A differentiated pipeline positions ImmunOS as a leader in the HLA field for both, immune-oncology and inflammatory diseases.
ImmunOS unique HLA-based molecules target specific checkpoints on various cells which are involved in inflammation or immune-oncology by using specifically tailored modalities.
The Company´s lead program, IOS-1002 (formerly iosH2), binds to and blocks the activation of specific leukocyte immunoglobulin-like receptors (LILRBs, also known as ILTs, i.e., immunoglobulin-like transcripts) and killer cell immunoglobulin-like receptors (KIRs) and has the potential to treat multiple types of solid tumors and hematologic malignancies. Specifically, IOS-1002 binds to LILRB1 (ILT2), LILRB2 (ILT4), and KIR3DL1 receptors on innate and adaptive immune cells that suppress immune responses when activated. IOS-1002 is designed as a potential monotherapy and as a combination therapy to improve medical outcomes in non-responders and patients that have progressed on currently approved adaptive immunity therapies. IOS-1002 is differentiated from competitor approaches as it targets multiple LILRB receptors and a KIR receptor instead of a single checkpoint receptor.
In non-clinical assays IOS-1002 has demonstrated activity against a variety of myeloid cells as well as T cells and NK cells (Rafiei et al, Cancers 2024). IOS-1002 activates immune cells to kill tumor cells through blocking the inhibitory activity of LILRB and KIR receptors expressed on innate and adaptive immune cells and through Fc-mediated activation of FcγR on immune cells. .
IOS-1002 is currently in phase I clinical trials in cancer patients with solid tumors. The trial design includes both a monotherapy arm as well as an arm with IOS-1002 in combination with an anti-PD1 antibody (Pembrolizumab) and evaluates the safety, tolerability and efficacy of IOS-1002.
IOS-1002 combines potentially multiple Mechanisms of Action by avidity: antogonistic on LILRB1/2 and KIR3DL1 and blocking their inhibotory activity and agonistic on FcγRs by activating them.
Immunosuppressive pathways are activated in both myeloid cells and tumor cells as a mechanism to create an immunosuppressive microenvironment in tumors. These pathways regulate the activation of myeloid cells as well as the recruitment and targeting of activated NK and T cells to the tumor stroma. The non-clinical IO pipeline includes multi-specific molecules that target receptors that are activated within both immune cells as well as tumor cells. The multi-specific molecules incorporate LILRB receptor targeting and targeting CD47 receptors expressed on tumor cells that suppress the activation of tumor specific macrophages. These multi-specific molecules are currently in non-clinical assays to assess their activity against both myeloid derived cells as well as their direct effect on activating immune cells, including macrophages, to target and kill tumor cells.
Diagram below represent the anticipated Mechanism of Action for ImmunOs innovative bispecific program.
