Our development pipeline comprises THREE PROJECTS – two autologous cell therapies targeting the novel master checkpoint inhibitor Cbl-b, and a small molecule project addressing a novel, undisclosed IMMUNO-ONCOLOGY target. Our lead cell therapy project is currently in CLINICAL PHASE 1 trials, while the other two candidates are in PRE-CLINICAL development.
|DISCOVERY||PRECLINICAL||PHASE 1||PHASE 2||PHASE 3|
autologous cell therapy targeting Cbl-b
first-in-human trial completed
adoptive cell therapy – TIL activation in solid tumors
|Novel IO targets||INV501|
oral application for tumor-specific immune activation
APN401 is an AUTOLOGOUS CELL THERAPY using siRNA mediated silencing of Cbl-b resulting in highly activated tumor-reactive white blood cells. APN401 is currently in a CLINICAL PHASE 1B TRIAL in patients with various solid tumors.
Amplification of effects with each cycle
For APN401, we use our proprietary manufacturing platform EPiC, which enables the generation of autologous anti-tumor immune cells with short treatment times in an out-patient setting. MULTIPLE TREATMENT CYCLES using freshly isolated PBMCs may increase the memory effect and can lead to an ENRICHMENT OF ANTI-TUMOR IMMUNE CELLS counteracting the treatment-induced resistance of cancer cells.
We have completed a first-in-human trial showing that single and multiple dose infusions of APN401 were safe and well tolerated, with no serious side effects observed.
Currently, a Phase 1b trial is ongoing at multiple clinical study centers in Austria. Part A of this trial is a multiple ascending dose in patients with various solid tumors (completion expected in Q2 2022). In Part B the maximum tolerated dose will be used in three distinct solid tumor indications to generate first data on clinical efficacy (study end expected in Q4 2023).
INV441 is an AUTOLOGOUS CELL THERAPY delivered via our EPiC platform that uses Tumor Infiltrating Lymphocytes (TILs) silenced for Cbl-b expression leading to HIGH POTENTIAL for tumor cell killing.
INV441 uses Tumor Infiltrating Lymphocytes (TILs) directly from the patient. USING EPiC, TILs are silenced for Cbl-b via siRNA leading to RE-ACTIVATION OF ANTI-TUMOR IMMUNITY. These freshly modified TILs are resistant to the immune-suppressive tumor microenvironment (TME).
1) Solid tumors are recognized by lymphocytes
2) The tumor microenvironment (TME) contains suppressive immune cells
3) Tumor infiltrating lymphocytes (TIL) could destroy the tumor but are inhibited by the TME
4) TILs upregulate Cbl-b in the TME, thus contributing to immune suppression
5) Mode of action of INV441: Cbl-b silenced TILs are re-activated specifically against the tumor and resist inhibition by TME
INV501 is a novel SMALL MOLECULE in pre-clinical development for tumor-specific immune activation upon ORAL APPLICATION.
INV501 activates tumor-specific immune cells by BINDING TO AN UNDISCLOSED TARGET currently under investigation.
We screened a small molecules library for their potential to enhance T cell activity in an antigen-specific manner (High Throughput Screen – HTS). This resulted in the identification of a distinct substance class, which has been developed further resulting in a lead candidate with profound capacity for TUMOR-SPECIFIC IMMUNE ACTIVATION.
INV501 is highly effective in tumor-specific immune cell activation as exemplified in in vitro cellular assays and preclinical models. The small molecule entity offers a distinct BENEFICIAL PHARMACOLOGIC PROFILE allowing for patient-friendly oral application. INV501 represents a VERY PROMISING AND HIGHLY SPECIFIC APPROACH for the treatment of various tumor indications.
First pre-clinical results show promising data on growth inhibition in a B16 melanoma model after oral application of INV501.