delivering on a range of opportunities for therapeutic discovery and development to bring prognosis-changing therapies to patients sooner.
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