Pipeline - Seismic Therapeutic | Seismic Therapeutic

Abnormal function of the adaptive immune system drives a diverse set of chronic and acute immune-driven diseases. At Seismic, we are building a pipeline of novel biologics derived from our IMPACT platform focused on addressing the unmet need in dysregulated adaptive immunity to have a broad impact on patients.

We have emerging novel, first-in-class and best-in-class antibody and enzyme programs modulating the two arms of the adaptive immune system, cell-mediated immunity and humoral immunity. For diseases of cell-mediated immunity characterized by inappropriately activated T cells, we are discovering and developing multi-functional antibody therapies that activate multiple inhibitory pathways in more than one cell type to regulate both sides of the immune cell synapse. For diseases of humoral dysfunction causing allergic disease, we are discovering and developing several immunoglobin E (IgE) targeted programs. For diseases of humoral immunity driven by autoantibodies that recognize one’s own tissues, we are discovering and developing multiple types of immunoglobulin sculpting (IgSc) enzyme therapeutics that modify different pathogenic Ig, including immunoglobin G (IgG) proteases.

PD-1:FcγRIIb Agonist Antibody

For diseases of cell-mediated immunity caused by dysregulated T cells, we are discovering and developing multi-functional antibody therapies that activate multiple inhibitory pathways in more than one cell type to restore immune homeostasis on both sides of the immune cell synapse. Our most advanced clinical program is S-4321, a non-depleting PD-1:FcγRIIb bifunctional antibody, which agonizes PD-1, a well-known inhibitory checkpoint receptor on T cells, and selectively engages and agonizes the inhibitory Fc gamma receptor, FcγRIIb, on B cells and other antigen presenting cells.

*Teff/T effector cells (including activated CD4/CD8 T cells; Tph/T peripheral helper cells; Trm/Tissue resident memory cells and others)

IgE-Targeted Programs

For IgE-mediated allergic diseases, we are developing multiple approaches engineered to disarm effector cells and shut down allergic responses at their source. These include: (i) cleaving and eliminating circulating IgE through IgE-specific proteases, (ii) dissociating IgE from effector cells and down-modulating effector function with an Fc-fused IgE dissociator, and (iii) sweeping free IgE from the tissue and circulation.

Disabling IgE effector function

Inhibiting effector cell degranulation

Internalizing and degrading IgE

Pan IgG Proteases

For diseases of humoral immunity driven by antibodies that recognize self or transplanted tissues, we are discovering and developing multiple immunoglobulin sculpting (IgSc) enzyme therapeutics that modify different pathogenic Ig, including immunoglobin G (IgG) and IgM proteases.

Degrades circulating IgG and immune complexes

Eliminates IgG effector function including complement-dependent (CDC) and antibody-dependent (ADCC) cell killing

Prevents memory B cell activation and antigen presentation