Pipeline

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.

PROGRAM

MECHANISM

INDICATIONS

RESEARCH

IND-ENABLING

PHASE 1

PHASE 2

S-4321

PD-1:FcγRIIb agonist antibody

Cell-Mediated Immune Diseases

Phase 1b

S-4321 is a bifunctional PD-1:FcγRIIb agonist antibody that simultaneously engages two inhibitory checkpoints to restore immune balance in autoimmune and inflammatory disease.

Attenuates overactive Teff (effector T) cells through affinity-tuned PD-1 agonism to put the “brakes” on overactive immune cells
Protects and strengthens Treg (regulatory T) cells through PD-1 agonism to promote immune homeostasis
Reduces inflammation through precision targeting of FcγRIIb-mediated B cell inhibition and cytokine avoidance

S-6204

IgE-targeted dissociator

Allergic Diseases

S-6204 is a multi-functional, IgE-targeted, single-domain antibody designed to disarm the cells that drive allergic responses at their source, for the treatment of allergic and atopic diseases.

Dissociates IgE from effector cells: rapidly and deeply removes bound IgE from mast cells and basophils, disarming them at the source
Neutralizes circulating IgE: binds soluble IgE to prevent it from binding or re-binding and triggering an allergic response
Dampens effector cell activation: FcγRIIb-selective Fc domain blocks activation of mast cells and basophils

Undisclosed

Exploratory