THREE ELEMENTS FOR OUR SUCCESS IN SCIENCE

EPiC
CELL THERAPY
PLATFORM

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  • invIOs’s innovative proprietary cell therapy platform
  • Applicable and expandable with siRNA, mRNA, CRISPR, etc.

SMALL MOLECULE
IO PROJECT

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  • Tumor specific immune cell activation
  • Oral availability
  • Broad therapeutic application window

INNOVATION
HUB

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  • Seeking promising IO projects to expand our pipeline
  • Entrepreneurial infrastructure to accelerate programme development

EPiC CELL THERAPY PLATFORM

The FLEXIBILITY OF RNAi TECHNOLOGY could expand the applicability of cell therapy to additional checkpoints and holds enormous potential for new therapeutic approaches.

EPiC enables treatment of patients using their OWN IMMUNE CELLS with short treatment times in an out-patient setting. Targeting the most promising intracellular checkpoints leads to enhanced and prolonged activation of existing tumor-reactive immune cells after REINFUSION to the patient, resulting in a BOOST OF TUMOR CELL KILLING.

A) Cancer patient referred to specialized local hospital for sourcing of cells

B) EPiC – specific and temporary (re)activation of immune cells, e.g., intracellular targets or signaling molecules

C) Finalization of drug product

D) EPiC – on-site QC release

E) Reinfusion of patient’s own cells

Advantages of EPiC:

  • GMP-certified process already in use in our APN401 multi-center Phase 1b clinical trial
  • Easily transferrable using an established transfer process
  • Manufacturing facility to supply single (on-site) or multiple treatment centers
  • Simple logistics, with no cryopreservation

See our pipeline for further information about APN401.

siRNA-BASED CELL THERAPIES TARGETING CBL-B

Cbl-b is a negative regulator and a major signaling hub for the activation of tumor-specific immune cells

By “patching” siRNA to the Cbl-b mRNA, Cbl-b is silenced

Cbl-b deficiency activates a variety of immune cells for tumor destruction

Cbl-b is a negative regulator and a major signaling hub for the activation of tumor-specific immune cells

By “patching” siRNA to the Cbl-b mRNA, Cbl-b is silenced

Cbl-b deficiency activates a variety of immune cells for tumor destruction

Cbl-b is a negative regulator of immune cell activation and has been described as a “master checkpoint” in immune function. Disrupting Cbl-b expression by silencing the Cbl-b gene enhances T cell and NK cell activity and results in reduced tumor growth in animal models. Blocking the Cbl-b function thereby activates both adaptive (T cells) and innate (NK cells) anti-tumor mechanisms, leading to more effective tumor destruction.

APN401 and INV441 are autologous cell therapies designed to inhibit the immune checkpoint Cbl-b using RNAi technology to enhance the immune response in cancer patients. Additionally, they benefit from repeated dosing of freshly modified cells, reducing immune escape of cancer cells.

Cbl-b silencing leads to:

  • Proliferation of T cells
  • Anti-tumor adoptive immune responses
  • Production of cytokines such as IL-2
  • Central memory effects
  • Reduction in T cell exhaustion
  • Lower activation threshold

Cbl-b-silenced PBMCs show a clear increase in proliferation and production of certain cytokines such as interferon gamma (IFN-γ) and interleukin 2 (IL-2) in response to stimulation. Importantly, neither proliferation nor cytokine production are induced in unstimulated T cells, indicating that Cbl-b silencing enhances T cell responses only in the context of antigen stimulation. This approach is superior to generalized systemic activation of all lymphocytes or to systemic administration of cytokines, which are often associated with severe toxicity and may also have negative immunoregulatory effects. Specifically, Cbl-b deficiency enhances anti-tumor activity of T cells and NK cells in vitro, resulting in: enhanced expression of inflammatory cytokines and activation markers when stimulated via the T cell receptor (TCR); enhanced proliferation and anti-tumor cell cytotoxicity; resistance to transforming growth factor beta (TGF-β)-mediated immune suppression (T cells); and increased activation of NK cells upon cytokine stimulation or tumor cell contact.

SMALL MOLECULE IO PROJECT

Our latest project focuses on SMALL MOLECULES and their potential to enhance T cell activity in an antigen-specific manner (High Throughput Screen – HTS). With this technology, we have identified a distinct substance class, which has been developed further resulting in a lead candidate with profound capacity for tumor specific immune activation.

The small molecule entity offers a distinct beneficial pharmacological profile, allowing for patient-friendly ORAL APPLICATION.

INV501 is a promising therapy currently in the preclinical development.

For further information please check INV501 in our pipeline.

OUR INNOVATION HUB

DEDICATED TO DELIVERING LIFESAVING IMMUNO-ONCOLOGY TREATMENTS

invIOs has deep expertise and a PROVEN TRACK RECORD of successful preclinical/clinical development of cancer treatments and in-licensing of novel projects.

We want to EXPAND our immuno-oncology (IO) pipeline by leveraging our expertise to DEVELOP product candidates to clinical proof of concept and beyond.

WE AIM TO ACCELERATE PROJECTS USING OUR
WELL-ESTABLISHED
ENTREPRENEURIAL INFRASTRUCTURE

Highly experienced staff

Fully equipped lab

Collaboration network

Clinical operations department

CMC unit

Regulatory experts

Patent management

Back-office support

Finance

To complement our own scientific programs, we are looking for:

    • Innovative, first-in-class targets/projects for IO therapies
    • Availability of proof-of-principle data (in vitro or in vivo)
    • All oncology indications, including orphan diseases

Submit your request or project offer: innovation@invios.com